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A    TEXT-BOOK 


PRACTICE  OF  MEDICINE. 


FOR  STUDENTS  AND  PRACTITIONERS. 


BY 

HOBART  AMORY  HARE,  M.D.,  B.Sc, 

PROFESSOR  OP  THERAPEUTICS  IN  THE    JEFFERSON    MEDICAL  COLLEGE   OF  PHILADELPHIA  ;    PHYSICIAN 

TO  THE  JEFFERSON  MEDICAL  COLLEGE  HOSPITAL  ;    ONE    TIME    CLINICAL    PROFESSOR  OF 

DISEASES   OF  CHILDREN  IN  THE  UNIVERSITY  OF  PENNSYLVANIA  ;    AUTHOR 

OF  "a  TEXT-BOOK  OF     PRACTICAL    THERAPEUTICS,"    AND 

"a  TEXT-BOOK  OF  PRACTICAL  DIAGNOSIS." 


SECOND  EDITION,  REVISED  AND  ENLARGED. 


ILLUSTRATED    WITH     131     ENGRAVINGS    AND    11     PLATES    IN 
COLORS    AND    MONOCHROME. 


LEA  BROTHERS  &  CO., 
PHILADELPHIA  AND   NEW  YORK. 

1907. 


H4^ 

Entered  according  to  the  Act  of  Congress,  in  the  year  1907,  by 

LEA  BROTHERS  &  CO., 
In  the  Office  of  the  Librarian  of  Congress.     All  rights  reserved. 


DORNAN,    PRINTER. 


PREFACE  TO  THE  SECOND  EDITION. 


In  presenting  the  second  edition  of  his  text-book  on  the  Practice  of 
Medicine  the  author  desires  to  express  his  appreciation  of  the  cordial 
reception  of  the  work  since  it  first  appeared,  a  reception  which  necessi- 
tated its  being  repeatedly  put  to  press. 

The  present  volume,  prepared  for  the  physician  and  student  of  medicine, 
embodies  the  experience  of  more  than  twenty-two  years  of  active  hospital 
and  private  practice,  during  which  time  the  author  has  been  constantly 
teaching  the  subjects  of  clinical  medicine  and  therapeutics.  With  this 
experience  he  has  attempted  to  present  the  facts  which  the  practitioner 
needs  and  which  the  student  must  thoroughly  grasp  if  he  is  to  be  successful 
in  gaining  his  degree  and  in  practising  his  art. 

In  the  preparation  of  many  portions  of  the  work  careful  collections  of 
statistics  have  been  made,  and  these  have  not  infrequently  given  results 
which  add  materially  to  our  conception  of  the  frequency  of  certain  dis- 
eases at  different  periods  of  life,  of  the  relative  frequency  of  different 
symptoms,  and  the  value  of  certain  plans  of  treatment. 

Particular  pains  have  been  taken  to  present  methods  of  treatment 
clearly  and  in  such  a  way  that  they  may  be  put  in  practice. 

Much  information  that  might  be  included,  which  deals  with  subjects 
which  are  still  uncertain  and  debatable,  has  been  excluded. 

Warm  thanks  are  due  to  my  colleague.  Dr.  W.  M.  L.  Coplin,  Professor 
of  Pathology  in  the  Jefferson  Medical  College,  for  valuable  suggestions  and 
criticisms,  in  which  he  has  shown  not  only  a  complete  grasp  of  his  own 
department  of  medical  study,  but  intimate  knowledge  concerning  the  latest 
developments  in  clinical  medicine. 

The  author  also  desires  to  acknowledge  the  valuable  suggestions,  made 
during  the  preparation  of  this  edition,  of  Dr.  Aller  G.  Ellis,  Demonstrator 
of  Pathology,  and  Dr.  Alfred  Gordon,  Instructor  in  Neurology  in  the  Jeffer- 
son Medical  College. 

The  fact  that  the  United  States  has,  within  the  last  few  years,  become 
possessed  of  territory  in  the  tropics  has  greatly  increased  our  interest  in 
the  many  tropical  diseases  heretofore  scarcely  known  by  practitioners  in  the 
temperate  zone,  and  the  investigations  by  surgeons  in  the  Army,  Navy,  and 

(iii) 


IV 


PREFACE 


the  Public  Health  and  Marine  Hospital  Service  have  thrown  much  light  upon 
these  aflfections.  Further  than  this,  the  investigations  by  English  physicians 
have  broadened  our  views  very  greatly  as  to  tropical  disease.  As  troops 
returning  from  tropical  service  often  bring  with  them  manifestations  of 
these  diseases,  it  behooves  every  practitioner  to  be  able  to  recognize  and 
treat  such  conditions.  It  seems  appropriate,  therefore,  that  a  modern  work 
on  medicine  should  contain  chapters  on  tropical  medicine,  the  more  so  as 
lectures  upon  this  subject  are  now  given  in  many  of  the  great  medical 
schools. 

In  the  preparation  of  this  second  edition  great  care  has  been  taken 
to  embody  the  latest  views  that  have  received  general  acceptance  as  being 
scientifically  and  chnically  correct,  it  being  constantly  borne  in  mind  that 
the  needs  of  the  student  and  practitioner  will  be  best  met  by  excluding 
statements  open  to  criticism  and  presenting  facts  which  will  prove  useful 
in  practice. 

H.  A.  H. 

Spruce  and  Eighteenth  Streets, 
Philadelphia,  January,  1907. 


CONTENTS. 


INFECTIOUS  DISEASES. 

PAGE 

Typhoid  Fever       ............  17 

Paratyphoid  Fever  .  .  .  .  .  .  .  .  .  .  .59 

Typhus  Fever         ............  61 

Relapsing  Fever     ............  68 

Variola  .  .  .  .  •  .  .  .  •  •  .  .  .70 

Vaccinia  and  Vaccination        ..........  88 

Varicella 90 

Scarlet  Fever          ............  93 

Measles 108 

Rubella 115 

Mumps 117 

Whooping-cough     ............  119 

Influenza        .............  125 

Dengue           .............  131 

Cerebrospinal  Fever        .          .          .          .          .          .          .          .          .          .          .  134 

Croupous  Pneumonia      ...........  143 

Diphtheria     .          .          .          .          .          •          .          .          .          .          .          .          .  171 

Gonorrhoeal  Infection     ...........  186 

Erysipelas 189 

Septicaemia  and  Pyaemia  .  .  .  .  .  .  .  .  .  .193 

Acute  Rheumatic  Fever  .  .  .  .  .  .  .  .  .  .196 

Cholera 204 

Yellow  Fever  .  . .  .  .212 

Plague  (Bubonic  Plague)           ..........  219 

Climatic  Bubo 226 

Dysentery      .............  227 

Epidemic  Gangrenous  Proctitis        .          .          .          .          .          .          .          .          .  239 

Hill  Diarrhoea 240 

Sprue  (Psilosis) 242 

Nasha  Fever           .          .          .          '. .          .  245 

Malta  Fever 245 

Beriberi  . '        .  .249 

Anthrax         .............  257 

Hydrophobia           ............  261 

Tetanus 267 

Glanders 271 

Actinomycosis         ............  273 

Mycetoma  (Madura  Foot,  Fungus  Foot  of  India)     ......  275 

Syphilis 276 

Hereditary  Syphilis        .          .          .          .          .          .          .          .          .          .  286 

(V) 


VI 

CONTENTS 

PAGE 

Tuberculosis 290 

Acute  Miliarv  Tuberculosis 

.      297 

Glandular  Tuberculosis 

.      299 

Tuberculosis  of  the  Serous  Membranes 

.      301 

Pulmonary  Tuberculosis 

.      309 

Tuberculosis  of  the  Alimentary  Canal 

.      334 

Tuberculosis  of  the  Liver 

.      338 

.      338 

Tuberculosis  of  the  Fallopian  Tubes,  Ovaries  a 

nd  Uterus 

.      342 

Tuberculosis  of  the  Heart 

.      343 

Tuberculosis  of  the  Thyroid  Gland 

.      343 

Tuberculosis  of  the  Brain  and  Cord 
Leprosy          ...... 

.      343 
.     344 

Febricula 

.      351 

Milk  Sickness 

.     352 

Weil's  Disease 

.      352 

Glandular  Fever 

,' 

.      353 

^lountain  Fever 

.      354 

Tick  Fever    . 

.      354 

Foot-and-Mouth  Disease 

.     356 

Miliar\^  Fever          .... 

.     356 

Japanese  River  Fever     . 

.     357 

Frambesia  (Frambcesia  Tropica,  Yaws) 

.      358 

Verruga  (Verruga  Peruviana)  . 

.      360 

Kubisagari     . 

. 

.     362 

DISEASES  OF  THE  RESPIRATORY  SYSTEM. 


Diseases  of  the  Nose        ...........  363 

Acute  Corj'za        ...........  363 

Chronic  Nasal  Catarrh           .........  365 

Atrophic  Nasal  Catarrh         .........  366 

Hay  Fever .  .367 

Epistaxis      ............  369 

Diseases  of  the  Larynx  ...........  369 

Acute  Catarrhal  Laryngitis   .          .          .          .          .          .          .          .          .  369 

Chronic  Catarrhal  Laryngitis          ........  371 

(Edematous  Laryngitis           .........  372 

Spasmodic  I^aryngitis    ..........  374 

Tuberculous  Laryngitis          .          .          .       ■  .          .          .          .          .          .  375 

Syphilitic  Larj-ngitis     .  .  .  .  .  .  .  .  .  .376 

Diseases  of  the  Bronchi   ...........  377 

Acute  Catarrhal  Bronchitis   .........  377 

Chronic  Catarrhal  Bronchitis           ........  382 

Bronchiectasis       ...........  383 

Fibrinous  Bronchitis     ..........  388 

Bronchial  Asthma         ..........  390 

Diseases  of  the  Lungs     ...........  397 

Bronchopneumonia         ..........  397 

Metastatic  Pneumonia  ..........  408 

Pneumonoconiosis  .  .  .  .         .  .  .  .  .  .411 


CONTENTS 


vu 


Diseases  of  the  Lungs: 

Emphysema  of  the  Lungs     . 

Compensatory  or  Acute  Emphysema 
Interstitial  Emphysema 
Small-lunged  Emphysema 

Gangrene  of  the  Lung 

Pulmonary  Abscess 

Congestion  of  the  Lungs 

Tumors  in  the  Lungs   . 
Diseases  of  the  Pleura 

Pleuritis 

Purulent  Pleural  Effusion  or  Empyema 

Chronic  Pleurisy   . 

Hydrothorax 

Pneumothorax,  Hydropneumothorax,  Pyopneumothorax 

Diseases  of  the  Mediastinum  ..... 


PAGE 

413 
419 
419 
420 
420 
423 
425 
428 
430 
430 
443 
448 
448 
449 
452 


of  the  Heart 


a  Result  of  Chronic 


Endocarditis 


DISEASES  OF  THE  CIRCULATORY  SYSTEM. 

Diseases  of  the  Pericardium 
Pericarditis 
Hy  dr  oper  i  cardium 
Hsemopericardium 
Pneumopericardium 
Pyopericardium     . 
Diseases  of  the  Heart 

Hypertrophy  and  Dilatation 
Disease  of  the  Myocardium 
Cardiac  Aneurysm 
Wounds  of  the  Heart   . 
Endocarditis 

Acute  Endocarditis 

Ulcerative  Endocardit 

Chronic  Endocarditis 
Chronic  Valvular  Disease  as 

Mitral  Regurgitation 

Mitral  Stenosis    . 

Aortic  Stenosis   . 

Aortic  Regurgitation 

Tricuspid  Regurgitation 

Tricuspid  Stenosis 

Disease  of   the  Pulmonary  Valves 
Neuroses  of  the  Heart 

Palpitation 

Tachycardia 

Bradycardia 

Arhythmia 
Angina  Pectoris    . 
Congenital  Cardiac  Defects 
Diseases  of  the  Arteries  . 
Arteriosclerosis 
Aneurysm    . 

Aneurysm  of  Thoracic  Aorta 

Aneurysm  of  the  Abdominal  Aorta 


457 
457 
466 
467 
467 
468 
468 
468 
473 
479 
481 
481 
482 
485 
488 
489 
494 
499 
504 
508 
513 
515 
515 
521 
521 
521 
522 
522 
523 
527 
528 
529 
534 
536 
542 


vm 


CONTENTS 


DISEASES  OF  THE  DIGESTIVE  TRACT. 

Diseases  of  the  Mouth     . 
Stomatitis    . 

Catarrhal  Stomatitis 
Aphthous  Stomatitis 
Ulcerative  Stomatitis 
Thrush 

Gangrenous  Stomatitis,  Cancrum  Oris  or  Noma 
Eczema  of  the  Tongue 
Leukoplakia  Euccalis    . 
Mucous  Patches  . 
Diseases  of  the  Salivary  Glands 

Functional  Disorders  of  the  Salivary  Glands 

Ptyalism 
Dry  Mouth 

Inflammation  of  the  Salivary  Glands 
Ludvig's  Angina 
Diseases  of  the  Pharj^nx 
Acute  Pharyngitis 

Ulcerative  or  Phlegmonous  Pharyngitis 
Croupous  Pharyngitis 
Chronic  Pharyngitis 
Follicular  Pharyngitis 
Diseases  of  the  Tonsils  . 
Acute  Tonsillitis  . 
Chronic  Hypertrophic  Tonsillitis 
Diseases  of  the  ffisophagus 
CEsophagitis 

Organic  Stricture  of  the  (Esophagus 
Dilatation  of  the  (Esophagus 
Spasms  of  the  (Esophagus    . 
Cancer  of  the  (Esophagus      . 
Diseases  of  the  Stomach 

Acute  Gastric  Catarrh 
Acute  Toxic  Gastritis 
Phlegmonous  Gastritis 
Diphtheritic  Gastritis 
Mycotic  Gastritis 
Chronic  Gastritis  . 
Gastric  Dilatation 

Acute  Gastrectasis 
Gastric  Ulcer        .... 
Cancer  of  the  Stomach 
Hypertrophic  Stenosis  of  the  Pylorus 
Hour-glass  Stomach 
Gastric  Neuroses  .... 
Cardiospasm 
Pylorospasm 
Gastric  Hj'perperistalsis 
Merycismus 
Nervous  Eructation    . 


PAGE 

545 

545 

545 

546 

546 

547 

548 

549 

550 

550 

550 

550 

550 

551 

551 

552 

552 

552 

554 

555 

555 

556 

556 

556 

558 

560 

560 

561 

561 

562 

563 

564 

564 

565 

566 

568 

568 

568 

572 

578 

579 

588 

595 

598 

601 

601 

602 

602 

603 

603 


CONTENTS 


IX 


Diseases  of  the  Stomach  : 

Hypersesthesia    . 

Gastralgia  .... 

Bulimia      .... 

Anorexia  Nervosa 

Nervous  Disorders  of  Secretion 
Hemorrhage  from  the  Stomach 
CycUc  Vomiting   .... 
Diseases  of  the  Intestines 

Diarrhoea     ..... 
Catarrhal  Enteritis 
Ileocolitis  of  Childhood 
Cholera  Infantum 
Appendicitis  .... 

Intestinal  Obstruction  . 

Congenital  Malformation 

Intussusception  . 

Internal  Strangulation 

Volvulus    .... 

Obstruction  from  Foreign  Bodies 
Duodenal  Ulcer    .... 
Enteroptosis  .... 

Colitis  ..... 

Acute  Colitis 

Mucous  Colitis    . 

Folliculus  and  Croupous  Colitis 

Pseudomembranous  Colitis  . 
Dilatation  of  the  Colon 


PAGE 

603 
603 
604 
604 
604 
604 
607 
608 
608 
609 
609 
613 
613 
623 
624 
624 
626 
627 
628 
628 
632 
636 
636 
637 
638 
639 
639 


DISEASES  OF  THE  PERITONEUM. 


Acute  Peritonitis  .... 

Chronic  Peritonitis 

Chronic  Adhesive  Sclerotic  Peritonitis 

Cancer  of  the  Peritoneum 

Other  Growths  of  the  Peritoneum   . 

Ascites  ..... 


641 
647 
648 
649 
649 
650 


DISEASES  OF  THE  LIVER. 

Inflammation  of  the  Liver     ..........  653 

Acute  Hepatitis  or  Hepatic  Abscess      .......  653 

Cirrhosis  of  the  Liver    ...........  658 

Atrophic  Cirrhosis         .          .          .          .          .          .          .          .         .          .  659 

Hypertrophic  Cirrhosis           .........  663 

Syphilitic  Cirrhosis        ..........  664 

Perihepatitis  (Capsular  Cirrhosis)    .........  665 

Affections  of  the  Hepatic  Bloodvessels     ........  666 

Amyloid  Liver        ............  667 

Fatty  Liver 668 

Tumors  of  the  Liver      ...........  668 

Acute  Yellow  Atrophy  of  the  Liver  .  .  .  .  .  .  .670 


CONTENTS 


DISEASES  OF  THE  BILIARY  TRACT 


Acute  Catarrh  of  the  Bile-ducts,  or  Acute  Cholangitis 

Chronic  Catarrh  of  the  Bile-ducts  . 

Suppurative  Inflammation  of  the  BUe-ducts 

Occlusion  and  Constrictions  of  the  Bile-ducts 

Acute  Cholecystitis  .... 

Cholelithiasis  ..... 

Malignant  Growths  of  the  GaU-bladder  and  Biliary  Passages 

Icterus  Neonatorum        .  .  ... 

DISEASES  OF  THE  PANCREAS 

Pancreatitis 

Acute  Pancreatitis 

Chronic  Pancreatitis 
Pancreatic  Calculus 
Pancreatic  Cysts    . 
Pancreatic  Tumors 
Hemorrhages  into  the  Pancreas 

DISEASES  OF  THE  KIDNEYS 

Malformations  of  the  Kidneys 

Movable  Kidney    . 

Circulatory  Disturbances  in  the  Kidney 

Acute  Hypergemia 

Chronic  Hypersemia 
Acute  Bright's  Disease 
Chronic  Bright's  Disease 
Chronic  Parenchymatous  Nephritis 
Chronic  Interstitial  Nephritis 
Amyloid  Disease  of  the  Kidneys 
UrEemia  .... 

Pyelonephritis  and  Pyelitis     . 
Hydronephrosis 
Cystic  Disease  of  the  Kidney 
Tumors  of  the  Kidney 
Nephrolithiasis 
Perinephritic  Abscess 
Disorders  of  Urinary  Secretion 

Anuria 

Haematuria 

Hsemoglobinuria 

Hsematinuria 

Albuminuria 

Pyuria 

Chyluria 

Phosphaturia 

Oxaluria 

Indicanuria 

Lithuria 

Melanuria    . 

Myelopathic  Albumo.suria 


PAGE 

671 
673 
673 
674 
675 
677 
683 
686 


687 
687 
691 
693 
694 
695 
695 


696 
696 
698 
699 
699 
700 
703 
704 
710 
718 
720 
725 
728 
730 
732 
733 
737 
737 
737 
738 
739 
739 
741 
744 
744 
745 
745 
745 
746 
746 
746 


CONTENTS 


XI 


DISEASES  OF  THE  DUCTLESS   GLANDS  AND  LYMPHATIC 

SYSTEM. 

PAGE 

749 
749 
750 
751 
751 
756 
758 
760 
760 
764 
765 
767 
767 
770 
772 


Diseases  of  the  Thyroid  Gland 

Goitre  .... 

•    SweUing  of  the  Thyroid 

Tumors  of  the  Thyroid  Gland 

Exophthalmic  Goitre    . 

Myxoedema 

Cretinism     .... 
Diseases  of  the  Suprarenal  Gland    . 

Addison's  Disease 
Diseases  of  the  Spleen   . 

Splenic  Anaemia  . 

Banti's  Disease    . 

Hodgkin's  Disease 

Status  Lymphaticus 
Diseases  of  the  Thymus  Gland 


DISEASES  OF  THE  BLOOD. 


Ansemia  .  .  .  •  • 

Secondary  Ansemia 

Primary  or  Essential  Anaemias 
Chlorosis    . 
Pernicious  Ansemia 
Leuksemia      .  .  .  .  • 

SplenomeduUary  Leuksemia  . 

Lymphatic  Leuksemia  . 
Chloroma       .  .  .  .  • 

Ansemia  Infantum 
Purpura         .  .  ,  . 

Haemophilia  .         .         .         »         . 


773 

773 
775 

775 
777 
780 
781 
782 
784 
785 
785 
787 


DISEASES  OF  NUTRITION. 


Diabetes  Mellitus  . 
Diabetes  Insipidus 
Gout     . 

Acute  Gout 
Chronic  Gout 
Irregular  Gout 
Arthritis  Deformans 
Chronic  Rheumatism 
Muscular  Rheumatism 
Rickets 
Scurvy- 
Obesity 
Adiposis  Dolorosa  . 


789 
806 
808 
813 
814 
814 
818 
823 
824 
825 
830 
833 
836 


Xll 


CONTENTS 


PAGE 

Acromegaly J          .          .          .          .  837 

Osteitis  Deformans         ...........  839 

Hypertrophic  Pulmonary  Osteoarthropathy 840 

Leontiasis  Ossea    ............  840 

Scleroderma  .............  840 

Ainhum          •••..........  841 


INTOXICATIONS. 


Alcoholism     ..... 

Acute  Alcoholism 

Subacute  and  Chronic  Alcoholism 
Morphinism  ..... 
Arsenical  Poisoning         ... 
Lead  Poisoning,  or  Plumbism 
Food  Poisoning       .... 

Bromat  otoxismus 

Mytilotoxismus     . 

Ichthyotoxismus  . 

Kreotoxismus 

Tyrotoxismus  and  Galactotoxismus 
Pellagra  (Maidismus) 
Lathyrism  (Chickpea  Disease;  Lupinosis) 
Atriplicism     ..... 
Lacquer  Poisoning 


843 
843 
844 
848 
850 
851 
855 
855 
856 
856 
856 
857 
857 
859 
860 
860 


DISEASES  DUE  TO  ANIMAL  PARASITES. 


Malarial  Fever  ..... 
Psorospermiasis  ..... 
Trypanosomiasis     ..... 

Trypanosoma  Fever 

African  Lethargy  (Sleeping  Sickness) 
Kala-Azar      ...... 

Nematodes    .  .  .  . 

Ascariasis    ..... 

Oxyuris  Vermicularis    . 

Trichina  Spiralis  .... 

Uncinariasis  (Ankylostomiasis) 

Filariasis  (Filaria  Sanguinis  Hominis) 

Filaria   Nocturna 

Elephantiasis 
Hsematochyluria 
Lymph  Scrotum 

Guinea-worm  Disease  (Dracontiasis) 

Strongyloides  Intestinalis 

Trichocephalus  Dispar  . 
Cestodes  or  Tapeworms 
Trematodes   ...... 

Bilharzia  Disease 

Distomatosis  of  the  Lung 

Distomatosis  of  the  Liver  (Liver  Flukes) 


863 
879 

879 
880 

881 
883 


885 
885 
887 
892 
893 
895 
895 
897 
897 
898 
900 
900 
904 
905 
907 
908 


CONTENTS  xiii 

PAGE 

Parasitic  Infusoria           ...........  909 

Dhobie  Itch 909 

Chigger  (Sand  Flea) 911 

Myiasis           .          . 911 

Intestinal  Myiasis          ..........  912 

Dermatobia  Cyaniventris       .........  912 


DISEASES  OF  THE  NERVOUS  SYSTEM. 

DISEASES  IN  WHICH  THE  CHIEF  MANIFESTATIONS  ARE  IN  THE  BRAIN 

AND  ITS  MEMBRANES. 

Hemorrhage  into  the  Brain,  Cerebral  Thrombosis  and  Embolism     .          .          .  913 

Infantile   Cerebral   Paralysis  ..........  925 

Little's  Disease     ...........  929 

Aphasia          .............  930 

Tumors  of  the  Brain  and  its  Membranes         .......  932 

Abscess  of  the  Brain      ...........  941 

Acute  Cerebritis  or  Encephalitis       .........  944 

Thrombosis  of  the  Venous  Sinuses           ........  945 

Cerebral  Meningitis         ...........  946 

Pachymeningitis  ...........  947 

Pachymeningitis  Interna        .........  947 

Leptomeningitis    ...........  948 

Dementia  Paralytica       ...........  950 

Disseminated  Sclerosis    ...........  954 

DISEASES  IN  WHICH  THE  CHIEF  MANIFESTATIONS  ARE  IN  THE  SPINAL 
CORD  OR  ITS  MEMBRANES. 

Locomotor  Ataxia           ...........  958 

Friedreich's  Ataxia          ...........  967 

Marie's  Cerebellar  Hereditary  Ataxia       .          .          .          .          .          .          .          .  970 

Acute  Anterior  Poliomyelitis            .          .          .          .          .          .          .          .          .  970 

Chronic  Anterior  Poliomyelitis         .          .          .          .          .          .          .          .          .  974 

Bulbar  Paralysis    ............  977 

Lateral  Sclerosis     ............  978 

Amyotrophic  Lateral  Sclerosis          .........  980 

Myelitis 983 

Acute  and  Subacute  Myelitis         ........  983 

Chronic  Myelitis  ...........  985 

Senile  Paraplegia   ............  987 

Myelomalacia          ............  987 

Syringomyelia 988 

Hemorrhage  into  the  Spinal  Cord  .........  990 

Hemorrhage  into  the  Spinal  Membranes 991 

Compression  of  the  Spinal  Cord 993 

Spinal  Meningitis  ............  997 

Chronic  Spinal  Meningitis     .........  999 

Acute  Ascending  Paralysis  (Landry's  Paralysis) 1000 

Caisson  Disease      ...,,,,.,,,.  1001 


CONTENTS 


DISEASES  IN  WHICH  THE  CHIEF  ]\IANIFESTATIONS  ARE  IN  THE  NERVES. 


Neuritis  .... 

Special  Forms  of  Neuritis 

Cervicobrachial  Neuritis 
Obstetrical  or  Birth  Neuritis 
Multiple  Neuritis 
Diseases  of  the  Cranial  Nerves 
The  Olfactory  Nerve    . 
The  Optic  Nerve 

Optic  Atrophy    . 

Hemianopsia 
The  Third  or  Oculomotor  Nerve 
The  Fourth  or  Trochlearis  Nerv^e 
The  Fifth  or  Trifacial  Nerve 
The  Sixth  Abducens  Nerve   . 

Disturbances  of  Motility  in  the  Ocular  Muscles 
Third,  Fourth,  and  Sixth  Nerves 

Ophthalmoplegia;  Paralysis  of  the   Internal  and 
of  the  Eyeball 
The  Seventh  or  Facial  Nerve 

Facial  Spasm 
The  Eighth  or  Auditory  Nerve 
The  Ninth  or  Glossopharyngeal  Nerve 
The  Tenth  or  Vagus  Nerv^e  . 
Eleventh  or  Spinal  Accessory  Nerve 
Twelfth  or  Hypoglossal  Nerve 


Muscular  Dystrophies     ...... 

Pseudomuscular  Hypertrophy 

Erb's  Juvenile  Muscular  Dystrophy 

Landouzy-Dejerine  Type  of  Muscular  Dystrophy 
Muscular  Atrophy  of  the  Peroneal  Type 

FUNCTIONAL  NERVOUS  DISEASES  AND  DISEASES  OF  DISPUTED 

PATHOLOGY. 


PAGE 

.  1003 

. 

.   1006 

. 

.  1006 

.  1007 

.  1007 

. 

.  1012 

. 

.  1012 

. 

.  1012 

. 

.  1014 

. 

.  1015 

. 

.  1018 

. 

.  1020 

.  1020 

.  1022 

Depending  on  the 

.  1022 

External  Muscles 

.  1023 

.  1024 

.  1027 

.  1028 

. 

.  1030 

. 

.  1030 

. 

.  1032 

• 

.  1034 

,E  IN  THE  MUSCLES. 

.  1035 

.  1035 

.  1036 

.  1037 

.  1037 

Myotonia  Congenita 
Paramyoclonus  Multiplex 
Paralysis  Agitans  . 
Chorea  Minor 
Other  Forms  of  Chorea 

Huntington's  Chorea    . 

Dubini's  Disease 
Hysteria         .... 
Epilepsy         .... 

Jacksonian  Epilepsy 

Petit  Mai,  or  Minor  Epilepsy 
Eclampsia      .... 

Infantile  Eclampsia 

Puerperal  Eclampsia    . 


1038 
1039 
1040 
1043 
1046 
1046 
1047 
1047 
1052 
1061 
1061 
1062 
1062 
1063 


CONTENTS 


XV 


Tetany 

Latah  . 

Amok  (Running  Amok) 

Astasia-abasia 

Neurasthenia 

Traumatic  Neuroses 

Occupation  Neuroses 

Raynaud's  Disease 

Angioneurotic  CEdema 

Erythromelalgia 

Migraine 

Sunstroke 

Heat  Exhaustion   . 

Facial  Hemiatrophy 

Periodical  Paralysis 


PAGE 

1064 
1066 
1066 
1067 
1068 
1070 
1072 
1075 
1075 
1076 
1077 
1080 
1082 
1083 
1083 


PRACTICE  OF  MEDICINE. 


DISEASES  DUE  TO  A  SPECIFIC  INFECTION. 


TYPHOID  FEVER. 

Definition. — ^Typhoid  or  Enteric  fever,  sometimes  called  Autumnal  or 
Gastric  fever,  is  an  acute  infectious  disease  due  to  the  entrance  into 
the  body  of  a  susceptible  individual  of  the  specific  bacillus  of  Eberth, 
commonly  known  as  Bacillus  typhosus.  The  entrance  of  this  organism 
into  the  system  results,  after  a  period  of  from  one  to  three  weeks  in  some 
persons,  but  not  in  all,  in  the  development  of  fever,  anorexia,  headache, 
mental  heaviness,  and  more  or  less  severe  pain  in  the  bowels,  back,  and 
limbs.  The  tongue  is  coated,  and  the  bowels  are  loose  or  constipated. 
With  these  symptoms  are  developed  enlargement  of  the  liver  and  spleen, 
and  swellings  and  ulceration  of  the  lymphoid  structures  of  the  small  and 
large  intestines,  and  a  rose  rash  on  the  skin. 

History. — ^Typhoid  fever  for  many  years  was  confused  with  typhus  fever 
and  malarial  fever,  and  its  very  name  means  "like  typhus."  In  1813  it 
was  considered  as  a  separate  disease,  but  this  separation  was  not  generally 
known  by  the  profession  until  Louis,  of  Paris  (1829),  first  emphasized  a 
number  of  its  cardinal  points.  Not  until  1837  was  the  identification  com- 
plete, when  Gerhard,  of  Philadelphia,  published  results  achieved  under 
the  guidance  of  Louis  which  proved  the  malady  to  be  a  distinct  entity. 
More  than  forty  years  later  (1880)  Eberth  isolated  the  specific  bacillus 
and  proved  it  to  be  the  sole  cause  of  the  disease.  Up  to  that  time  various 
causes  had  been  thought  to  exist,  but  it  had  been  recognized  for  many 
years  as  a  "filth  disease,"  and,  therefore,  preventable  to  some  degree. 

Distribution. — Enteric  fever  is  one  of  the  diseases  which  may  be  said  to 
be  pandemic,  since  it  is  found  with  some  degree  of  constancy  all  over  the 
world,  its  prevalence  depending  upon  the  introduction  into  the  body  of 
the  specific  bacillus  usually  with  water  or  food. 

Etiology. — The  cause  of  this  disease,  as  just  stated,  is  the  specific  bacillus 
of  Eberth,  a  short,  thick,  actively  motile  bacillus,  with  rounded  ends  and 
flagella,  growing  readily  in  ordinary  suitable  media.  It  is  killed  by  expo- 
sure to  60°  C.  (140°  F.),  but  it  can  withstand  a  freezing  temperature  for  many 
days.  Exposed  to  sunlight  it  is  slowly  killed,  but  drying,  except  in  very 
2 


18  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

thin  layers,  does  not  destroy  it.  It  remains  alive  for  months,  and  even  for 
years,  in  clothing  and  in  soil,  if  the  conditions  are  favorable.  It  is  readily 
destroyed  by  the  stronger  germicides,  such  as  carbolic  acid  (1:200)  and 
bichloride  of  mercury  (1:2000).  The  bacillus  of  Eberth  bears  a  close 
resemblance  to  the  Bacillus  coli  communis,  which  is  always  present  in  the 
intestine,  and  to  the  so-called  paracolon  bacillus  and  the  Bacillus  dysenterice. 

The  second  etiological  factor  in  the  development  of  the  disease  is  the 
mode  by  which  the  bacillus  gains  access  to  the  body.  Almost  invariably 
this  access  is  through  the  mouth,  stomach,  and  intestine,  more  rarely  by 
inhalation  of  the  bacillus  in  dust  by  the  lungs.  Infection  takes  place  by 
the  mouth  in  a  host  of  ways,  as  by  infected  water,  or  milk  diluted  with 
infected  water,  or  chilled  by  infected  ice;  by  vegetables  and  oysters  and 
clams,  which,  when  eaten  raw,  are  often  the  means  of  carrying  infection. 
It  has  recently  been  proved  at  Ogdensburg,  New  York,  that  infected  ice 
may  transmit  the  organism  after  it  has  been  stored  in  an  ice-house  for  at 
least  nine  months.  In  still  other  instances  persons  nursing  cases  of  this 
disease  get  the  finger-tips  infected  and  so,  on  putting  the  fingers  to  the  mouth, 
introduce  the  organism  into  the  body.  Again,  it  has  been  proved  beyond 
doubt  that  flies  after  lighting  upon  the  discharges  of  a  case  of  typhoid  fever 
may  carry  the  bacillus  to  otherwise  pure  food,  and  so  spread  the  infection 
as  long  as  twenty-three  days  after  feeding  on  infected  stools  (Ficher). 
Stokes  describes  an  epidemic  in  a  factory  employing  1500  women  and  400 
men.  As  many  as  200  of  the  women  were  ill  at  one  time  with  typhoid 
fever,  but  none  of  the  men  fell  ill.  All  the  men  drank  beer  at  luncheon, 
whereas  all  the  women  used  milk.  The  milk  was  found  to  have  been  in- 
fected by  flies  from  a  neighboring  privy.  Cockroaches  may  also  spread 
the  bacillus. 

Every  great  epidemic  of  the  disease  has  been  due  to  contamination  of  the 
water  supply.  In  the  Maidstone  epidemic  in  England  1  person  in  every  17 
in  the  town  was  infected ;  while  in  the  Plymouth  epidemic  in  Pennsylvania 
1  in  every  7  v/as  stricken,  for  there  were  1200  cases  in  a  population  of  8000. 
As  only  a  part  of  these  8000  persons  used  the  contaminated  water,  the  pro- 
portion of  actual  infection  to  exposure  was  far  higher  than  1  in  7.  The 
influence  of  a  bad  and  good  water  supply  is  shown  in  Figs.  1,  2  and  3. 

In  1888  the  use  of  filtered  drinking  water  was  begun  in  the  French  army, 
as  a  result  of  which  the  morbidity  of  typhoid  fever  was  diminished  49  per 
cent,  in  1890,  and  the  mortality  34  per  cent. 

Prevention. — From  what  has  just  been  said  it  is  evident  that  typhoid  fever  is 
an  entirely  preventable  disease,  provided  that  the  bacilli  as  they  escape  in 
the  feces,  the  urine,  the  sputum,  and,  perhaps,  in  the  sweat,  are  destroyed  as 
soon  as  they  pass  from  the  patient's  body.  The  destruction  of  the  dis- 
charges and  so  of  the  bacilli  is  therefore  absolutely  essential,  and  in  addition 
careful  antisepsis  on  the  part  of  the  attendant  as  to  personal  cleanliness 
and  the  protection  of  the  discharges  from  flies  are  to  be  enforced.  As 
careless  or  ignorant  persons  do  not  disinfect  the  stools,  the  additional 
measures  of  prophylaxis  are  the  boiling  of  all  water  that  is  to  be  placed 
in  the  mouth,  and  the  use  of  nothing  but  well-cooked  foods,  which  have 
not  been  exposed  to  flies  or  dust  after  cooking.    The  vessel  which  receives 


TYPHOID  FEVER 


19 


the  discharges  of  the  patient  should  contain  carboUc  acid  (1 :  200),  corro- 
subHmate    (1:2000),  or  chlorinated   lime  (a  heaping  teaspoonful   to 


sive 


the  pint).    Formaldehyde  solution  (40  per  cent.)  may  also  be  used.    If  the 


FlQ.  1 


■rt«05^l»50t-l»050 


oo 

1 

OS 
oo 

OS 
oo 

ao 

o 

Oi 

1 

1000 

1 

2000 
1 

3000 
1 

4000 
1 

6000 
1 

6000 
1 

1 

7000 

1 

1 

8000 

1 
9000 

1 

1 

10000 

1 

1 

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Fig.  2 

ODOOG^OOOOQCOOodQCOO 


e»es3i393S»3>Sa3SS9 
ooooacaooooocoooaoao 


1 

■ 

n 

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r 

1000 

1 

2000 

1 

3000 

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-  ■■■ 

1 

4000 

1 
5000 

1 

6000 

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TOGO 

1 
8000 

1 
9000 

1 

10000 

1 

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1 

2000 
1 

3000 
1 

4000 
1 

5000 

1 

6000 

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7000 
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■mi" 

Fig.  1.— Mortality  in  Chicago  of  typhoid  fever.  In  1891  and  1892  the  water  was  contaminated  with 
sewage  and  the  death  rate  was  about  1  to  450  to  1  to  1500.  With  a  change  in  water  supply  the  mor- 
tality has  fallen  to  1  to  6000  or  even  1  to  9000.     (Seibert.) 

Fig.  2.— Mortality  of  typhoid  fever  in  Berlin  before  the  supply  of  drinking  water  was  filtered.  In 
the  decade  1843  to  1853  the  average  yearly  mortality  was  1  per  900  of  inhabitants. 

Fig.  3.— Mortality  of  typhoid  fever  in  Berlin  after  water  was  filtered.     (Seibert.) 


stool  is  formed,  it  should  be  broken  up  by  stirring  it  with  a  rod,  so  as  to 
expose  all  the  fecal  matter  "to  the  germicide. 

Physicians  and  nurses  are  not  careful  enough  about  the  destruction  of  the 
stools,  and  the  average  individual  is  willing  to  take  his  chances  on  the  use  of 


20  DISEASES  DUE    TO   A   SPECIFIC  INFECTION 

unboiled  water.  Another  of  the  difficulties  is  that  patients  may,  when  no 
longer  kept  in  the  house  by  the  disease,  continue  to  cast  off  bacilli  in  the 
urine  or  feces  which  are  capable  of  infecting  water  supplies.  This  danger 
is  of  great  importance,  because  at  each  urination  or  defecation  the  con- 
valescent patient  may  produce  a  new  source  of  infection.  Further,  it  is 
toward  the  close  of  the  attack  and  during  convalescence  that  the  urine 
contains  these  specific  organisms  in  pure  culture  and  in  enormous  numbers, 
and  they  may  remain  persistently  present,  not  only  for  days  but  for  months. 
The  patient  should  be  told  of  this  danger,  should  be  directed  to  disinfect 
his  discharges,  and  should  receive  daily  doses  of  uritone  or  urotropin  to 
destroy  the  bacilli  in  the  urine  before  they  are  passed  in  that  fluid.  If  he 
is  also  informed  that  bacilluria  is  a  danger  to  himself,  in  that  it  may  result 
in  secondary  diseases  in  his  genito-urinary  tract,  he  may  be  interested 
enough  to  aid  the  physician  in  arresting  the  spread  of  the  bacillus  by 
adhering  to  a  plan  of  careful  medication. 

All  clothing,  instruments,  bedding,  pillows,  utensils,  bath-tubs  and  ordi- 
nary wash-tubs,  which  may  be  contaminated  by  the  discharges  of  a 
patient,  should  be  disinfected  thoroughly  as  soon  as  their  function  is  per- 
formed.   The  hands  of  the  nurses  should  be  repeatedly  disinfected. 

Another  preventive  of  typhoid  fever  consists  in  the  injection,  or  inocu- 
lation, of  the  individual  with  bouillon  containing  the  toxins  of  Bacillus 
typhosus,  the  organisms  themselves  being  destroyed  beforehand  by  heat. 
Such  an  injection  produces  local  swelKng  and  some  pain,  a  sense  of  nausea 
and  depression,  and  some  febrile  movement,  which  symptoms  speedily 
disappear,  the  patient  at  the  end  of  twenty-four  to  thirty-six  hours  being 
well  again.  A  fortnight  later  the  individual  is  injected  a  second  time.  It 
is  interesting  to  note  that  these  injections  increase  the  bacteriolytic  power 
of  the  blood,  cause  in  some  degree  the  so-called  Widal  reaction,  or  agglutina- 
tion of  the  Bacillus  typhosus,  to  take  place  when  the  serum  of  the  injected 
person  is  used  for  this  test,  and  in  many  hundred  cases  have  probably  served 
to  act  as  a  protective  agent  against  infection,  akhough  the  protection  is  by 
no  means  so  complete  as  that  afforded  by  vaccination  against  smallpox, 
nor  has  it  been  tried  sufficiently  widely  to  place  its  use  upon  a  sunilar  cHnical 
basis.  It  has,  however,  had  complete  tests  in  the  last  few  years.  Thus,  of 
29,650  individuals  in  South  Africa,  Egypt,  Cyprus,  India,  and  Ireland,  who 
were  similarly  exposed  to  infection  by  typhoid  fever,  7055  received  pre- 
ventive inoculations.  Of  this  number  333,  or  4.72  per  cent.,  contracted  the 
disease;  34,  or  1.03  per  cent.,  died.  Of  the  22,595  who  were  not  inoculated, 
2763,  or  12.22  per  cent.,  contracted  the  disease;  507,  or  2.7  per  cent.,  died.' 

It  has  been  shown  in  the  United  States  Government  Laboratories  at 
Washington  and  in  the  City  Laboratory  of  Philadelphia  that  the  intro- 
duction of  so  small  an  amount  of  sulphate  of  copper  as  1:1,000,000, 
or  even  1  : 4,000,000,  will  destroy  the  t}T)hoid  bacillus  in  a  very  few  hours, 
and  already  this  means  has  been  successfully  used  in  large  reserv'oirs  for 
the  purification  of  the  water  supply  of  towns.  It  is  said  to  be  efficient,  is 
very  cheap,  and  entirely  harmless  to  human  beings  who  drink  the  water 

1  "These  statistics  are  compiled  from  tlie  reports  of  Wright,  Leishman,  Luck,  Fawcett,  and  Burt. 


TYPHOID  FEVER 


21 


and  to  the  fish  in  the  water.  How  the  copper  acts  is  not  known.  If 
water  containing  typhoid  baciUi  is  placed  in  burnished  copper  vessels  for 
a  few  hours  most  of  the  typhoid  germs  are  also  destroyed.  More  recently, 
Gage  and  Clark  have  thrown  doubt  on  this  method,  and  its  value  must  be 
considered  sub  judice. 

Frequency. — Typhoid  fever  affects  males  oftener  than  females,  and  occurs 
most  frequently  between  fifteen  and  thirty  years  of  age.  It  may,  how- 
ever, affect  infants  or  aged  persons.  It  occurs  more  frequently  in  August, 
September,  and  October  than  any  other  quarter  of  the  year,  but  is  by  no 
means  limited  to  this  period.     (See  Fig.  4.) 


Chart  from  the  United  States  census,  showing  the  period  of  the  year  when  the  mortality  from 
typhoid  fever  reaches  its  maximum. 

Typhoid  fever  is  becoming  less  and  less  frequent,  and  less  severe  all 
over  the  world.  In  Munich  the  mortality  in  the  decade  from  1851  to 
1861  ranged  from  123  in  100,000  inhabitants  to  453  in  100,000  inhabi- 
tants, whereas  in  the  years  from  1890  to  1897  the  mortality  was  from  57  or 
14.8  in  100,000  people  to  10  or  2.5  per  100,000;  in  Vienna  it  has  fallen 
from  120  per  100,000  to  10  per  100,000;  in  Dantzig,  from  100  per  100,000 
to  10.5.  In  Massachusetts  the  mortality  from  typhoid  fever  in  1901  was 
less  than  in  any  year  since  1842.  In  33  cities  in  that  State  it  was  only  one- 
fourth  of  what  it  was  thirty  years  ago.  In  Philadelphia  a  similar  decrease 
is  seen  in  both  mortality  and  morbidity.  (See  Fig.  5.)  The  rise  in  mor- 
bidity in  1898  is  due  to  the  soldiers  returning  from  the  Spanish-American 


22 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


war,  for  the  careless  sanitation  of  large  camps  always  makes  it  epidemic. 
Thus,  in  this  war  about  1  in  every  5  of  the  soldiers  in  the  United  States 
army  became  infected,  and  nearly  87  per  cent,  of  all  the  deaths  in  the  army 


Fig.  5 

NUMBER 
OF 

CASES 

BETWEEN 

8100 — 7800 

7800 — 7500 

__    _          __    . 

7500 — 7200 

::::::::::::::::::::::::::::::::::::::::::::: 

7200 — 6900 

_ 
J 

6900 — 6600 

I 

f 

6600 — 6300 

f 

: 

6300 — 6000 

I 

600© — 5700 

1 

5700 — 5400 

I 

.____! 

5400 — 5100 

__  [ 

5100 — 4800 

4800 — 450O 

oi         ^              ,                                                                    A                      -          I 

2^:r::::f:::::::::::::_:_: 1___. / 

4500 — 4200 

on  A^  ^  J  ^         -  -    --     I    .       -      l- 

^°  __L4_i--\ 1- 

4200 — 3900 

.0  -Y-XU-^-^-^ /- 

^^  _/_4L______\t H I— 

3900 — 3600 

,./  L              \            _^J /-  — 

18^-^-j^-—-_  —  -\ t l____ 

3600 — 3300 

^-7        J   '  \       »             ^         ^                           -I 

n—'-^—A           V__/_). ,_ U 

3300 — 3000 

.:""   V   t^  ^          ^^.ti t- 

^^ :__________[ ^__J 

3000 — 2700 

.,              ^            ,  ]__ 

^^ '::::: : .^__\.! 

2700 — 2400 

1^    \y1s__l______\ 

2400  —  2100 

.o       ]/  5/    ^ , 

^^ "":::: f j, A^ 

2100 — 1800 

io                                     -5^      /           ^ 

^2""::: I-a-,^- ^s- 

1800 — 1500 

. \y^_ ^_ 

11                      *^ 

Showing  the  decreasing:  mortality  of  typhoid  fever  in  Philadelphia.    Solid  line,  morbidity  with  sharp 
rise  in  1898-99,  due  to  returned  soldiers  of  Spanish  war.     Broken  line,  mortality. 

were  due  to  this  cause.  In  Melbourne,  Australia,  there  has  also  been  a 
decrease  in  the  mortality  rate  which  is  very  noticeable,  being  over  50  per 
cent.     This  decrease  is  due  chiefly  to  care  in  regard  to  water  supplies. 


TYPHOID  FEVER 


23 


The  general  mortality  rate  of  the  world  may  be  said  fifty  years  ago  to 
have  been  almost  universally  25  per  cent.,  whereas  it  is  now  from  15  to  10 
per  cent. 

With  advancing  years  of  age  the  morbidity  decreases,  but  the  mortality 
greatly  increases.     (See  Fig.  6.) 

Pathology  and  Morbid  Anatomy. — In  studying  the  morbid  anatomy  of 
typhoid  fever  it  must  be  remembered  that  it  is  not,  when  fully  developed, 
a  local  infection,  restricted  to  one  or  more  foci  from  which  the  Bacillus 
typhosus  distributes  its  toxin  through  the  body.  On  the  contrary,  the 
typhoid  infection  is  practically  universal,  and  the  bacillus  may  be  found  in 
varying  numbers  in  every  organ  of  the  body,  including  the  bone-marrow 
and  skin.  Contrary  to  general  belief,  they  may  not  be  demonstrable  in 
the  intestinal  contents  in  large  numbers  until  the  disease  is  well  advanced, 
and  their  presence  in  the  stools  depends  largely  upon  the  intensity  of  the 


Fig.  6 


AGE 

10 

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10-20 

21-25 

20-30 

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Showing  the  increased  mortality  of  typhoid  fever  with  age.    (Curschmann.) 


changes  which  take  place  in  the  intestinal  glands.  It  is  true,  however, 
that  the  agminated  glands  (Peyer's  patches)  and  the  solitary  glands  of 
the  small  bowel  are  the  parts  of  the  body  which  usually  are  the  seat  of 
the  most  evident  and  constant  lesions.  On  the  other  hand,  it  is  not  to  be 
forgotten  that  cases  of  undoubted  typhoid  fever  occasionally  occur  in 
which  no  ulceration  of  the  intestinal  mucosa  takes  place. 

The  alterations  from  the  normal  in  the  bowel  may  be  discussed  under 
three  heads :  (1)  a  diffuse  catarrhal  inflammation  of  the  intestinal  mucosa  of 
varying  severity,  but  usually  resulting  in  desquamation  of  epithelium;  (2) 
hyperemia,  swelling,  endothelial  hyperplasia,  necrosis,  and  finally  ulceration 
of  the  agminated  glands  or  Peyer's  patches;  and  (3)  a  similar  change  in  the 
so-called  solitary  lymph  follicles  of  the  intestine,  although  the  changes  in  the 
agminated  glands  are  distinctly  the  more  conspicuous.  These  changes  begin 
in  the  very  earliest  stages  of  onset,  and  do  not  wait  until  the  symptoms  of  the 


24 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


disease  are  well  developed.  If  by  some  accident  the  patient  comes  to  autopsy 
at  this  time,  the  intestinal  mucosa  will  not  only  be  found  inflamed,  but  in 
addition  the  lymphoid  structures  just  named  will  also  be  found  swollen  and 
reddened  by  hypersemia.  Their  edges  are  not  well  defined,  and  the  entire 
gland  is  hyperplastic  and  spongy.  A  little  later  in  the  progress  of  the  disease 
these  areas  become  less  red  in  hue  and  begin  to  look  somewhat  gray  in 
color;  they  are  firmer  and  project  above  the  surrounding  mucous  membrane 
to  a  marked  degree,  so  that  they  extend  well  into  the  lumen  of  the  bowel. 


Fig.  7 


Ulceration  of  a  Peyer  patch  in  typhoid  fever,  with  associated  swelling  of  soUtary  glands. 

Sometimes  the  hyperplasia  within  the  gland  is  so  great  that  its  edges  overhang 
the  surrounding  tissue.  Still  later  the  lymphatic  tissue  may  become  so  infil- 
trated that  neighboring  patches  of  glandular  tissue  coalesce,  and  when 
they  reach  the  stage  of  necrosis  result  in  large  areas  of  slough,  so  that 
the  entire  thickness  of  the  intestinal  wall  may  be  involved  (Fig.  7),  The 
presence  of  so  severe  an  ulcerative  process  naturally  results  in  deep  infil- 
tration of  the  bowel  wall,  and  the  inflammatory  condition  may  extend  to 
the  peritoneal  coat,  so  that  this  serous  membrane  is  reddened  or  even  grayish 


PLATE  I. 


Showing  Typhoid  Ulcers  in  Small  Bowel  and  near  the 
Appendix.      (Kast  and  Rumpler.) 


TYPHOID  FEVER  25 

from  exuded  lymph.  The  severest  forms  of  ulceration  usually  take  place 
in  the  lower  part  of  the  ileum. 

While  ulceration  of  the  tissues  composing  Peyer's  patches  is  the  usual 
result  of  this  infection,  necrosis  does  not  always  ensue.  The  gland  may 
become  red  and  swollen  and  the  inflammatory  process  go  no  farther,  pro- 
ceeding from  this  state  to  that  of  resolution  and  healing.  Not  infrequently 
this  agminated  patch  is  not  equally  affected  in  all  its  parts,  and  this  gives 
it  an  uneven  appearance,  which  is  emphasized  when  the  portions  which 
are  most  affected  ulcerate,  so  that  small  ulcers  are  dotted  over  the  sur- 
face of  the  swelling,  which,  if  the  process  is  severe,  finally  coalesce.  In 
severe  types  of  the  disease  the  process  is  so  well  diffused  that  a  huge 
slough  forms  which,  when  it  drops  off,  leaves  a  swollen,  ulcerated  surface, 
the  excavation  being  usually  very  deep.  It  is  this  type  of  necrosis  that 
results  in  perforation,  the  opening  in  the  bowel  wall  being  usually  found 
at  a  point  directly  opposite  the  mesenteric  attachment.  Rarely  the  perfor- 
ation takes  place  between  the  layers  of  the  mesentery  and  causes  a  retro- 
peritoneal abscess.  Harte  states  that  in  140  cases  out  of  190  the  perforation 
occurred  in  the  small  bowel  within  twelve  inches  of  the  caecum.  If  the 
patient  survives  the  severer  periods  of  the  disease,  the  swelling  of  the 
glandular  tissue  gradually  diminishes,  granulations  develop,  new  connective 
tissue  largely  takes  the  place  once  occupied  by  the  gland,  and  the  ordinary 
intestinal  epithelium  covers  the  exposed  area.  While  it  is  true  that  the 
solitary  glands  are  rarely  so  markedly  affected  as  the  agminated  glands, 
they  may  suffer  much  more  severely  and  be  found  diseased  over  a  larger 
area  than  are  the  glands  of  Peyer. 

The  number  of  ulcers  in  the  bowel  in  typhoid  fever  varies  greatly.  Usually 
they  are  hmited  in  number,  but  occasionally  they  cover  very  large  areas. 
They  may  be  more  numerous  in  the  caecum  than  elsewhere  in  the  colon.  Out 
of  577  autopsies  upon  cases  of  this  disease  in  Hamburg  and  in  Leipzig,  the 
csecum  was  ulcerated  in  510,  or  88.39  per  cent.;  the  csecum  and  appendix 
in  247,  or  42.81  per  cent.;  the  colon  in  184  cases,  or  31.89  per  qent. ;  the 
jejunum  in  41  cases,  or  7.10  per  cent.;  the  rectum  in  12  cases,  or  2.08  per 
cent.  The  percentage  of  csecal  lesions,  in  these  statistics  of  Curschmann, 
just  given,  is  much  higher  than  is  generally  noted;  40  per  cent,  is  more 
nearly  correct.  As  already  stated,  the  lower  part  of  the  small  bowel  is  the 
area  chiefly  affected. 

Next  to  the  changes  in  the  intestine  the  most  noteworthy  alterations 
may  be  said  to  take  place  in  the  lymph  nodes  of  the  jnesentery,  which  lie 
between  the  intestinal  lesion  and  the  general  system.  These  tissues  go 
through  a  similar  process  of  hypersemia,  swelling,  and  endothelial  prolifer- 
ation, which  usually  falls  short  of  extensive  necrosis.  Small  necrotic  patches 
are  not  infrequent.  More  rarely  large  foci  of  softening  or  even  suppuration 
may  occur  in  these  nodes,  and  as  recovery  takes  place  small  septic  areas 
are  gradually  walled  off  by  lymph,  become  encysted,  or  are  absorbed. 
Rupture  of  enlarged  mesenteric  nodes  has  been  observed. 

The  spleen,  in  addition  to  its  swelling,  which  begins  early  and  lasts  for 
the  first  three  weeks  or  more  of  the  illness,  is  full  and  tense,  and  of  a  darker 
hue  than  normal.    Later,  as  the  attack  wanes,  it  becomes  soft  and  darker 


26  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

in  hue.  The  splenic  blood  sinuses  are  distended  by  erythrocytes,  the  endo- 
thelial cells  proliferate,  and  the  pulp  here  and  there  becomes  the  seat  of 
small  areas  of  coagulation  necrosis.  The  splenic  lesions  may  also  consist 
in  infarction  and  rupture,  but  the  latter  accident  is  very  rare. 

Until  a  few  years  ago  the  presence  of  the  typhoid  bacillus  in  the  blood 
was  unknown,  but  we  now  know  that  this  organism  is  present  in  this  part 
of  the  body  with  great  constancy  during  an  attack  of  typhoid  fever. 
It  is  usually  present  as  early  as  the  fifth  day  and  persists  until  the  close  of 
the  third  week,  or  even  longer  than  this.  Rosenberger  has  recently  collected 
535  cases  of  typhoid  fever  in  which  the  blood  was  examined  for  the  bacillus. 
It  was  found  in  80  per  cent,  of  these  cases.  The  examination  of  the  blood 
has  therefore  become  of  great  importance  in  the  early  diagnosis  of  the 
disease.  (See  Diagnosis.)  The  bacillus  probably  gains  access  to  the  blood 
through  the  mesenteric  glands. 

The  liver  is  usually  somewhat  swollen,  but  the  changes  in  its  appearance 
are  not  peculiar  to  this  disease.  The  hepatic  cells  manifest  more  or 
less  cloudy  swelling,  and  areas  of  coagulation  necrosis  containing  endothelial 
cells  are  present.  The  cells  lining  the  bile-ducts  may  be  swollen,  granular, 
and,  in  some  cases,  undergo  a  process  of  desquamation.  Abscess  of  the 
liver  may  develop  or  gallstones  may  by  their  presence  aid  in  the  produc- 
tion of  a  cholecystitis,  but  more  commonly  typhoid  fever  probably  induces 
gallstones.     (See  Complications.) 

The  heart  muscle  nearly  always  suffers  from  typhoid  infection  in  direct 
proportion  to  the  severity  of  the  toxaemia  present.  The  myocardium  is 
granular  and  may  suffer  from  fatty  or  hyaline  changes.  Very  rarely  the 
endocardium  becomes  affected  and  the  specific  bacillus  has  been  obtained 
from  vegetations  on  the  valves. 

The  kidneys  show  no  typical  changes.  They  usually  show  cloudy  swell- 
ing, and  even  an  acute  nephritis  may  be  present.  Sometimes  as  the  result 
of  a  terminal  infection  multiple  abscesses  may  form  in  the  kidneys  and  a 
croupous  exudate  in  the  pelvis  of  these  organs  may  develop. 

Reference  is  made  elsewhere  to  the  lesions  of  the  respiratory  tract  which 
may  complicate  the  course  of  the  malady,  such  as  laryngeal  perichondritis, 
ulcerative  laryngitis,  hypostatic  congestion,  pneumonia  in  both  its  forms, 
pulmonary  infarction,  simple  pleurisy,  and  empyema.    (See  Complications.) 

An  endarteritis  (which  may  be  a  thromboendarteritis)  has  been  shown 
to  occur  in  a  small  percentage  of  cases,  and  it  is  reasonable  to  assume  that 
the  thrombotic  processes  occasionally  observed  in  the  veins  depend  upon 
a  similar  involvement  of  the  lining  membrane  of  these  vessels. 

Longcope  has  shown  that  the  lesions  in  the  bone-marrow  closely  resemble 
the  changes  in  the  lymphoid  tissues  of  the  mesentery  and  of  the  bowel. 
There  are  present  many  lymphoid  cells,  large  phagocytes  and  foci  of 
necrosis. 

A  very  important  factor  to  be  recalled  in  the  study  of  the  pathology  of 
typhoid  fever  is  the  presence  of  additional  infecting  micro-organisms 
which  aid  the  Bacillus  typhosus  in  producing  severe  lesions  and  often 
are  equally  responsible  for  a  fatal  termination.  This  view  is,  however, 
based  on  post-mortem  findings,  and  is  not  supported  by  the  results  of 


TYPHOID  FEVER  27 

ante-mortem  examinations  of  the  blood,  for  of  150  cases  of  typhoid  fever  in 
which  the  blood  was  examined  during  life  Cole  found  but  one  in  which 
mixed  infection  was  present;  the  case  was  one  of  staphylococcsemia,  with 
multiple  boils,  and  terminated  in  death. 

Incubation. — ^The  period  of  incubation  of  the  infection  by  typhoid  fever 
is  generally  stated  to  be  from  one  to  three  weeks.  That  the  period  of 
incubation  may  be  much  shorter  than  this  would  seem  to  be  proved  by  the 
case  reported  by  Duflocq  and  Voisin  of  a  girl  nineteen  years  of  age  who 
deliberately  swallowed  a  virulent  culture  of  the  typhoid  bacillus  with  the 
intention  of  committing  suicide.  She  began  to  feel  ill  on  the  third  day, 
had  fever  on  the  fourth  day,  rose  spots  on  the  fifth  day,  and  the  Widal 
reaction  appeared  on  the  sixth  day. 

Sjnmptoms. — Typhoid  fever  usually  begins  with  a  sense  of  wretchedness 
and  general  illness,  no  particular  symptom  being  especially  well  marked, 
unless  it  be  more  or  less  severe  frontal  headache  and  aching  in  the  back  and 
limbs.  The  facial  expression  very  early  in  typhoid  fever  usually  becomes  list- 
less and  later  stupid  and  heavy,  and  the  patient  is  often  a  little  deaf  because 
his  mental  state  is  benumbed  rather  than  because  there  is  any  actual  trouble 
with  the  auditory  apparatus.  Not  infrequently  there  may  be  a  considerable 
amount  of  cough  without  expectoration,  and  there  may  be  exaggeration 
of  the  sounds  of  bronchial  breathing  on  auscultation. 

The  tongue  is  somewhat  coated,  and  very  early  its  edges  become  clean 
and  red,  while  the  central  coating  remains.  This  appearance  of  the  tongue 
is  very  characteristic,  even  in  mild  cases. 

Headache,  thirst,  and  sleeplessness  are  usually  prominent  symptoms  during 
the  first  week.  A  mild  fever  develops  simultaneously  and  nose-bleed  may 
occur  repeatedly.  Usually  the  liver  and  spleen  become  swollen  toward 
the  end  of  the  first  week,  and  the  belly  becomes  somewhat  tumid  and 
tender. 

The  characteristic  enlargement  of  the  spleen  in  enteric  fever  may  be 
undemonstrable  because  of  the  distention  of  the  stomach  and  intestine  with 
gas;  but  while  the  presence  of  an  enlarged  spleen  is  of  some  importance  in 
reaching  a  diagnosis  of  typhoid  fever,  inability  to  discover  any  increase  in 
its  size  does  not  negative  the  diagnosis  of  typhoid  fever  in  any  degree. 

An  undue  amount  of  gurgling  can  be  felt  and  heard  in  the  right  iliac 
fossa. 

Constipation  is  usual  in  the  first  week,  but  diarrhoea  may  be  marked,  and 
if  loose  the  stools  may  be  brownish,  but  later  resemble  okra-soup  or  pea- 
soup. 

The  temperature  in  typhoid  fever  during  the  first  week  rises  step  by 
step.  Each  morning  it  is  higher  than  on  the  previous  morning,  and  each 
evening  higher  than  on  the  night  before,  although  the  morning  temperature 
is  often  lower  than  that  of  the  preceding  evening.  (See  Fig.  8.)  Usually 
by  the  end  of  this  week  it  reaches  in  the  morning  102°  or  103°,  and  at 
night  103°  to  104°,  and  remains  at  this  level  until  the  fourteenth  or 
twenty-first  day. 

The  pulse  is  more  rapid  than  normal,  ranging  from  90  to  100  beats  per 
minute,  and  it  is  usually  soft  and  compressible;  the  pulse  of  debility,  not 


28 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


of  vigor.  Often  the  pulse  is  a  little  dicrotic.  As  the  disease  progresses  the 
pulse  rate  usually  increases  to  about  110,  but  the  pulse  force  distinctly 
diminishes. 

At  about  the  seventh  to  the  ninth  day  a  very  important  diagnostic  sign 
first  makes  its  appearance,  namely,  the  so-called  rose  spots,  which  usually 
develop  on  the  skin  of  the  abdomen  and  chest,  sometimes  on  the  back,  and 
more  rarely  on  the  limbs.  These  spots  are  small,  faint  macules,  usually 
scanty  in  number,  which  lose  their  color  momentarily  when  pressed  upon 
or  when  the  skin  on  which  they  exist  is  stretched  between  the  finger  and 
thumb  of  the  physician.  As  a  rule  these  spots  are  isolated,  but  very  rarely 
they  may  be  so  profuse  as  to  produce  the  appearance  of  an  ordinary  rash. 


Fig.  8 


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The  tongue  becomes  dry  and  it  may  be  fissured,  the  mental  stupor 
increases,  diarrhoea  is  also  active,  and  the  moderate  tympanites  of  the 
earHer  days  becomes  more  marked.  If  the  patient  has  received  httle 
care,  or  if  the  case  is  essentially  severe,  his  condition  is  manifestly  one  of 
profound  toxsemia,  and  by  the  end  of  the  second  week  he  is  evidently  at 
the  very  acme  of  his  infection.  Death  not  infrequently  takes  place  during 
this  period  as  a  result  of  profound  toxaemia,  hemorrhage,  perforation,  or 
pulmonary  complications. 

Because  of  the  toxaemia  delirium  may  be  marked,  and  it  is  usually  of 
the  low  muttering  type,  the  patient  seems  to  be  in  a  semi-stupor,  the  teeth 
are  covered  with  sordes,  and  the  tongue  is  foul  and  dry. 

These  symptoms  gradually  carry  the  patient  into  his  third  week,  with 
increasing  diarrhcea,  greater  tympanites,  deeper  stupor,  and  more  manifest 
signs  of  profound  toxaemia,  with  muscular  tremors  or  true  suhsultus  tendinum. 
Emaciation  by  this  time  is  marked  and  the  skin  dry  and  harsh.  The  heart 
is  feeble,  its  sounds  distant  and  muffled,  and  myocardial  degeneration  is 


TYPHOID  FEVER 


29 


manifestly  advanced.  To  the  possibility  of  the  appearance  of  the  fatal 
complications  named  in  the  succeeding  pages  as  appearing  at  the  end  of  the 
second  week  are  added  at  this  time  still  greater  danger  of  pulmonary  hypo- 
static congestion  and  pneumonia.  The  patient  may  be  so  profoundly 
poisoned  by  the  toxic  products  of  the  disease  that  he  seems  almost 
moribund. 

If  the  pathological  process  is  not  so  severe  that  recovery  is  impossible, 
the  first  sign  of  the  ending  of  the  malady  may  develop  at  any  time  between 
the  fourteenth   and   twenty-eighth   day,   according  to   the  severity  of   the 


Fig.  9 


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Part  of  a  chart  showing  the  period  of  steep  curves  from  the  fourteenth  to  the  twentieth  day 
of  an  attack  of  typhoid  fever. 


disease.  This  consists  in  a  slight  modification  of  the  temperature  range 
and  the  development  of  a  low  morning  temperature  with  a  well-maintained 
high  evening  temperature,  so  that  the  daily  range  may  amount  to  from 
2°  to  3°.  This  is  called  the  "'period  of  steep  curves,^^  and  the  appearance 
of  these  steep  curves  at  this  time  in  the  course  of  the  disease  is  usually  a 
promise  of  approaching  convalescence.  An  equally  good  description  of  this 
period  is  that  of  Murchison,  who  called  it  the  "stage  of  changing  fortunes," 
or  that  of  Wunderlich,  who  described  it  as  the  "period  of  ambiguity." 


30  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

The  last  stage  of  the  acute  febrile  period  having  been  reached,  the 
temperature  falls  to  normal  during  the  next  few  days  by  lysis,  and  then 
may  be  subnormal  until  convalescence  is  well  established,  the  patient 
being  wasted  and  feeble,  but  usually  ravenously  hungry. 

Atypic.u.  Forms. — While  the  train  of  symptoms  just  described  may  be  con- 
sidered typical  of  an  attack  of  typhoid  fever  occurring  under  conditions  favor- 
able for  its  full  development,  it  is  often  so  modified  by  various  causes  that  a 
large  proportion  of  cases  do  not  present  many  of  the  most  prominent  and  diag- 
nostic symptoms,  but,  in  their  place,  manifestations  so  at  variance  with  those 
of  ordinary  cases  as  to  greatly  perplex  the  physician.  Thus,  very  marked 
variations  in  onset  may  occur  and  completely  mislead  the  medical  attendant 
if  he  be  not  on  his  guard.  In  some  cases  instead  of  manifesting  itself  grad- 
ually the  disease  has  a  sudden  onset  with  a  sharp  chill  followed,  it  may  be, 
by  a  profuse  sweat  and  a  continued  fever.  This  variation  is  perhaps  most 
apt  to  occur  in  children.  Headache  may  be  so  severe  in  the  beginning  as  to 
rouse  the  suspicion  of  meningeal  inflammation,  and  active  delirium  may 
be  an  early  symptom,  being  severe  enough  to  be  maniacal  in  type.  In  other 
instances  a  pneumonia  is  the  earliest  sign  of  the  malady,  while  in  still  others 
a  severe  choleraic  diarrhcea  may  begin  the  illness.  It  is  also  important  to 
recall  the  fact  that  well-developed  signs  of  appendicitis  may  appear,  due 
to  the  swelling  of  the  lymphoid  tissues  of  the  intestine  and  appendix  by 
reason  of  the  infection.  This  has  frequently  resulted  in  enthusiastic  sur- 
geons removing  the  appendix  only  to  find  it  slightly  diseased  as  part  of  the 
general  lymphatic  change,  the  speedy  appearance  of  the  rose  rash  and  per- 
sistent temperature  soon  showing  the  true  character  of  the  case.  Rarely  a 
severe  attack  of  vomiting  begins  the  illness,  and  still  more  rarely  acide 
renal  disease,  nephro-typhoid,  or  the  fievre  typhoide  h  forme  renale  of  the 
French  observers,  develops. 

Although  diarrhcex  was  correctly  considered  at  one  time  to  be  one  of  the 
most  constant  symptoms  of  enteric  fever  it  is  now  absent  in  more  than  half 
the  cases  during  the  whole  course  of  the  disease,  and  splenic  enlargement 
in  many  instances  is  too  slight  to  be  discovered,  so  that  it  is  to  be  borne  in 
mind  that  while  these  two  symptoms  possess  a  positive  diagnostic  value  when 
present,  their  absence  in  no  way  contradicts  the  diagnosis  of  typhoid  fever. 

In  other  instances  the  course  of  the  fever  greatly  varies  from  that  just 
described.  It  may  rise  very  abruptly,  and  it  may  end  equally  suddenly,  the 
lysis  being  completed  in  twenty  hours.  Sometimes  the  morning  temperature 
is  the  higher  of  the  two,  although  this  is  rare.  The  regular  course  of  the 
temperature  may  also  be  greatly  altered  by  intercurrent  chills.  (See  Chills.) 
Very  rarely,  strange  as  it  may  seem,  no  febrile  movement  is  present  at  any 
time  in  the  course  of  the  malady. 

The  most  important  variations  from  what  may  be  called  the  normal 
course  of  the  temperature  in  the  second  and  third  week  of  this  disease  are 
those  produced  by  free  hemorrhage  from  an  intestinal  ulcer  and  by  perfora- 
tion of  the  bowel.  A  sudden  fall  of  several  degrees  should  always  arouse 
suspicion  of  one  of  these  accidents,  for  the  drop  in  the  fever  may  be  noted 
before  any  of  the  other  signs  of  hemorrhage  or  perforation  manifest  them- 
selves. 


TYPHOID  FEVER 


31 


Marked  rises  and  falls  of  temperature 
who  are  markedly  ancemic  as   the  result 
causes    a    marked    fall    of     the 
fever. 

The  course  of  the  temperature 
may  resemble  that  of  remittent 
malarial  fever,  and  it  has  fre- 
quently misled  physicians  into  the 
belief  that  malarial  infection  and 
not  typhoid  infection  was  present. 
(See  Chills.)  Infectious  complica- 
tions of  the  disease  such  as  otitis 
media,  phlebitis,  f  urunculosis,men- 
ingitis,  and  erysipelas  may  also 
cause  sudden  variations  in  tem- 
perature. Ai\d  in  cases  which  have 
been  gravely  ill  it  not  rarely  hap- 
pens that  fever  continues  after  the 
typhoid  infection  has  run  its  course 
because  of  post-typhoidal  septicae- 
mia— that  is,  a  multiple  infection 
due  to  the  presence  of  pyogenic 
organisms,  which  have  found  a 
favorable  field  for  growth  in  a 
patient  whose  vitality  has  been 
impaired  by  the  specific  fever. 

As  the  stage  of  convalescence 
approaches,  or  when  it  is  reached, 
a  sharp  return  of  active  febrile 
movement  may  come  on  for  a  day 
or  two,  the  temperature  being  as 
high  or  higher  than  ever  before. 
It  then  returns  to  its  ordinary  level. 
This  is  called  a  recrudescence,  and 
possesses  no  grave  significance.  It 
often  follows  mental  excitement 
and  the  taking  of  improper  or  too 
much  food.  When  this  rise  of 
temperature  persists,  it  usually  is 
indicative  of  some  complicating 
malady,  or  of  a  relapse  called  an 
"intercurrent  relapse"  if  it  takes 
place  during  the  continuance  of 
the  primary  febrile  period.  (See 
Fig.  10.)  After  the  fever  has  disap- 
peared there  may  be  a  prolonged 
continuance  of  a  slight  evening 
rise  of  temperature  as  the  result 


are  also  often  seen  in  patients 
of  hemorrhage.    Abortion  also 


aiVOS     XI3.HN3.aHVJ 


32  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

of  nervous  irritability  and  anaemia,  or  it  depends  upon  the  abuse  of  strych- 
nine, with  the  mistaken  idea  that  it  is  a  valuable  heart  tonic  at  this  time. 
In  other  cases  a  subnormal  temperature  for  the  entire  twenty-four  hours  may 
persist  for  days.  This  is  of  no  importance  save  that  it  indicates  that  the 
patient  is  feeble  and  needs  good  feeding  and  fresh  air.  The  other  variations 
met  with  depend  upon  the  age  of  the  patient.  Old  persons  often  have  an 
irregular  febrile  movement,  and  children  may  have  marked  rises  and  falls  of 
temperature  which  do  not  necessarily  indicate  any  complications. 

Persistence  of  distinct  febrile  movement  after  the  fourth  week  in  any  case 
of  typhoid  fever  in  which  a  relapse  has  not  occurred  nearly  always  means  a 
complicating  or  secondary  infection.  The  number  of  cases  of  rapid  tuber- 
culosis called  typhoid  fever,  until  the  persistent  loss  of  flesh  and  fever  forces 
the  correct  diagnosis  upon  the  physician,  is  by  no  means  small.  The  possi- 
bility of  ulcerative  endocarditis,  cholecystitis  with  ulceration,  with  or  without 
impacted  gallstones,  and  septic  infection  due  to  suppuration  as  causes  of 
fever  are  to  be  borne  in  mind  and  their  presence  carefully  looked  for.  (See 
Complications.) 

That  a  patient  with  this  disease  may  suffer  not  only  from  the  infec- 
tion due  to  the  bacilli  of  Eberth,  but  from  multiple  infections  by  other 
organisms  which  aid  in  decreasing  his  vital  resistance  should  be  borne  in 
mind. 

Closely  associated  with  the  study  of  the  temperature  is  that  of  chills. 
They  may  usher  in  an  acute  complicating  inflammatory  process,  or  be 
entirely  without  such  significance.  Sometimes  they  occur  in  cases  which 
suffer  from  constipation,  apparently  as  a  result  of  the  absorption  of  fecal 
poisons.  (See  Fig.  11.)  In  other  cases  they  are  due  to  a  true  coincident 
malarial  infection,  but  it  is  a  noteworthy  fact  that  during  the  course  of 
typhoid  fever,  even  if  the  patient  is  also  suffering  from  malarial  infection, 
the  latter  usually  remains  in  abeyance  until  the  former  has  about  run  its 
course.  It  is  better  for  the  physician  to  regard  such  chills  as  being  an  indi- 
cation of  some  acute  complication  than  to  consider  them  as  malarial,  unless 
he  can  prove  the  existence  of  the  last  possibility  by  finding  malarial 
organisms  in  the  blood. 

The  skin  is  sometimes  covered  by  a  fugacious  scarlatiniform  rash  in 
the  early  stages.  In  certain  cases  it  desquamates  in  large  flakes  or  in 
fine,  branny  scales,  the  latter  appearing  oftenest  in  those  who  have  been 
actively  bathed  and  rubbed. 

Very  commonly  if  sweating  takes  place,  sudamina,  or  tiny  sweat  drops 
retained  beneath  the  superficial  epiderm  are  found  on  the  abdomen,  chest, 
or  limbs.  Herpes  about  the  mouth  is  very  rare  in  typhoid  fever,  but  it 
does  occur,  notwithstanding  the  denial  of  this  fact  by  some  observers. 

Under  the  name  of  tache  bleudtre  or  peliomata,  faint  blue  or  steel-gray 
spots  of  fairly  good  size  are  sometimes  met  with.  They  are  not  due  to 
the  disease,  but  are  found  only  in  those  who  are  infested  with  lice.  The 
so-called  tache  cerebrale  is  not  characteristic  of  this  disease,  but  is  some- 
times seen  during  its  course,  and  consists  in  a  red  line  with  white  borders 
produced  by  drawing  the  finger-nail  over  the  skin.  It  is  probably  due  to 
vasomotor  palsy  of  the  cutaneous  vessels. 


TYPHOID  FEVER 


33 


Of  the  deeper  lesions  of  the  skin,  we  meet  with  hed-sores,  which  rarely 
occur  in  cases  seen  from  the  first  and  which  receive  proper  care.  They  appear 
usually  over  the  sacrum.  Cases  of  superficial  gangrene  of  the  skin  have 
been  reported  by  Stahl  and  the  author.     Erysipelas  occurs,  usually  of  the 


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34  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

face,  by  reason  of  infection  through  fissures  in  the  buccal  or  nasal  mucous 
membrane.  Sometimes  erysipelas  migrans  develops.  In  very  malignant 
cases  petechioe  may  be  present. 

Patients  suffering  from  typhoid  fever  rarely  suffer  from  other  eruptive 
diseases,  but  instances  of  scarlet  fever,  chicken-pox,  and  measles  occurring 
as  complications  are  on  record.  In  women  in  particular  the  hair  often  falls 
out  freely  during  or  after  an  attack.  Boils  are  by  no  means  rare  lesions, 
and  even  carbuncles  may  develop  as  a  result  of  multiple  infection. 

The  blood  in  typhoid  fever  suffers  from  an  increasing  degree  of  anoemia 
in  respect  to  the  number  of  the  red  cells  and  of  their  richness  in  haemoglobin. 
Indeed,  the  color-index  is  more  markedly  lowered  than  the  corpuscular 
count.  When  an  inadequate  supply  of  liquids  has  been  allowed  the  result- 
ing concentration  of  the  blood  may  produce  an  apparent  corpuscular  richness 
not  actually  present. 

The  bacteriolytic  power  of  the  blood  in  severe  cases  is  probably  always 
diminished.  The  leukocytes  are  slightly  decreased  in  number,  the  large 
mononuclear  and  transitional  cells  are  relatively  increased,  and,  according 
to  Thayer,  the  polymorphonuclear  cells  are  decreased.  Cabot  asserts  that 
a  leukocytosis,  non-inflammatory  in  origin,  sometimes  occurs. 

Complications  and  Sequelae.  Circulatory  Complications. — The  heart, 
as  already  stated,  is  weakened,  and  if  severely  affected  may  develop  em- 
bryocardia  or  fetal  heart  sounds.  There  are  few,  if  any,  diseases  which 
do  not  have  special  predilection  for  the  heart  muscle  or  its  valves,  which  so 
greatly  interfere  with  this  organ  as  does  typhoid  fever.  A  pulse  rate  above 
125  is  ominous,  and  one  of  130  or  140  dangerous.  The  danger  is  usually  in 
direct  proportion  to  the  feebleness  of  the  first  sound  of  the  heart.  When 
the  cardiac  sounds  are  those  of  the  foetus  in  utero  (embryocardia),  the  prog- 
nosis is  grave.  A  very  rapid  pulse  and  irritable  cardiac  action  are  sometimes 
seen  in  cases  in  which  strychnine  has  been  used  to  excess  with  the  idea  that 
it  is  a  stimulant.  A  soft  systolic  murmur  is  occasionally  audible,  which 
may  be  hsemic  in  origin  or  due  to  relative  insufficiency  of  the  mitral  valves. 
Rarely  it  may  be  due  to  endocarditis  or  pericarditis,  but  pericarditis  is  a 
very  rare  complication  of  typhoid  fever.  Gaudy  and  Gourand  state  that 
pericarditis  arising  during  the  course  of  typhoid  fever  occurs  in  two  forms, 
namely,  the  fibrinous,  which  is  characterized  by  an  abundant  pseudo- 
membranous exudation  with  only  slight  serous  effusion,  and  the  fibrino- 
purulent  form,  in  which  a  considerable  effusion  may  occur.  Pericarditis 
may  exist  alone  or  may  occur  in  connection  with  endocarditis,  myocarditis, 
pleuritis,  or  pulmonary  complications.  As  a  rule,  it  develops  very  slowly 
and  may  remain  latent,  so  that  only  most  careful  auscultation  over  the 
prsecordial  region  will  reveal  the  presence  of  friction  fremitus,  and  later 
careful  percussion  may  be  required  to  distinguish  an  effusion.  The  patho- 
genesis of  this  complication  is  obscure.  The  purulent  form  when  it  occurs 
may  be  due  to  secondary  infection,  although  the  fibrinous  variety  is  prob- 
ably due  to  a  direct  infection  with  the  Eberth  bacillus.  Typhoid  fever 
complicated  by  purulent  pericarditis  is  always  fatal,  but  the  existence  of 
the  serofibrinous  pericarditis  influences  prognosis  slightly  if  at  all,  unless 
the  effusion  be  profuse. 


TYPHOID  FEVER  35 

Sudden  cardiac  failure  may  occur  as  the  result  of  myocarditis,  or  of 
embolism  or  thrombosis  of  the  coronary  arteries,  from  heart  clot,  throm- 
bosis of  the  cavse  and  pulmonary  veins  or  from  pericarditis  with  effusion. 
Sometimes  the  cardiac  failure  is  gradual  when  due  to  these  causes. 

So  far  as  the  bloodvessels  are  concerned  the  most  common  lesion  is 
phlebitis,  which  usually  affects  the  veins  of  the  left  leg,  especially  the  femoral 
vein.  The  frequency  of  involvement  of  the  veins  in  the  left  leg  depends 
upon  the  pressure  exercised  by  the  right  common  iliac  artery  upon  the  left 
common  iliac  vein,  which  tends  to  obstruct  the  flow  of  blood.  Sometimes 
the  tendency  to  the  formation  of  a  thrombus  is  greatly  increased  by  a  local 
infection  of  the  endothelial  lining  of  the  vessel,  and  it  is  not  uncommon  for 
a  severe  chill  or  chills  to  mark  the  onset  of  the  lesion.  Wright  and  Knapp 
have  recently  shown  that  the  tendency  to  the  formation  of  a  thrombus  in 
typhoid  fever  is  augmented  by  the  increase  of  calcium  in  the  blood.  When 
milk  is  the  exclusive  diet  the  rise  in  the  proportion  of  calcium  oxide  sup- 
plied to  the  body  is  very  noteworthy.  They  also  recommend  that  for  the 
prevention  of  this  state  the  physician  add  20  to  40  grains  of  citrate  of  soda 
to  each  pint  of  milk  taken  by  the  patient  in  order  to  decalcify  it. 

Thromboses  of  extraordinary  size  and  number  may  form  and  extend  from 
the  femoral  vein  to  the  vena  cava.  When  venous  plugging  seriously  inter- 
feres with  the  circulation,  the  gangrene  which  results  is  usually  moist,  but 
in  the  vast  majority  of  cases  of  phlebitis  of  the  leg  partial  recovery  takes 
place,  although  varicosity  of  the  veins  of  the  limb  may  persist  after  con- 
valescence is  completed.  The  rarity  of  plugging  of  the  veins  of  the  upper 
extremity  is  remarkable. 

Arterial  thrombosis  is  much  more  rare  than  is  venous  thrombosis.  This 
complication  usually  develops  after  the  second  week  of  the  fever,  and  is 
manifested  by  pain  and  tenderness  along  the  course  of  the  vessel  affected. 
Usually  the  leg  is  the  limb  involved.  After  a  temporary  increase  in  the 
force  of  pulsation  in  the  affected  vessel  the  pulse  becomes  small  and  may 
be  lost.  The  part  becomes  cold  and  discolored,  and  finally  gangrene  ensues. 
In  other  cases,  in  which  the  vessel  which  is  involved  is  small,  recovery  takes 
place  by  the  establishment  of  a  collateral  circulation.  Even  in  the  mild 
cases  the  patient  suffers  afterward  from  fatigue  in  the  affected  limb  on 
exertion,  and  intermittent  claudication  may  develop.  The  condition  is  due 
to  an  arteritis. 

Thayer  has  published  statistics  which  seem  to  indicate  that  typhoid  fever 
is  prone  to  produce  early  senile  changes  in  the  bloodvessels  in  after  years. 

Complications  in  the  Alimentary  Canal. — The  complications  in  the 
upper  digestive  tract  are  pharyngitis,  which  is  rarely  severe  enough  to  cause 
much  discomfort,  and  oesophagitis,  which  is  still  more  rare,  although  several 
observers  have  recorded  ulceration  of  the  cesophagus.  Inflammation  of  the 
parotid  gland  is  a  rare  complication  of  typhoid  fever,  and  usually  occurs 
about  the  third  week  in  cases  of  severe  infection.  This  inflammatory  state 
may  be  due  to  infection  of  the  gland  from  the  mouth  by  ordinary  pus 
organisms,  or  more  rarely  be  due  to  the  specific  bacillus.  Rarely  parotitis 
occurs  in  the  first  week.  In  the  only  case  the  author  has  seen  in  which 
this  complication  developed  at  this  time  there  was  no  pain  or  redness,  and 


36  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

the  swelling  disappeared  in  about  ten  days.  It  was  also  bilateral.  In 
advanced  typhoid  fever  it  is  usually  bilateral;  is  often  followed  by  ugly 
sloughing,  and  is  a  very  dangerous  complication. 

The  stomach  in  typhoid  fever  is  rarely  much  affected.  Digestion  in  this 
viscus  is,  as  a  rule,  feeble  because  in  all  fevers  there  is  a  lack  of  gastric 
secretion,  and  this  is  particularly  true  of  typhoid  fever.  Vomiting  may 
come  on  usually  as  a  result  of  indiscretions  in  food  and  medicine.  Some- 
times, however,  late  in  the  disease  a  persistent,  pernicious  vomiting  develops 
which  only  ends  with  exhaustion  and  death.  A  few  cases  of  gastric  ulcer 
occurring  in  typhoid  fever  are  recorded. 

When  there  are  more  than  three  or  four  stools  a  day  diarrhoea  is  to  be 
considered  excessive.  AVlien  a  far  greater  number  occur,  it  is  usually 
the  result  of  improper  feeding.  The  stools  are  thin  and  resemble  pea- 
soup  save  that  they  are  apt  to  be  a  httle  more  yellow.  They  are  alkaline 
in  reaction,  offensive,  and  may  contain  particles  of  undigested  food,  as 
curds  of  milk,  and  also  small  shreds  of  lymphoid  tissue  from  the  sloughs 
of  the  bowel.  The  specific  bacillus  usually  is  not  to  be  found  in  the  stools 
until  about  the  seventh  or  tenth  day.  The  significance  of  active  diarrhoea 
as  to  the  gravity  of  the  case  has  been  much  discussed,  some  believing  that 
it  is  a  sign  of  a  severe  infection.  The  real  significance  is  not  of  severity  of 
infection,  but  of  severity  of  intestinal  involvement,  catarrhal  or  ulcerative, 
although  in  some  cases  even  the  latter  state  does  not  provoke  active  diar- 
rhoea. General  diffuse  pain  in  the  bowels  is  often  present  early  in  the 
disease,  but  is  apt  to  disappear  later. 

Hemorrhage  from  the  bowel  in  typhoid  fever  is  one  of  the  inevitable 
complications  in  a  certain  percentage  of  cases,  and  usually  takes  place 
after  the  second  week  of  the  disease.  Very  rarely  slight  loss  of  blood  may 
occur  in  the  first  week.  Proper  treatment  of  the  patient  all  through  his 
attack  may  diminish  toxaemia  and  prevent  a  fatal  terminal  infection,  but  no 
form  of  treatment  so  far  devised  has  materially  diminished  the  frequency  of 
hemorrhage  or  the  mortality  from  this  cause,  although  the  frequency  of 
the  occurrence  and  mortal  effects  vary  greatly  in  different  epidemics.  The 
general  average  of  its  occurrence  may  be  placed  at  5  per  cent.  In  52,196  cases 
of  typhoid  fever  collected  from  several  series  of  cases  reported  by  French 
and  German  physicians,  and  from  the  official  reports  of  hospitals  in  the 
United  States  and  Canada,  England  and  Ireland,  Germany,  Austria,  South 
Africa,  and  Australia,  hemorrhage  is  stated  to  have  occurred  in  2725  cases, 
which  gives  a  percentage  of  5.22.  The  mortality  in  persons  suffering  from 
it  is  about  35  to  50  per  cent.,  although  in  271  cases  of  intestinal  hemorrhage 
complicating  typhoid  fever,  collected  from  the  official  reports  of  hospitals 
in  the  United  States,  Canada,  England,  and  Germany,  71  cases  proved 
fatal,  which  gives  a  percentage  of  26.2.  Hemorrhages  usually  arise  from 
ulcers  in  the  small  intestine  and  are  very  rare  in  children.  The  symptoms 
consist  of  sudden  fall  in  the  temperature  and  it  may  be  in  the  pulse  rate, 
but  this  primary  decrease  is  usually  followed  by  a  more  rapid  pulse  than 
existed  before  the  accident  occurred.  A  diagnosis  of  hemorrhage  is  to  be 
reached  not  only  by  the  observance  of  the  symptoms  just  described,  but 
in  addition  by  the  presence  of  blood  in  the  stools  and  by  examining  the 


TYPHOID  FEVER  37 

blood  to  discover  a  paucity  of  hsemoglobin.  The  gravity  of  a  hemorrhage 
depends  upon  the  relation  of  the  quantity  of  blood  lost  to  the  vitality  of 
the  patient  and  the  frequency  with  which  the  bleeding  occurs.  Thus  a 
fairly  profuse  hemorrhage  in  a  strong  patient  may  be  followed  by  no 
severe  symptoms,  whereas  repeated  small  hemorrhages  may  greatly  exhaust 
the  most  lusty  individual.  When  the  patient  is  at  the  end  of  a  long  and 
severe  attack  of  the  fever,  even  a  comparatively  small  hemorrhage  may  be 
fatal.  The  existence  of  small  losses  of  blood  not  sufficient  in  size  to  be 
manifest  to  the  eye  when  the  stools  are  examined,  may  be  discovered  by 
the  tests  for  occult  blood  named  in  the  Article  on  Gastric  Ulcer. 

Perforation  of  the  bowel,  the  most  serious  of  all  the  complications  of 
this  disease  that  is  commonly  met  with,  has  no  relation  to  the  severity  of 
the  general  symptoms,  for  it  occurs  as  often  in  mild  as  in  severe  cases. 
Indeed,  in  nearly  50  per  cent,  of  recorded  cases  this  accident  occurred  in 
mild  cases.  When  perforation  occurs  the  symptoms  are  apt  to  be  ushered 
in  by  agonizing  pain,  usually  felt  in  the  appendicular  region,  which  may  be 
severe  enough  to  rouse  the  patient  from  a  considerable  degree  of  stupor. 
If  the  patient  is  not  too  apathetic  the  pain  is  often  described  as  being  in 
the  lower  zone  of  the  belly  near  the  median  line,  and  most  commonly 
slightly  to  the  right.  The  belly- wall  is  sensitive  to  palpation,  speedily 
becomes  tense  and  tympanitic,  and  all  the  symptoms  of  a  general  dif- 
fuse peritonitis  may  quickly  ensue.  The  pain  may,  however,  not  be  per- 
sistent, but  pass  away  or  become  modified,  as  the  peritoneal  condition 
resulting  from  the  escape  of  fecal  matter  into  its  cavity  becomes  more  and 
more  septic.  The  pulse  becomes  rapid  and  running,  and  collapse  may 
speedily  assert  itself.  When  this  occurs,  death  speedily  comes  on,  the 
patient  dying  in  a  few  hours,  or,  again,  he  may  rally  and  survive  for  several 
days.  Early  death  is,  however,  the  more  common  result.  Thus  in  the 
collection  of  34  cases  made  by  Fitz,  of  Boston,  37.3  per  cent,  died  on  the 
first  day,  29.5  per  cent,  on  the  second,  and  83.4  per  cent,  in  the  first  week. 
During  the  second  week  9  died,  in  the  third  w^eek  4  died,  and  2  other  cases 
lived  thirty  and  thirty-eight  days,  respectively.  If  collapse  does  not  ensue, 
the  rally  of  the  system  results  in  a  rise  of  the  temperature  to  a  point  higher 
than  before  the  accident,  and  this  movement  is  often  accompanied  by 
chills  and  rigors.  Usually  by  the  second  or  third  day  the  peritoneal  symp- 
toms become  more  and  more  marked,  the  condition  of  the  patient  more 
and  more  asthenic  and  depressed,  and  death  results  by  the  fourth  day 
from  a  general  peritonitis  with  toxaemia  from  the  absorption  of  toxic  materials. 
In  other  cases  the  onset  of  the  perforation  is  insidious ;  the  belly  before  the 
perforation  may  have  been  moderately  tympanitic,  but  now  becomes  intensely 
hard  and  rigid;  the  pain,  which  in  some  cases  is  so  severe,  does  not  develop, 
but  the  great  fall  in  fever  followed  by  a  rise,  and  this  again  by  rigors,  it 
may  be,  give  evidence  of  the  grave  accident  which  has  occurred.  The 
pulse  becomes  increasingly  rapid  and  running,  and  the  respiration  more 
and  more  costal  and  less  and  less  diaphragmatic,  until  the  patient  sinks  out 
of  Hfe,  without  much,  if  any,  suffering,  in  generally  the  same  manner  as  one 
sees  death  come  to  a  case  of  diffuse  septic  peritonitis  due  to  a  pyosalpinx  or 
to  septic  appendicitis.     In  such  cases  the  perforation  is  usually  very  small. 


38  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

and  is  so  surrounded  by  adhesions  that  the  escape  of  the  intestinal  con- 
tents is  very  gradual  and  insidious,  infecting  the  peritoneum  without  the 
escaping  fluid  being  copious  enough  at  any  one  time  to  produce  great  pain 
or  reaction. 

In  this  connection  it  is  important  to  note  that  a  sudden  fall  in  temperature 
is  not  a  symptom  necessary  to  the  diagnosis  of  intestinal  perforation.  On 
the  contrary,  there  are  many  cases  on  record  in  which  a  rise  of  temperature 
has  followed  this  accident. 

The  diagnosis  of  perforation  is  to  be  reached  by  the  following  signs  in 
addition  to  those  just  given:  The  hand  of  the  physician,  when  lightly  placed 
upon  the  abdominal  wall,  not  only  develops  the  fact  that  it  is  hypersensitive, 
but  that  its  muscles  are  unduly  tense.  If  the  perforation  has  occurred 
very  recently  the  rather  swollen  and  tumid  belly  may  be  slightly  scaphoid. 
Percussion  may  indicate  the  presence  of  gas  in  the  peritoneal  cavity,  and 
the  Uver  may  be  pushed  away  from  the  abdominal  wall  in  such  a  manner 
that  the  ordinary  area  of  Hver  dulness  is  largely  decreased.  Percussion  of 
the  right  hypochondrium  is,  therefore,  an  essential  procedure  in  the  physical 
diagnosis  of  these  cases.  A  fallacy  underlying  this  test  is  the  possibility  of 
a  portion  of  the  colon,  when  greatly  distended  with  gas,  slipping  up  between 
the  liver  and  the  belly  wall,  and  thus  giving  resonance;  but  this  is  a  rare 
occurrence. 

In  some  cases,  however,  as  intimated,  the  symptoms  are  so  insidious  that 
the  absence  of  this  sign  does  not  negative  the  diagnosis  of  perforation. 
Indeed  a  positive  diagnosis  may  not  be  possible,  and  cases  are  sometimes 
met  with  in  which  the  perforation  has  not  been  suspected,  and  is  found 
only  at  the  autopsy. 

The  diagnosis  of  peritonitis  due  to  perforation  is  aided,  but  not  confirmed, 
if  an  examination  of  the  blood  reveals  a  leukocytosis  of  polymorphonuclear 
cells. 

There  are  several  conditions  causing  pain  which  must  be  carefully  excluded 
before  the  physician  can  arrive  at  the  diagnosis  of  perforation,  even  if  the 
symptoms  and  signs  just  described  are  present.  These  are  diaphragmatic 
pleurisy,  pneumonia  of  the  bases,  appendicitis,  iliac  thrombosis,  and  intes- 
tinal obstruction.  Further  than  this,  peritonitis  may  develop  from  extension 
of  the  inflammatory  process  in  the  bowel  or  by  reason  of  the  migra- 
tion of  micro-organisms  through  those  parts  of  the  bowel  wall  which 
have  been  impaired  by  the  ulcerative  process.  In  such  cases  the  pain, 
swelling,  and  diaphragmatic  paralysis  may  all  be  present  without  being 
due  to  perforation,  and  so  closely  may  the  symptoms  of  perforation  be 
aped  that  operation  has  been  performed,  with  the  discovery  that  no  perfora- 
tion had  occurred;  thus  in  a  case  under  the  care  of  Herringham,  nothing 
was  found  at  the  section  and  the  patient  recovered.  Perforation  may  also 
be  simulated  by  suppuration  and  rupture  of  a  swollen  mesenteric  gland. 
Other  causes  of  peritonitis  are  necrosis  of  the  mesenteric  glands,  infarc- 
tion of  the  spleen,  or  the  development  of  abscess  in  an  ovary  or  Fallopian 
tube.  Very  rarely  peritonitis  arises  from  cholecystitis  or  cholangitis,  with 
or  without  gallstones.  Liebermeister  has  recorded  two  cases  in  which 
rupture  of  the  gall-bladder  with  escape  of  gallstones  into  the  abdominal 


TYPHOID  FEVER  39 

cavity  took  place.  An  ulcer  in  the  appendix  may  perforate  or  an  inter- 
current appendicitis  may  complicate  the  case. 

The  percentage  of  frequency  of  occurrence  of  perforation  is  generally 
stated  to  be  about  2.2,  but  in  30,966  cases  of  typhoid  fever  collected  from 
several  series  of  cases  reported  by  French  and  German  physicians,  and 
from  the  official  reports  of  hospitals  in  the  United  States  and  Canada, 
England  and  Ireland,  Germany,  Austria,  South  Africa,  and  Australia, 
perforation  is  stated  to  have  occurred  in  1 144  cases,  which  gives  a  percentage 
of  3.69.  The  percentage  of  its  mortality,  when  surgical  interference  is  not 
resorted  to  at  the  most  favorable  time,  is  90  to  95  per  cent.,  and  with 
operative  interference  it  may  be  as  high  as  81  per  cent.     (See  Treatment.) 

Perforation  is  very  much  more  frequently  seen  in  men  than  in  women. 
Fitz  in  444  cases  found  71  per  cent,  in  men  and  29  per  cent,  in  women.  In 
21  cases  of  perforation  in  Basle,  15  were  men  and  6  were  women;  and 
Griesinger  in  14  cases  had  10  men  and  4  women.  Murchison  also  found 
in  24  cases  16  men  and  8  women,  although  the  general  mortality  of  the 
disease  among  women  was  slightly  higher  than  among  men.  So,  too, 
Bristowe,  of  London,  met  with  this  accident  in  men  in  11  of  15  cases,  and, 
again,  Nacke  collected  106  perforation  cases,  of  which  72  were  in  men 
and  34  were  in  women. 

Perforation  is  responsible  for  a  large  proportion  of  the  deaths  which  occur 
from  typhoid  fever.  Out  of  1721  cases  which  came  to  autopsy  the  per- 
centage of  deaths  due  to  perforation  was  11.3,  according  to  Murchison. 
According  to  Hdlscher,  it  was  found  in  2000  Munich  cases  114  times  (5.7 
per  cent.),  and  in  20  out  of  80  of  his  cases  which  ended  in  death.  In  4680 
cases  tabulated  by  different  writers,  Fitz  found  the  proportion  to  be  6.58 
per  cent.,  which  agrees  with  Holscher's  statistics.  Hoffman  found  that  out 
of  250  deaths  in  typhoid  fever  20  were  due  to  perforation. 

Perforation  takes  place  most  commonly  in  the  third  and  fourth  weeks  of 
the  malady,  but  is  by  no  means  rare  in  the  second  week.  It  occurs  most 
commonly  in  patients  between  twenty  and  thirty  years  of  age.  Elsberg  has 
reported  a  case  of  a  child  of  three  and  a  half  years  who  suffered  from 
this  accident,  but  whose  life  was  saved  by  abdominal  section. 

The  relation  of  typhoid  fever  to  appendicitis  is  one  of  great  interest. 
It  has  been  thought  by  some  that  appendicitis  arising  in  typhoid  fever  was 
a  mere  coincidence;  by  others,  that  its  origin  depended  upon  a  general  infec- 
tious process;  and,  again,  by  others,  that  it  was  due  to  the  direct  infection  of 
the  appendix  with  the  bacillus  of  Eberth.  Probably  all  these  views  hold  true 
in  individual  cases.  The  richness  of  the  appendix  in  lymphoid  tissue,  and 
the  fact  that  typhoid  fever  is  particularly  prone  to  attack  such  tissues, 
renders  this  organ  peculiarly  susceptible  on  theoretical  grounds.  That  this 
view  is  correct  is  proved  by  the  research  of  Hopfenhausen,  who  collected 
the  appendices  obtained  from  30  cases  of  typhoid  fever  and  studied  them 
under  Stilling  in  the  University  of  Lausanne.  She  concludes  that  moderate 
changes  in  the  appendix  may  be  found  in  nearly  all  cases  of  this  disease, 
that  it  is  most  marked  in  the  earlier  stages  of  the  malady,  and  consists 
chiefly  in  cellular  infiltration,  specific  lesions  being  rare  and  not  suffi- 
cient to  produce  the  more  severe  forms  of  appendicular  disease. 


40  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

True  appendicitis  complicating  typhoid  fever,  in  the  sense  of  inflammation 
of  the  appendix  severe  enough  to  produce  abscess,  is  undoubtedly  a  very 
rare  affection.  Hopfenhausen  has  collected  statistics  of  743  cases  of  appen- 
dicitis, of  which  5  per  cent,  were  due  to  typhoid  fever.  This  must  be  a 
very  much  larger  percentage  than  usually  exists. 

It  is  a  noteworthy  fact  that  appendicular  symptoms  are  not  infrequent 
in  early  typhoid  fever,  and  often  disappear  under  rest  in  bed,  and  with 
the  full  development  of  the  infection.  Rarely  the  inflammation  goes  on 
to  the  formation  of  an  appendicular  abscess  or  perforation.  The  swelling 
of  the  lymph  node  in  the  mesoappendix  and  the  presence  of  ulcers  in  the 
caecum  explain  why  it  is  that  pain  in  the  appendicular  area  is  by  no  means 
rare.  (See  Plate  I.)  Sudden  pain  in  the  lower  zone  of  the  abdomen  may  be 
indicative,  not  of  appendicitis,  but  of  the  presence  of  an   iliac  thrombosis. 

Tympanites  in  typhoid  fever  is  always  present  to  some  degree  at  some 
stage  of  the  disease.  AVhen  very  marked,  it  is  an  evil  symptom  because 
it  indicates  active  fermentation  in  the  bowel,  and  the  presence  of  intestinal 
atony,  and  because  the  gas  presses  on  the  abdominal  thoracic  viscera  and 
disturbs  their  functions.  By  distending  the  intestine  it  may  also  predispose 
the  patient  to  a  hemorrhage  or  perforation  by  the  strain  on  a  severely  ulcer- 
ated Peyer's  patch. 

Hepatic  Complications. — ^The  liver  and  gall-bladder  rarely  show  signs  of 
active  infection  during  the  early  part  of  an  attack  of  typhoid  fever.  Jaundice 
is  one  of  the  rarest  complications  of  this  disease.  Aside  from  some  swelling 
and  tenderness  in  the  hepatic  region,  no  symptoms  in  the  hypochondrium  are 
usually  observable.  It  is,  however,  important  to  note  that  secondary  involve- 
ment of  the  gall-bladder  as  a  sequel  of  this  malady  is  by  no  means  rare,  a  true 
cholecystitis  developing  in  a  goodly  proportion  of  cases  as  a  result  of  infec- 
tion of  this  viscus  by  the  bacillus  of  Eberth.  This  cholecystitis  may  be 
severe  enough  to  result  in  empyema  of  the  gall-bladder  and  perforation 
of  its  walls  with  symptoms  resembling  intestinal  perforation.  A  still  more 
interesting  fact  is  that  such  a  cholecystitis  due  to  this  organism  may  develop 
many  years  after  the  attack  of  typhoid  fever,  and  again  that  the  clumping 
of  these  organisms  in  the  gall-bladder  may  give  rise  to  the  formation  of 
gallstones. 

Louis,  in  his  work  on  typhoid  fever,  published  in  1836,  states  that  changes 
in  the  bile  and  gall-bladder  occur  more  frequently  in  typhoid  fever  than 
in  other  acute  diseases,  and  cites  3  fatal  cases  in  which  cholecystitis,  unrecog- 
nized during  life,  was  found  at  autopsy.  Grisolle  and  Andral  mention 
similar  cases.  In  3  instances  French  found  the  gall-bladder  of  persons 
who  had  died  of  typhoid  fever  filled  with  turbid  albuminous  fluid,  and 
Rokitansky  speaks  of  having  found  "fibrinous  exudations"  in  the  gall- 
bladder of  several  patients  who  died  from  the  disease.  Murchison  refers 
to  the  cholangitis  and  cholecystitis  which  may  accompany  typhoid  fever, 
and  reports  a  case  of  rupture  of  the  gall-bladder,  followed  by  general  peri- 
tonitis. In  1876  Hagenmiiller  reported  18  cases  of  cholecystitis  complicating 
typhoid  fever.  He  concluded  that  it  was  a  more  frequent  complication 
than  had  generally  been  supposed.  Holscher,  in  the  2000  Munich  autop- 
sies, found  empyema  of  the  gall-bladder  5  times. 


TYPHOID  FEVER  41 

In  1889  Bernheim  suggested  that  typhoid  bacilh  might  give  rise  to  gall- 
stones by  producing  alteration  or  stagnation  of  the  bile.  In  1893  Defourt 
reported  19  cases  of  cholelithiasis,  in  which  the  first  attack  of  biliary  colic 
occurred  at  varying  periods  after  typhoid  fever.  Osier  has  reported  a  case 
of  hepatic  colic  occurring  for  the  first  time  in  the  fifth  week  of  typhoid 
fever.  At  operation  nothing  could  be  found  to  account  for  perforation 
of  the  gall-bladder,  but  nine  months  later  a  gallstone  was  discharged. 

Fournier  found  bacteria  in  38  out  of  100  gallstones  which  he  removed 
at  autopsies."  The  colon  bacilli  predominated,  while  the  typhoid  bacilli 
were  found  to  be  second  in  frequency.  Milian,  Chantemesse,  and  Horton 
Smith  report  similar  experiences. 

Chiari  found  typhoid  bacilli  present  in  the  gall-bladder  in  19  out  of  22 
cases,  and  obtained  pure  cultures  from  15.  In  9  out  of  10  cases  at  St. 
Bartholomew's  Hospital,  London,  Bacilli  typhosi  were  found.  Gushing 
mentions  5  cases  of  cholecystitis  complicating  typhoid  fever,  in  which  pure 
cultures  of  colon  bacilli  were  obtained  from  the  pus.  Marsden  reports  a 
case  in  which  cultures  resembling  Bacillus  typhosus  were  obtained.  Van 
Dungern  obtained  pure  cultures  of  typhoid  bacilli  from  pus  surrounding 
the  gall-bladder  fourteen  years  and  a  half  after  an  attack  of  typhoid  fever. 
Pure  cultures  have  often  been  obtained  from  six  to  eight  months  after  the 
attack  (Chantemesse,  Dupr^). 

Mason  thinks  that  the  bacilli  gain  entrance  through  the  biliary  ducts. 
Councilman  believes  that  they  are  carried  through  the  blood,  and  that  areas 
of  necrosis  in  the  liver  afford  them  portals  of  entrance.  Hagenmiiller,  Mayo 
Robson,  and  Mark  Richardson  believe  that  biliary  complications,  espe- 
cially cholecystitis,  are  due  to  ascending  infection  of  the  ducts.  Marsden  is 
of  the  opinion  that  the  most  important  passage  of  bacilli  into  the  gall- 
bladder is  through  the  blood,  the  liver,  and  the  biliary  ducts.  He  is 
undoubtedly  correct. 

Typhoid  cholecystitis  during  the  course  of  the  fever  is  frequently  latent. 
In  more  than  one-half  the  recorded  cases,  either  on  account  of  latency  of 
symptoms  or  typhoidal  stupor,  nothing  unusual  was  observed  during  life. 

The  two  most  constant  symptoms  are  pain  and  swelling,  the  former  being 
paroxysmal  and  most  marked  in  the  region  of  the  gall-bladder  and  under 
the  scapula.  Maurice  Richardson  says  that  it  may  be  in  the  epigastrium 
or  over  McBurney's  point.  According  to  Mayo  Robson,  if  a  line  be  drawn 
from  the  umbilicus  to  the  ninth  rib  on  the  right  side,  there  is  almost  always 
tenderness  at  the  beginning  of  the  second  third  of  this  line.  Jaundice  is 
rarely  met  with,  but  there  may  be  repeated  chills  and  sweats. 

Genito-urinary  Complications. — Albuminuria  in  typhoid  fever  is  quite 
a  constant  condition,  occurring  as  frequently  as  in  70  per  cent,  of  all  cases, 
and  being  most  marked  in  the  second  week.  Usually  its  presence  is  not  asso- 
ciated with  that  of  tube  casts  unless  the  patient  is  already  a  sufferer  from 
nephritis  prior  to  the  attack.  When  casts  are  present,  the  albumin  is  usu- 
ally present  in  large  amount.  Albuminuria  without  casts  is  not  a  serious 
complication.  Probably  true  nephritis  is  present  in  almost  20  per  cent,  of 
the  cases,  but  this  is  usually  not  productive  of  renal  symptoms.  An  ante- 
cedent nephritis  may  take  on  renewed  activity  and   a   true  hemorrhagic 


42  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

nephritis  may  occur,  usually  in  severe  cases  only.  The  urine  is  apt  to  be 
scanty  and  of  high  specific  gravity  unless  the  physician  insists  upon  the 
patient  drinking  freely  of  water. 

Pyuria  in  slight  degree  is  common.  Blumer  says  it  occurs  in  17  per  cent., 
but  it  is  a  noteworthy  fact  that  pyelitis  due  to  typhoid  fever  is  almost  unknown. 
While  this  is  true,  it  is  also  of  interest  to  note  that  enormous  numbers  of 
the  bacillus  of  Eberth  are  to  be  found  in  the  urine  after  the  second  week 
of  the  disease,  and  often  far  into  convalescence.  Petruschky  has  estimated 
that  1  c.c.  may  contain  170,000,000  bacilli.  A  profuse  polyuria  is  often 
present  when  the  stage  of  convalescence  is  entered  upon. 

Orchitis  and  epididymitis  rarely  occur  as  a  result  of  a  direct  infection  with 
the  specific  bacillus.  They  differ  from  the  changes  due  to  gonorrhoea  in 
that  they  are  less  painful  and  more  rapid  in  their  course  to  suppuration  or 
recovery.  They  are  usually  unilateral  and  the  testicle  is  first  affected. 
Typhoidal  cystitis  due  to  the  presence  of  the  bacillus  of  Eberth  rarely  occurs. 

Respiratory  Complications. — The  respiratory  disorders  met  with  in 
connection  with  the  course  of  typhoid  fever,  aside  from  the  bronchitis  already 
mentioned,  are  quite  numerous.  In  the  later  stages  of  the  disease  we  may 
meet  with  severe  laryngeal  ulceration,  which  in  turn  may  be  complicated  by 
perichondritis  or  oedema  of  the  glottis.  Hoffman  found  28  cases  of  ulcer  of 
the  larynx  in  250  autopsies  in  this  disease,  and  Griesinger  in  26  per  cent,  of 
those  dying  of  the  malady,  so  that  it  is  by  no  means  rare.  Keen  collected 
146  cases  of  severe  laryngeal  disease  due  to  this  cause,  and  found  that 
necrosis  of  the  laryngeal  cartilages  when  it  occurred  was  a  very  fatal 
complication,  death  occurring  in  95  per  cent,  of  the  cases. 

Intense  hypostatic  congestion  is  one  of  the  most  constant  pulmonary 
changes  seen  at  autopsy;  in  some  cases  the  blood  may  inundate  the  air 
vesicles,  causing  solidification.  How  often  this  change  is  agonal  cannot  be 
determined  with  any  degree  of  certainty,  but  as  it  depends  on  more  or  less 
prolonged  maintenance  of  one  position  aided  by  an  enfeebled  circulation 
the  danger  can  be  greatly  lessened,  if  not  avoided,  by  frequent  changes 
in  posture. 

Pneumonia  develops  in  typhoid  fever  in  three  forms  and  in  different  stages 
of  the  disease:  (1)  As  an  acute  lobar  pneumonia  ushering  in  the  attack  of 
enteric  fever,  and  due  to  the  Micrococcus  lanceolatus,  or,  it  is  thought  by 
some,  to  the  infection  of  the  lung  by  the  bacillus  of  Eberth,  the  so-called 
''pneumotyphoid."  True  croupous  pneumonia  in  the  later  stages  is  very 
rare.  (2)  Bronchopneumonia,  probably  arising  from  terminal  infection  or 
by  hypostatic  congestion  due  to  the  profound  toxsemia  and  cardiac  degenera- 
tion and  feebleness,  is  more  common.  (3)  Acute  tuberculous  pneumonia 
sometimes  seizes  the  typhoid  fever  patient  when  he  seems  about  to  begin 
his  convalescence. 

It  is  not  to  be  forgotten  that  infarction  of  the  lung  may  occur  as  the 
result  of  cardiac  or  venous  emboli.  Such  an  infarction  may  mislead  the 
physician  into  a  diagnosis  of  lobar  or  lobular  pneumonia  by  reason  of 
the  dulness  on  percussion,  the  rise  of  temperature,  and  blood-tinged 
sputum.  An  infarction  may,  if  the  patient  survives,  result  in  pulmonary 
abscess  or  gangrene. 


TYPHOID  FEVER  43 

Pleurisy  arises  very  rarely  as  a  primary  lesion.  It  is  usually  secondary  to 
infarction,  pneumonia,  or  gangrene.  Cases  of  empyema  due  to  the  specific 
bacillus  have,  however,  been  recorded. 

Nervous  Complications. — The  nervous  disturbances  vary  very  greatly. 
In  the  average  case  there  is  in  the  early  part  of  the  onset  no  mental  change 
save  that  of  unfitness  for  mental  occupation,  with  dreamful  sleep  which  is  apt 
to  be  restless.  Later  the  patient  continually  dozes  off,  yet  awakens  easily,  and 
for  a  moment  may  be  a  little  confused  between  the  mental  impressions  left 
on  his  brain  by  the  dream  and  the  conditions  he  finds  about  him  on  returning 
to  consciousness.  Still  later,  if  the  infection  is  severe,  he  becomes  more 
apathetic  when  awake,  less  easily  aroused  when  asleep,  and  often  delirious 
in  his  sleep,  his  dreams  being  evidently  vivid,  so  that  he  keeps  muttering 
the  conversation  he  thinks  he  is  actually  having,  or  calls  out  loudly,  as  his 
dream  seems  to  lead  him  to  a  point  where  an  imperative  call  or  sudden 
action  is  needed.  Sometimes  the  delusions  in  the  delirium  amount  to 
imperative  conceptions,  and  the  patient  believes  that  he  is  away  from  home 
and  must  return  there  at  once,  or  that  he  is  being  restrained  by  force,  or, 
again,  that  some  member  of  his  family  is  in  distress  and  needs  his  aid  or 
is  calling  for  him.  Often  this  form  of  mental  disturbance  is  painful  to 
witness,  difficult  to  overcome,  and  harassing  to  the  patient.  In  these  cases 
the  hands  may  be  moved  continually  in  active  motions,  as  if  to  illustrate 
the  ideas  of  the  patient.  Such  cases  are  apt  to  be  grave  if  for  no  other 
reason  than  that  they  exhaust  themselves  if  relief  is  not  given.  The 
more  encouraging  type  of  delirium  is  of  the  quiet,  muttering  form,  as  if 
the  patient  was  gently  "speaking  in  his  sleep"  as  in  health,  and  this  may 
be  taken  as  the  natural  form  of  delirium  in  the  disease.  Later  the  stupid 
condition  becomes  more  and  more  marked  in  some  cases,  and  absolute 
mental  stillness  is  reached,  in  which  only  rough  shaking  or  loud  calling 
will  arouse  the  patient.  In  severe  cases  with  marked  toxaemia  we  find  at 
times  a  state  of  mental  confusion,  staring  eyes,  and  semi-stupor,  with  per- 
sistent muttering,  the  so-called  coma  vigil. 

During  convalescence  mental  aberration,  depending  usually  upon  exhaus- 
tion, may  develop.    The  prognosis  in  such  cases  is  usually  good. 

Rarely  in  the  course  of  typhoid  fever  symptoms  of  irritation  or  inflamma- 
tion of  the  meninges  of  the  brain  develop,  and  it  is  important  to  remember 
that  these  symptoms  may  arise  from  several  causes.  The  most  common  of 
these  is  congestion  and  engorgement  of  the  meningeal  vessels  without  any 
true  inflammatory  process;  the  next  most  common  form  is  that  due  to  the 
extension  of  an  infection  from  abscess  in  the  middle  ear;  the  third  form  is 
that  in  which  there  is  infection  with  the  streptococcus  or  pneumococcus, 
and  very  rarely  the  meningitis  is  due  to  the  bacillus  of  Eberth.  Cole 
has  recorded  three  instances  in  which  the  typhoid  bacillus  was  obtained 
from  the  cerebrospinal  fluid  by  lumbar  puncture  in  typhoid  fever.  In  one 
the  meningitis  was  serous,  in  another  purulent;  the  character  of  the  other 
is  not  stated. 

The  frequency  of  this  complication  in  the  different  periods  of  the  disease 
when  due  to  true  typhoid  infection  of  the  meninges  is  in  direct  ratio  to 
the  length  of   the   malady,  namely,  in  the  third  or  fourth  week.     In  the 


44  DISEASES  DUE   TO   A    SPECIFIC  INFECTION 

great  majority  of  instances  in  which  the  complication  has  appeared  the 
patient  was  under  thirty  years,  and  usually  between  twenty  and  thirty 
years.  That  is  the  period  in  which  typhoid  fever  is  most  conmionly 
seen. 

In  every  case  of  true  typhoid  meningitis,  so  far  recorded,  death  has 
occurred,  but  this  is  a  statement  which  does  not  possess  as  great  prognostic 
value  as  would  appear  at  first  glance,  since  an  absolute  diagnosis  of  true 
typhoid  meningitis  can  not  be  made  during  life,  for  the  positive  test  is 
the  bacteriological  examination  of  the  skull  contents.  Nevertheless,  the 
presence  of  marked  meningeal  symptoms  is  of  the  gravest  import  in  all 
cases. 

Sometimes,  because  of  degenerative  changes  in  the  vessels,  a  hemorrhagic 
effusion  into  the  meninges  of  the  brain  takes  place,  but  this  does  not 
commonly  produce  marked  symptoms  unless  it  is  profuse. 

Convulsions,  generalized  or  localized,  with  coma  and  delirium  may  arise 
from  thrombosis  of  the  cerebral  sinuses  or  of  the  cerebral  arteries,  but  they 
are  very  rare  from  any  cause.  Murchison  only  met  with  them  in  6  cases  out 
of  2960.  If  due  to  the  lesions  named,  they  indicate  a  fatal  termination 
in  the  near  future.  In  Osier's  case  death  followed  convulsions,  produced  by 
thrombosis  of  the  branches  of  the  left  middle  cerebral  artery,  in  twelve 
hours.  If  they  occur  in  neurotic  children  or  females,  the  outlook  is  not 
so  gloomy,  as  they  probably  do  not  depend  upon  an  actual  lesion  in  the 
brain. 

Sometimes  acute  otitis  media  produces  violent  headache  and  finally 
symptoms  of  meningitis,  but  its  presence  is  often  unrecognized  as  a  cause 
until  a  discharge  takes  place  from  the  ear. 

Neuritis,  generalized  or  localized,  is  met  with  occasionally  in  the  later 
stages,  producing  wrist-drop  or  toe-drop,  and  sometimes  causing  severe 
pain.  ^Vhen  there  is  a  multiple  neuritis  the  symptoms  may  closely  resemble 
locomotor  ataxia  or  anterior  poliomyelitis.  Sometimes  the  skin  of  the  toes 
or  of  the  whole  foot  becomes  exquisitely  sensitive. 

When  hemiplegia  occurs,  which  is  quite  rare,  it  results  from  cerebral 
embolism  or  thrombosis  or  very  rarely  from  actual  hemorrhage. 

Complications  in  the  Bones,  Joints,  and  Muscles. — Secondary 
disease  of  the  bones,  consisting  of  post-typhoidal  osteomyelitis  due  to  the 
specific  bacillus  or  to  infection  by  associated  micro-organisms,  may  occur. 
The  tibia  and  the  ribs  are  the  bones  most  commonly  involved,  and  the 
changes  are  subacute  or  chronic  rather  than  acute.  vSo,  too,  arthritis  may 
be  due  to  pyogenic  micro-organisms  or  to  the  Eberth  bacillus,  and  is  usually 
of  a  subacute  or  chronic  type.  Spontaneous  dislocation  of  the  hip  may  occur 
in  very  rare  instances. 

IMany  years  ago  V.  P.  Gibney,  of  New  York,  described,  under  the  name 
of  typhoid  spine,  a  condition  in  which  there  develops,  often  some  days 
after  the  patient  is  up  and  about,  and  often  only  after  some  very  slight  jar 
or  trauma,  great  tenderness  of  the  spine,  with  pain  in  the  back,  and  in  the 
legs  when  they  are  moved.  Usually  it  is  held  that  this  condition  is  not 
dependent  upon  a  spondylitis,  neuritis,  or  Pott's  disease,  and  is  probably 
a  neurosis  closely  allied  to  the   neuroses  seen  in  cases  of  severe  trauma. 


TYPHOID  FEVER  45 

Fraenkel  has  recently  shown  that  in  fatal  cases  of  typhoid  fever  the 
bacillus  may  be  obtained  from  the  cancellous  tissue  of  the  bodies  of 
the  vertebrae  and  some  of  these  cases  of  so-called  typhoid  spine  may  be 
instances  of  osteomyelitis  involving  these  structures. 

Sometimes  in  the  stage  of  convalescence  a  curious  state  is  developed  in 
which  the  muscles  of  the  lower  extremities  become  painful,  somewhat 
brawny,  and  even  slight  redness  may  appear  in  the  skin  covering  them. 
Usually  this  is  unilateral,  but  it  may  be  bilateral.  Most  commonly  it 
affects  the  calf  of  the  leg,  and  pain  is  developed  on  pressure  or  on  move- 
ment, active  or  passive.  This  is  due  to  a  myositis.  It  should  not  be 
confused  with  phlegmasia  dolens  due  to  thrombosis. 

Typhoid  Fever  Complicating  Pregnancy. — In  a  very  large  number  of 
cases  of  typhoid  fever  complicating  pregnancy,  abortion  or  premature  labor 
comes  on.  Corbin  collected  364  cases  of  typhoid  fever  occurring  in  pregnant 
women,  and  Fellner,  of  Vienna,  has  added  7  others  to  this  number,  making  a 
total  of  371  cases.  Of  these  371  cases  228,  or  61  per  cent.,  ended  in  prema- 
ture births,  and  in  202  cases  pregnancy  terminated  before  the  sixth  month. 
Most  of  the  full-term  children  were  born  dead,  and  those  who  were  born 
alive  were  weak  and  did  not  long  survive.  The  mortality  in  the  mother 
under  these  circumstances  is  about  16  per  cent. 

Diagnosis. — ^The  diagnosis  of  typhoid  fever  is  to  be  based  on  the  char- 
acteristic ascent  of  the  temperature,  the  general  malaise  of  the  patient,  the 
peculiarly  coated  tongue  with  red  edges,  the  tumid  belly,  and  the  develop- 
ment of  the  rash  about  the  seventh  to  the  ninth  day.  If  to  these  symptoms 
are  added  an  enlargement  of  the  spleen  and  liver,  the  diagnosis  becomes 
still  more  certain,  and  is  confirmed  if  the  laboratory  tests  mentioned  on 
the  following  pages  are  positive.  The  laboratory  aids  to  diagnosis  are 
the  Widal  or  agglutination  test;  the  isolation  of  the  bacillus  from  the 
blood,  from  the  stools,  from  the  urine,  and  from  the  rose  spots,  and 
the  diazo  reaction.  The  objection  to  these  tests  is  the  difficulty  as  to 
technique  for  the  general  practitioner,  and,  more  important  still,  the  fact 
that  some  of  them  are  obtainable  in  many  instances  so  late  in  the  course 
of  the  disease  as  only  to  confirm  the  clinical  diagnosis  already  made.  (See 
page  48.) 

Typhoid  fever  must  be  separated  from  a  number  of  maladies  which 
closely  resemble  it.  Pure  typhoid  infection  may  result  in  the  production 
of  a  fever  which  closely  follows  the  remittent  or  intermittent  malarial 
types,  and  which  is  often  associated  with  so  much  gastric  disturbance  and 
vomiting  and  so  lacking  in  the  more  prominent  typhoid  symptoms  usually 
seen  that  the  picture  of  remittent  malarial  fever  is  clear,  while  the  true 
picture  of  typhoid  fever  is  clouded.  Again,  there  can  be  no  doubt  that 
cases  of  true  malarial  infection  occur  in  which  the  symptoms  so  closely 
resemble  those  of  typhoid  fever  that  a  purely  clinical  diagnosis  is  almost 
impossible  if  an  epidemic  of  typhoid  fever  is  in  full  swing  at  the  time. 
Finally,  there  can  also  be  no  doubt  that  it  is  possible  for  the  patient  to  have 
a  double  infection  with  the  bacillus  of  Eberth  and  the  plasmodium  of 
Laveran,  in  which  case,  however,  the  malarial  manifestations  are  usually 
dwarfed  by  the  typhoid  poison,  and  only  are  marked  at  the  onset  of  the 


46 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


enteric  fever  and  at  its  termination.  To  this  mixed  infection  the  term 
typhomalarial  fever  may  be  correctly  apphed  to  indicate  not  a  separate 
disease,  but  a  double  infection.  Etymologically,  this  term  might  also  be 
used  to  define  a  condition  of  malarial  fever  in  which,  because  of  profound 
debility,  the  patient  was  in  a  typhoid  state — that  is,  in  a  condition  of  which 
typhoid  fever  is  a  type.  Practically,  however,  it  should  be  discarded  or 
limited  in  its  use  to  the  double  infection  just  described. 

How  far  constant  fever  occurring  day  after  day  and  associated  with 
manifestations  of  general  loss  of  strength  and  debility  can  be  relied  upon 
in  the  diagnosis  of  typhoid  fever  is  hard  to  determine.  Certain  it  is  that  if 
a  physician  makes  a  diagnosis  of  enteric  fever  upon  these  symptoms  alone, 
without  bearing  in  mind  the  fact  that  similar  conditions  are  equally  well 
developed  under  other  forms  of  infection,  he  will  find  himself  in  error  in 
not  a  few  instances.  Chief  among  these  conditions  may  be  mentioned 
tuberculosis  of  the  lungs  or  peritoneum,  that  form  of  influenza  in  which 
the  chief  symptoms  are  abdominal,  cases  of  ulcerative  endocarditis,  septi- 
coemia,  and  pyaemia,  and  those  of  cholecystitis  with  ulceration,  as  from 
impacted  gallstones.  It  must  not  be  forgotten,  too,  that  syphilitic  fever 
may  in  very  susceptible  persons  resemble  typhoid  infection.  The  febrile 
movement,  rose  rash  (if  it  be  scanty),  malaise,  and  signs  of  general  infection 
in  this  disease  may  readily  mislead  the  physician.  Again,  in  the  more 
advanced,  or  tertiary,  stages  of  syphilis  a  prolonged  low,  septic  fever  may 
be  present.  Any  case  of  so-called  typhoid  fever  which  lasts  more  than 
four  weeks  without  the  attack  being  prolonged  by  a  relapse  is  almost 
certainly  suffering  from  another  disease,  often  tuberculosis. 

It  is  not  to  be  forgotten  that  trichiniasis  may  resemble  typhoid  fever, 
for  in  it  we  have  fever,  pains  in  the  limbs  and  back,  headache,  stupor,  and 
nausea,  with  pain  in  the  belly  and  diarrhoea. 

The  differentiation  of  typhoid  from  other  fevers  is  aided  by  a  study  of 
the  following  table: 

Typhoid  Fever. 
Onset  gradual. 
Face  dull  and  apathetic. 


Delirium  a  late  symptom. 

Coma  a  late  symptom. 

Eruption  very  late. 

Eruption  chiefly   on  trunk,  well  defined,  and 

appeal's    in  several  crops  of  small  rose-red 

spots. 
Leukocytes  decreased. 
Widal  test  positive. 
Bacilli  of  Eberth  in  blood. 

Typhoid  Fever. 
Kash  appears  in  crops. 
Profuse  sweats  rare. 
Temperature  curves  regular. 
Pulse  rarely  over  100. 
Bacillus  of  Eberth  in  blood. 
Widal  test  positive. 
No  eye  changes. 
Respirations  slightly  increased. 
Cyanosis  rare, 


Typhus  Fever. 

Onset  abrupt. 

Face  livid,  anxious,  swollen,  conjunctiva  red- 
dened.    Pupils  contracted. 

Delirium  an  early  symptom. 

Coma  an  early  symptom. 

Eruption  early. 

Eruption  over  trunk  and  limbs  and  ill- 
defined.  Does  not  appear  in  crops,  and  is 
dusky  red  or  petechial  in  character. 

Leukocytes  increased. 

Widal  test  negative. 

Bacilli  absent. 

Acute  Miliary  Tuberculosis. 
Bash,  if  present,  not  in  crops. 
Profuse  sweats  constant. 
Temperature  curves  irregular. 
Pulse  usually  rapid. 
Absent  from  blood. 
Negative. 

Choroidal  tubercles. 
Greatly  increased. 
Cyanosis  common, 


TYPHOID  FEVER 

Typhoid  Fever  of  the  Cerebral  Type.  Cerebral  Meningitis. 


47 


Regular  temperature. 
No  marked  blood  change. 
Herpes  very  rare. 
Eose  rash  on  trunk  chiefly. 
Cerebrospinal  fluid  negative. 

Typhoid  Fever. 

Onset  gradual. 
Fever  gradually  rises. 
Chills  rare  in  onset. 
Unaffected  by  quinine. 
Heavy  facial  expression. 

Herpes  rare. 

Early  delirium  rare. 

Anaemia  moderate. 

Moderate  reduction  in  leukocytes. 

Eose  rash. 

Bacilli  in  blood. 


Irregular  temperature. 

Increase  in  polynuclear  white  cells. 

Very  common. 

Petechise  over  whole  surface. 

Positive  for  the  specific  bacillus. 

JEstivo-autumnal  Fever. 

Onset  acute. 
Fever  rises  irregularly. 
Severe  chills  common. 
Improved  by  quinine. 

Anxious  facies  with  slightly  icteroid  conjunc- 
tiva. 
Herpes  common. 
Early  delirium  common. 
Ansemia  marked. 
Great  reduction  in  leukocytes. 
No  rash. 
Plasmodium  in  blood. 


Typhoid  Fever. 


Onset  gradual. 
Enlarged  spleen. 
Eose  rash. 
Prostration  gradual. 
Lasts  several  weeks. 


Influenza. 

Onset  sudden. 

No  enlargement  of  spleen. 

No  rash. 

Prostration  rapid. 

Lasts  a  few  days. 


Typhoid  Fever. 

Onset  gradual. 

Nervous  symptoms  moderate. 

No  leukocytosis. 

Widal  test  positive. 

Bacilli  in  blood. 

Lasts  weeks. 

Disease  of  youth. 

Typhoid  Fever. 

No  cardiac  murmurs. 
Eegular  temperature. 
Sweats  rare. 
No  leukocytosis. 
No  cardiac  dyspnoea. 
No  petechise. 
No  infarctions. 
No  leukocytosis. 
Widal  test  positive. 
No  retinal  emboli. 
No  chills. 
Bacilli  in  blood. 


Typhoid  Pneumonia. 

Onset  more  rapid. 
Nervous  symptoms  severe. 
Marked  leukocytosis. 
Widal  test  negative. 
None  in  blood. 
Lasts  a  shorter  time. 
Disease  of  old  age. 

Ulcerative  Endocarditis, 

Cardiac  murmurs. 

Irregular  septic  temperature. 

Sweats  common. 

Marked  leukocytosis. 

Cardiac  dyspnoea. 

Petechise. 

Infarctions. 

Leukocytosis. 

Negative. 

Eetinal  emboli. 

Eepeated  chills. 

No  bacilli  in  blood. 


Typhoid  Fever. 


Eose  rash. 
Face  not  swollen. 
Muscles  normal. 
Eosinophiles  decreased. 
A  common  disease. 


Triehiniasis. 

No  rash. 
Face  swollen. 
Myositis. 

Eosinophiles  numerous, 
A  rare  disease, 


48  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

For  the  diagnosis  of  paratyphoid  fever  from  typhoid  fever,  see  the  article 
on  that  disease. 

Tests. — ^The  so-called  Widal  test  depends  upon  the  fact  that  if  a  small 
amount  of  blood,  or  blood  serum,  or  even  the  breast  milk  or  tears  from  a 
patient  having  or  recently  having  had  typhoid  fever,  are  brought  in  proper 
dilutions  in  contact  with  living  typhoid  bacilli  these  organisms  soon  cease 
to  move,  that  is,  lose  their  motility,  and  gradually  come  together  in  clumps, 
or,  in  other  words,  agglutinate. 

Nahrt  and  Bolton  have  found  that  agglutinating  properties  are  trans- 
mitted from  mother  to  child  by  means  of  the  milk,  and  that  the  typhoid 
bacillus,  when  present  in  the  foetus,  produces  agglutinins  in  its  blood. 
They  were  unable  to  determine  whether  agglutinins  were  transmitted  from 
mother  to  foetus  through  the  placenta. 

The  typhoid  bacilli  to  be  employed  in  the  test  are  not  such  as  have  been 
recently  isolated  from  a  case  of  typhoid  fever,  but  those  which  have  been 
modified  by  repeated  transplantation  on  artificial  media.  These  bacilli  are 
kept  in  sealed  tubes  of  nutrient  agar-agar  in  an  ice-chest;  from  such  a  stock 
culture  inoculations  are  made,  and  when  the  test  is  to  be  used  are  placed 
in  broth-bouillon,  incubated  for  twenty-four  hours  at  a  temperature  of  37°  C, 
and  then  employed  for  the  test.  It  is  essential  that  it  be  proved  beforehand 
that  this  culture  is  composed  of  organisms  reacting  to  known  typhoid 
serum  and  not  to  healthy  serum.  From  this  test  culture  a  proper  dilution 
is  made  by  adding  the  bacilli  to  blood  diluted  with  normal  salt  solution. 
A  hanging  drop  is  now  placed  under  the  microscope  and  examined  with 
a  magnifying  power  of  about  800  diameters.  The  bacilli  should  appear  as 
actively  motile  organisms  which  do  not  clump. 

The  finger-tip  or  lobe  of  the  ear  is  pricked,  and  by  means  of  the  "white 
pipette"  of  a  blood-cell  counting  apparatus  the  blood  is  drawn  up  to  the 
mark  0.5.  Then  the  pipette  is  dipped  in  distilled  water  and  the  water  is 
drawn  up  till  the  figure  11  is  reached.  This  gives  us  a  dilution  of  1:20. 
One  drop  of  the  mixture  of  bacilli  in  salt  solution  and  one  drop  of  the  diluted 
blood  are  then  placed  on  a  cover-glass,  which  is  inverted  over  a  hollow  slide 
and  the  drop  examined.  A  positive  reaction  consists  in  an  absolute  immo- 
bilization of  all  the  baciUi  and  of  a  clumping  of  a  majority  of  them.  This 
reaction  should  occur  in  five  minutes  if  the  dilution  of  blood  has  been  1 :  20, 
and  in  thirty  minutes  if  it  has  been  1 :  40,  and  in  two  hours  if  the  dilution 
has  been  1 :  60.  A  rapid  clumping  with  a  weak  dilution  is  to  be  regarded 
as  a  very  positive  test.  On  the  other  hand,  it  is  to  be  remembered  that  a 
dilution  of  blood  in  the  proportion  of  1 :  10  may  give  a  reaction  even  if  nor- 
mal blood  is  used.  An  exact  estimate  of  the  strength  of  the  solution  and  of 
the  time  of  reaction  is  therefore  of  importance. 

This  test  is  an  exceedingly  accurate  one,  if  properly  employed.  The  chief 
difficulty  about  it  is  that  the  reaction  is  often  absent  until  the  seventh  or 
even  the  twelfth  day  of  the  disease.  Out  of  over  8000  cases  reported  by  a 
number  of  observers,  the  test  was  positive  in  94  per  cent.  A  negative  result 
is  unimportant  if  it  is  obtained  prior  to  the  third  week.  But  cases  have  been 
recorded  in  which  bacilli  have  been  isolated  from  the  blood  during  life  and 
at  autopsy  the  lesions  were  those  of  typhoid  fever,  but  at  no  time  during 


TYPHOID   FEVER 


49 


the  course  of  the  disease  did  the  blood  yield  the  agglutinative  reaction. 
Repeated  tests  should  also  be  made  before  it  is  decided  that  the  blood  does 
not  give  the  reaction.  When  dried  blood  is  used  its  volume  as  near  as  may  be 
should  be  restored  by  the  addition  of  distilled  water,  and  from  this  the  proper 
dilution  is  to  be  prepared  and  the  resulting  dilution  used  as  already  indi- 
cated. The  fallacies  of  this  test  lie  in  the  possibility  that  the  patient  may 
have  had  typhoid  fever  at  some  previous  time  and  so  give  the  reaction, 
and  in  mistaking  irregular  and  delayed  clumping  as  true  agglutination  or 
as  a  partial  reaction. 

This  test  has  now  been  brought  within  the  reach  of  everyone  by  the  use 
of  an  agglutometer  which  has  been  placed  on  the  market  by  a  well-known 
house.     (See  Fig.  12.) 

Fig  12 


Agglutometer  for  the  agglutination  test  for  typhoid  fever. 

This  apparatus  is  designed  to  obviate  the  use  of  the  microscope  and  the 
fresh  live  culture  of  typhoid  bacilli  necessary  in  the  Widal  test  when  made 
in  the  old  way.  Laboratory  experiments  have  shown  it  equal  in  delicacy 
to  the  former  method.  The  limits  of  the  reaction  are  more  distinct  than  in 
the  old  process. 

One  bottle  of  a  sterile  permanent  suspension  of  typhoid  bacilli  is  fur- 
nished, together  with  four  test  tubes,  one  lancet  and  tube  for  collecting 
blood,  one  vial  for  diluting  the  serum,  one  small  pipette  for  distributing 
the  diluted  serum,  and  one  large  pipette  with  two  graduations  (each  cor- 
responding to  ten  drops  of  the  size  delivered  by  the  small  pipette)  for 
filling  the  tubes  with  suspension.  The  three  tubes  labelled  50,  100,  and 
200,  are  to  be  used  for  the  test;  the  fourth  is  a  control  tube  to  which  no 
serum  should  be  added. 

Let  blood  flow  into  the  blood  tube  until  the  bottom  is  covered  with  a 
layer  one-eighth  to  one-fourth  inch  thick.  The  blood  will  flow  much  more 
4 


50  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

rapidly  if  the  lobe  of  the  ear  is  squeezed  intermittently  between  the  thumb 
and  index  finger. 

Cork  the  tube  and  replace  in  an  upright  position. 

In  a  short  time  (an  hour)  the  serum  will  have  separated,  or  may  be  readily 
made  to  do  so  by  carefully  loosening  the  edges  of  the  clot  with  the  lancec. 

After  the  serum  has  separated,  insert  the  pipette  into  the  blood  tube,  the 
point  resting  in  the  lateral  depression,  and  incline  both  slightly,  when  the 
serum  will  readily  enter  the  pipette. 

Add  one  drop  of  serum  to  ten  drops  of  clear  water  in  the  diluting  tube, 
and  shake  well.  If  the  diluted  serum  is  cloudy,  let  it  clear  by  standing 
a  few  minutes  before  distributing  to  the  tubes  of  suspension. 

By  means  of  the  large  pipette  put  20  drops  (two  graduations)  of  the 
suspension  of  typhoid  bacilli  in  each  of  the  four  test-tubes. 

Add  the  serum  dilution  to  the  typhoid  suspension  in  the  following  amounts : 
four  drops  added  to  the  tube  marked  50  gives  a  dilution  of  1 :  50 ;  two  drops 
added  to  the  tube  marked  100  gives  a  dilution  of  1 :  100;  one  drop  added  to 
the  tube  marked  200  gives  a  dilution  of  1 :  200. 

No  serum  should  be  added  to  the  control  tube. 

After  adding  the  serum  dilution,  cork  the  tubes  and  shake  well.  Put 
away  in  a  warm  place. 

Examine  the  tubes  at  the  end  of  one  and  four  hours,  and  again  on  the 
following  day.  The  rapidity  of  the  reaction  depends  both  upon  the  agglu- 
tinating power  of  the  blood  serum  and  the  temperature  at  which  the  tubes 
are  kept.  The  reaction  may  be  seen  with  the  greatest  distinctness  when  one 
stands  near  the  middle  of  the  roo  n  facing  a  window.  The  tubes  should  be 
held  on  a  level  with  the  eye  and  inclined  slightly  away  from  the  observer. 

When  the  reaction  is  positive,  floccules  appear  in  one  or  more  of  the 
tubes,  depending  upon  the  agglutinating  power  of  the  serum  tested. 
These  flakes  are  small  at  first  and  disseminated  through  the  fluid.  They 
gradually  increase  in  size  and  settle  to  the  bottom  of  the  tube. 

In  a  complete  reaction  the  supernatant  fluid  is  perfectly  clear. 

In  a  positive  but  incomplete  reaction,  floccules  are  seen  in  the  still  cloudy 
fluid. 

In  a  negative  reaction  the  fluid  in  the  tubes  remains  uniformly  clouded, 
as  in  the  control. 

All  apparatus  and  corks  should  be  thoroughly  washed  before  using  a 
second  time. 

The  diazo  reaction,  sometimes  called  Ehrlich's  reaction,  depends  upon 
the  fact  that  in  typhoid  fever  the  urine  of  the  patient  contains  a  chromogen 
which,  when  treated  with  diazo-benzene-sulphonic  acid  and  ammonia,  pro- 
duces a  distinct  red  hue  in  the  urine,  which  may  be  as  deep  as  garnet  red. 
Other  diseases  give  this  reaction,  such  as  tuberculosis  and  some  cases  of 
pneumonia,  but  it  is  of  considerable  value  in  determining  the  presence  of 
typhoid  fever  if  taken  in  conjunction  with  other  signs.  It  is  usually  present 
as  early  as  the  sixth  day,  and  lasts  until  about  the  eighteenth  day.  The  test 
itself  consists  in  using  two  solutions.  One  of  these  consists  of  a  5  per  cent, 
solution  of  hydrochloric  acid  to  which  has  been  added  sulphanilic  acid  in 
the  proportion  of  1  gram  for  each  100  c.c.     The  other  is  a  0.5  per  cent. 


TYPHOID  FEVER  51 

solution  of  sodium  nitrite.  When  the  test  is  to  be  made  the  two  solutions 
are  mixed  in  the  proportion  of  40 : 1 .  Equal  parts  of  urine  and  this  mix- 
ture are  then  shaken  together  and  rendered  alkaline  by  the  addition  of 
ammonium  hydrate,  which  is  allowed  to  flow  down  the  side  of  the  tube, 
forming  the  layer  above  the  mixture  just  named.  At  the  dividing  line 
between  these  two  fluids  the  reaction  appears.  If  typhoid  fever  is  present 
a  garnet-red  hue  develops.  If  it  is  not  present,  only  an  orange  tint  is 
seen  unless  one  of  the  other  maladies  which  give  this  test  is  present.  After 
the  test  tube  containing  these  liquids  has  stood  for  some  time  a  green 
sediment  forms,  which  Ehrlich  considers  very  characteristic  of  a  true 
reaction. 

Another  method  of  reaching  a  positive  diagnosis  is  the  examination  of 
the  blood  itself  for  the  specific  bacillus,  which,  as  already  stated,  is  present 
in  this  fluid  in  nearly  all,  if  not  all,  cases  of  typhoid  fever.  While  it  is 
true  that  this  examination  is  not  possible  for  one  who  is  not  trained  in  its 
technique  from  the  bacteriological  standpoint,  it  is  also  a  fact  that  this  test 
is  not  open  to  the  fallacies  of  the  Widal  test,  and  that  the  bacilli  are  often 
found  as  early  as  the  fifth  day,  whereas  the  Widal  test  is  frequently  not 
positive  till  the  ninth  day,  or  even  later.  The  urine  and  stools  may  be 
examined  for  the  specific  infecting  micro-organism,  but  they  are  rarely  dis- 
coverable in  these  discharges  early  enough  to  aid  the  diagnosis. 

The  Widal  test  and  the  discovery  of  the  bacillus  of  Eberth  in  the  blood 
enable  us  to  differentiate  true  typhoid  fever  from  paratyphoid  fever. 

Finally,  it  is  to  be  remembered  as  a  valuable  diagnostic  fact  that  the 
fever  of  the  first  stages  of  typhoid  fever  is  more  resistant  to  the  cold  bath 
than  in  any  other  malady,  although  it  yields  readily  enough  later  on  in 
the  course  of  the  malady  to  this  therapeutic  measure. 

Prognosis. — The  prognosis  in  typhoid  fever  depends  upon  several  important 
factors.  One  of  these  is  the  time  at  which  the  patient  comes  under  medical 
care,  not  because  active  medication  is  of  great  advantage,  but  rather  because 
patients  that  go  to  bed  late  in  the  onset  of  the  disease  usually  become  more 
seriously  ill  than  those  who  conserve  their  vital  forces  by  rest  from  the  very 
beginning  of  the  malady.  Patients  who  travel  long  distances  in  the  early 
stages  of  typhoid  are  wont  to  have  severe  attacks,  and  if,  after  the  disease 
is  well  developed,  travelling  is  resorted  to  the  illness  nearly  always  increases 
in  violence.  Another  factor  is  the  state  of  the  patient  at  the  beginning  of 
the  malady,  as  to  his  vital  resistance  and  general  health.  Fat  persons  usually 
do  not  withstand  it  well.  Children  nearly  always  recover  from  typhoid 
fever  in  its  uncomplicated  forms,  and  aged  persons,  while  rarely  affected, 
succumb  when  attacked  in  direct  proportion  to  their  years.     (See  Fig.  6.) 

A  third  factor  is  the  degree  of  toxaemia  which  develops  in  severe  cases, 
particularly  if  they  are  not  treated  skilfully  at  first. 

Aside  from  these  general  considerations  it  is  impossible  to  make  an 
accurate  prognosis  as  to  the  severity  of  the  attack  or  probable  recovery  of 
the  patient  in  the  first  week  of  the  disease,  because  the  malady  develops 
slowly  and  because  a  fatal  termination  is  nearly  always  due  to  some 
intercurrent  complication  which  cannot  be  foreseen.  Even  when  the 
disease  is  ushered  in  with  violence  of  all  the  symptoms,  particularly  an 


52  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

exceedingly  high  temperature,  it  often  happens  that  it  follows  a  very  short 
and  fairly  mild  course,  so  that  a  severe  onset  justifies  the  physician  in 
expecting  a  speedy  recovery  in  many  instances.  When,  however,  compli- 
cating conditions  such  as  pulmonary,  cerebral,  or  meningeal  manifestations 
develop,  the  prognosis  is  of  course  correspondingly  grave. 

Recovery  in  typhoid  fever,  under  the  modern  and  favorable  methods  of 
treatment,  takes  place  in  about  93  per  cent,  of  cases  in  the  best  t}^es  of 
private  practice  and  in  hospitals  in  which  the  patients  are  received  early 
and  in  fairly  good  condition.  In  private  practice  among  the  poor  it  is  much 
lower.  In  army  practice  the  mortality  may  vary  from  2  or  3  per  cent,  in 
time  of  peace  to  50  per  cent,  in  time  of  war,  illustrating  very  well  the  fact, 
already  stated,  that  early  rest  in  bed,  perfect  quiet  of  mind  and  body,  and 
proper  nursing  are  most  favorable  in  their  influence,  whereas  an  absence 
of  these  aids  to  recovery  is  most  harmful.  Under  the  cold-bath  treatment 
of  typhoid  fever,  when  it  is  instituted  early,  the  mortality  of  about  7  per  cent, 
is  laro-ely  due  to  those  unavoidable  accidents,  hemorrhage  and  perforation 
of  the  bowel. 

]\Iuch  depends  in  all  cases  upon  the  severity  of  the  infection.  In  some 
widespread  epidemics  the  mortaHty  is  singularly  low  even  when  the  care 
of  the  patients  is  not  in  many  cases  very  skilful;  in  others  it  is  corre- 
spondingly liigh.  In  the  United  States  army  in  the  Spanish  war  it  was 
only  7  per  cent.,  a  remarkably  low  rate  for  war  time;  whereas  in  the 
Boer  war  the  English  troops  suffered  from  a  death  rate  of  nearly  21 
per  cent. 

Sudden  death  sometimes  occurs  in  typhoid  fever  without  the  autopsy 
reveahng  any  adequate  cause,  the  real  cause  being  in  all  probabiHty  an 
acute  cardiac  dilatation. 

Treatment. — The  following  is  the  plan  pursued  by  the  author  in  the 
treatment  of  this  disease.  As  soon  as  the  patient  comes  under  observation, 
unless  his  bowels  have  already  been  moved  by  the  aid  of  calomel,  he  is  given 
1  to  2  grains  of  this  drug  in  quarter-grain  doses  every  hour.  If  his  bowels  are 
not  moved  in  twelve  hours,  a  movement  is  produced  by  the  aid  of  a  large 
rectal  injection  of  soap  and  water,  and  if  need  be  by  the  ingestion  of  a  Seid- 
litz  powder.  Twelve  hours  later  he  receives  5  to  10  minims  of  dilute  hydro- 
chloric acid  ^ath  a  teaspoonful  of  essence  of  pepsin  ;  this  is  repeated  regu- 
larly every  six  hours  throughout  the  disease  after  food. 

Hydrotherapy. — An  order  is  given  that  if  the  temperature  rises  as  high  as 
102.5°  the  patient  is  to  be  rubbed  with  tepid,  cool,  cold,  or  ice-water,  or  even 
with  a  piece  of  ice,  according  to  the  degree  with  which  his  temperature  resists 
the  bath  and  according  to  the  degree  of  toxaemia  present.  If  toxtemia  is  very 
great,  it  is  often  necessary  to  give  a  thorough,  brief  and  brisk,  rub-off  with  a 
small  piece  of  ice,  not  so  much  to  reduce  the  fever  as  to  cause  reaction  and 
arouse  the  patient's  vitality.  With  this  application  of  cold,  in  different  degrees 
according  to  the  needs  of  the  case,  there  must  be  employed  by  another 
nurse,  or  by  the  free  hand  of  the  nurse  who  uses  the  cold,  active  friction  to 
the  skin  as  the  cold  comes  in  contact  with  the  integument,  because  friction 
increases  the  heat  loss  50  per  cent.,  aids  in  producing  those  most  essential 
conditions,  reaction  and  equalization  of  the  capillary  circulation,  and  prevents 


TYPHOID  FEVER  53 

the  patient  from  being  chilled.  It  is  a  cardinal  rule  that  if  the  patient  has 
been  ill  so  long  that  reaction  does  not  occur  under  the  bath,  it  is  contra- 
indicated  and  we  must  endeavor  by  gentle  measures  and  the  use  of  tepid 
or  even  of  hot  water  to  redevelop  the  power  of  the  body  to  react.  In 
other  words,  that  temperature  of  water  should  be  used  which  is  necessary 
when  combined  with  active  friction  to  reduce  the  temperature  at  least  2° 
in  fifteen  to  twenty  minutes,  provided  reaction  can  be  produced.  Without 
reaction  we  simply  increase  internal  congestions  by  the  use  of  cold  water. 
It  is  interesting  to  note  that  Hirschfeld  has  treated  over  1000  cases  with 
tepid  immersion  baths  of  80°  to  90°  with  a  mortality  of  only  3.4  per  cent. 

Whenever  cold  is  used,  an  ice-bag  or  cold  cloth  should  be  applied  to  the 
head  to  prevent  cerebral  congestion. 

While  the  method  of  bathing  just  described  is  that  nearly  always  pursued 
by  the  writer,  it  is  proper  to  give  definite  information  concerning  the  so-called 
Brand  method  of  cold  bathing,  a  plan  v/hich  was  introduced  by  Brand,  of 
Stettin,  many  years  ago,  but  which  has  only  received  its  full  share  of  credit 
during  the  past  fifteen  years.  This  plan  consists  in  immersing  the  patient, 
when  his  temperature  reaches  102°  or  102.5°,  in  a  tub  of  water  the  tempera- 
ture of  which  is  70°,  and  keeping  him  there  with  active  friction  for  fifteen 
or  twenty  minutes,  until  the  temperature  is  reduced  to  100°.  In  order  to 
combat  chilling  and  aid  the  circulation  it  is  customary  to  give  the  patient 
one-half  to  one  ounce  of  whiskey  before,  during,  or  after  the  bath.  The  bath 
is  repeated  whenever  the  temperature  rises  to  102°.  Usually  it  is  needed 
every  two  or  three  hours.  In  order  that  the  patient's  strength  may  be 
conserved  he  should  be  lifted  into  and  out  of  the  tub.  When  cold  is  prop- 
erly used  it  should,  after  the  first  week  of  the  disease,  produce  changes  in 
the  temperature,  as  shown  in  the  following  chart  (Fig.  13). 

This  so-called  plunge  bath,  or  Brand  bath,  is  a  remedy  of  the  greatest 
possible  value,  but  is  not  needed  in  every  case  as  a  matter  of  routine. 
When  used  it  is  essential  to  produce  reaction  and  to  use  friction,  and  to 
apply  ice  to  the  head.  The  indications  for  its  use  are  identical  with 
those  just  named.  It  is  actually  contraindicated  in  the  very  young  and  very 
old,  in  whom  it  is  often  difficult  to  produce  reaction,  and  if  the  case  comes 
under  treatment  so  late  as  the  beginning  of  the  third  week,  since  reaction  to 
cold  is  usually  then  lost.  The  presence  of  a  complicating  pneumonia  also 
contraindicates  it.  Other  disadvantages  are  that  the  back  cannot  be  rubbed, 
although  the  muscles  in  that  part  of  the  body  contain  much  heat  and  the 
skin  is  most  prone  to  suffer  from  bed-sores,  and  that  the  patient  must 
be  lifted  or  raise  himself  out  of  the  tub.  The  temperature  of  the  plunge 
bath  when  its  use  is  deemed  wise  should  not  be  placed  at  a  tepid  level  and 
then  reduced  while  the  patient  is  in  the  water,  as  this  does  not  administer 
a  stimulating  and  awakening  shock  to  the  system,  but  simply  chills  the 
patient,  thereby  doing  no  good,  for  the  object  in  using  water  in  typhoid 
fever  is  to  produce  reaction,  eliminate  poisons,  and  reduce  temperature,  and 
the  means  by  which  this  is  best  accomplished  can  be  determined  in  each 
case  by  the  physician. 

Personally  the  writer  has  never  failed  to  successfully  accomplish  all 
these  results  by  cold  rubbing,  with  friction,  if  it  is  properly  given,   but 


54 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


many  physicians  prefer  to  follow  the  method  of  Brand  as  a  routine 
practice.  An  enormous  array  of  statistics  prove  its  value  as  a  life-saving 
agent/ 

Some  form  of  bath  at  least  once  a  day  is  absolutely  necessary  even  if  the 
temperature  never  exceeds  normal,  to  estabhsh  cleanliness  and  equalize  the 
circulation  everywhere,  and  he  who  treats  typhoid  fever  without  resort  to 
efficient  hydrotherapy,  if  it  can  be  used,  is  not  doing  all  for  his  patient  that 
can  be  done. 

The  use  of  hydrotherapy  greatly  lowers  the  mortality,  saving  about  10  in 
every  100  cases,  but  it  does  not  diminish  the  frequency  of  perforation  or 
hemorrhage,  and  it  apparently  increases  the  frequency  of  relapse.  This 
may  be  due  to  the  fact  that  more  are  saved  to  run  the  chance  of  relapse, 


Fig.  13 


Chart  showing  the  falls  in  temperature  and  reactions  following  the  use  of  cold  spongings  in  a  case  of 
typhoid  fever.  The  dotted  lines  show  the  fall  The  broken,  nearly  horizontal  line  shows  the  morn- 
ing and  evening  range  unaffected  by  sponging.     Thirty-four  baths  were  given  in  eight  days. 

but  also  may  depend  upon  the  fact  that  mild  cases  are  more  prone  to 
relapse  than  severe  ones.  Hydrotherapy  does  not  shorten  the  duration  of 
the  fever,  but  it  often  shortens  the  length  of  the  illness  by  preventing 
complications. 

Diet.— The  diet  consists  of  milk  in  the  first  week  and  often  for  most  of  the 
second  week,  about  a  quart  to  a  quart  and  a  half  a  day  being  given,  so 
divided  that  the  patient  gets  it  every  three  or  four  hours.  It  is  followed 
by  the  acid  and  pepsin  already  named,  unless  the  stomach  is  irritable,  when 
a  little  lime-water  may  be  given  as  a  substitute,  or  a  little  Celestins  Vichy 
water  may  be  used.  When  the  digestion  of  milk  is  difficult  it  is  well  to 
add  to  it  hot  water  or  to  dilute  it  with  an  alkaline  or  carbonated  water. 
If  the  taste  of  the  milk  is  unpleasant  to  the  patient,  it  may  be  flavored 

I  See  article  by  the  author  in  Therapeutic  Gazette  for  March,  1898. 


TYPHOID  FEVER 


55 


by  the  addition  of  vanilla,  nutmeg,  coffee,  tea,  or  cocoa  in  small  amounts. 
After  the  first  week  or  ten  days  the  patient  is  allowed  from  one  to  two  soft- 
boiled  eggs  each  day,  so  soft  that  they  can  better  be  taken  as  a  drink  than 
eaten  with  a  spoon,  and  flavored  with  a  little  salt.  Well-boiled  rice  strained 
through  a  fine  sieve,  and  even  thin  cornstarch  or  barley-gruel,  if  well 
cooked,  may  be  given  at  this  time  with  advantage,  particularly  if  at  the 
same  time  a  little  taka-diastase  is  used  to  aid  their  digestion.  The  author 
is  firmly  convinced  that  by  this  means  terminal  infections  and  general 
feebleness  can  be  largely  avoided  and  the  patient  brought  to  the  stage  of 
convalescence  ready  for  speedy  return  to  health  and  with  greater  vital 
force.  Broths  and  other  liquid  animal  soups  are  inadvisable,  for  they  are 
good  culture-media,  and  often  tend  to  increase  tympanites  and  diarrhoea. 
They  are  largely  used  by  many  physicians,  but  never  by  the  writer.  When 
curds  appear  in  the  stools,  the  quantity  of  milk  should  be  diminished  or  it 
should  be  peptonized,  or  its  digestion  aided  by  the  use  of  pancreatin  given 
after  it  is  taken.  The  use  of  5  to  10  grains  of  citrate  of  soda  in  the  milk 
will  also  prevent  the  formation  of  curds. 

The  use  of  cows'  milk  in  large  amounts  for  a  considerable  time  has  been 
shown  to  increase  the  coagulability  of  the  blood,  as  cows'  milk  contains 
an  excess  of  calcium  salts.  Wright  has  suggested  that  this  is  one  of  the 
reasons  why  thrombosis  is  so  common  in  typhoid  fever.  To  prevent  the 
increase  in  coagulability  a  mixed  diet  should  be  given  and  a  few  grains  of 
citric  acid  be  administered  daily  for  a  few  days  at  intervals  of  a  week. 

Medicines. — Drugs  are  not  to  be  given  if  they  can  be  avoided — that 
is,  they  are  not  to  be  used  unless  they  are  certainly  needed  to  combat  some 
definite  condition  which  should  be  alleviated.  In  the  great  majority  of 
cases,  if  not  in  all,  the  so-called  antipyretic  drugs  are  not  only  useless  but 
harmful,  and  particularly  harmful  if  their  use  is  resorted  to  simultaneously 
with  bathing.  Their  only  justifiable  use  in  a  case  which  can  be  properly 
nursed  and  bathed  is  for  the  purpose  of  relieving  headache  and  backache, 
when  they  may  be  given  in  small  doses,  such  as  2  grains  of  acetanilid  three  or 
four  times  a  day.  Quinine  is  of  little,  if  any,  value  except  as  a  tonic  in 
small  doses. 

Stimulants  are  to  be  used  when  the  pulse  is  actually  weak  and  the  car- 
diac first  sound  distant  or  feeble.  The  best  of  them  is  whiskey  or  brandy, 
diluted  with  milk  or  water,  and  given  in  doses  of  half  an  ounce  every  three 
to  six  hours  as  needed.  Many  cases  do  better  without  any  stimulation, 
whereas  others  need  much  larger  doses  of  alcohol  than  those  just  named. 
Digitalis  is  rarely  of  any  service  because  it  does  not  act  well  in  the  presence 
of  fever,  rarely  supports  the  degenerated  muscle  fibres  of  the  heart,  and  is 
apt  to  disorder  the  stomach.  When  the  cardiac  condition  is  desperate, 
Hoffmann's  anodyne  in  drachm  doses  every  two  hours  in  cool  water  is 
very  valuable.  When  profound  adynamia  develops  and  the  patient  is 
critically  ill,  much  good  may  result  from  the  injection  hypodermically  of 
^  grain  of  camphor  in  30  drops  of  sterilized  olive  oil  every  eight  hours 
for  five  or  six  doses.  Another  method  of  value  when  the  vascular  system 
is  relaxed  and  the  patient  adynamic  is  the  use  of  hypodermoclysis,  adding 
to  the  pint  of  a  0.9  per  cent,  saline  solution  1  drachm  of  adrenalin  chloride 


56  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

solution  of  the  strength  of  1 :  1000.  Strychnine  may  also  be  used,  but  it  is 
a  mistake  to  employ  it  for  more  than  a  few  doses  in  the  active  stage  of  this 
disease.  It  is  better  to  keep  it  in  reserve  for  attacks  of  sudden  circulatory 
failure. 

Antisepsis. — Absolute  intestinal  antisepsis  can  not  be  produced  by  any 
known  means,  although  it  is  possible  to  modify  very  materially  the  growth  of 
micro-organisms  in  the  bowel  by  the  use  of  proper  remedies.  If  the  physician 
takes  the  ground  that  by  the  use  of  these  substances  he  destroys  the  Bacillus 
typhosus  and  so  benefits  the  patient,  he  is  largely  in  error,  and  his  use  of  them 
is  not  rational  because  the  bacillus  in  the  early  stages  at  best  is  not  free  in  the 
bowel,  and  in  the  later  stages  is  widely  distributed  in  every  part  of  the  body. 
If,  on  the  other  hand,  these  remedies  are  given  to  combat  intestinal  fer- 
mentation, as  shown  by  foul-smelling  stools  and  tympanites  and  other 
evidences  of  an  excessive  growth  of  the  non-specific  bacteria  which  throng 
the  bowel  during  the  progress  of  this  disease,  his  use  of  them  is  rational  in 
that  by  this  means  other  toxic  materials  are  prevented  from  being  gene- 
rated in  excess.  So  far  as  we  know,  the  most  active  and  harmless  intes- 
tinal antiseptic  is  acetozone  given  in  the  daily  dose  of  30  grains  dissolved  in  ^ 
gallon  of  pure  water  flavored  with  some  one  of  the  volatile  oils,  but  not 
with  sugar.  This  quantity  may  be  given  the  patient  as  a  drink  in  the 
course  of  one  or  two  days.  Another  is  the  sulphocarbolate  of  zinc  in  the 
dose  of  2  to  3  grains  in  pill  form  three  or  four  times  a  day.  Still  another 
drug  of  far  older  use  is  turpentine  in  emulsion  in  the  dose  of  10  to  20  drops 
three  or  four  times  a  day.  The  latter  I  prefer.  In  many  of  these  cases  also 
the  use  of  a  few  small  doses  of  calomel  or  salol  is  advantageous. 

Treatment  of  Special  Symptoms. — Constipation  is  to  be  relieved  pref- 
erably by  the  use  of  enemata  of  soap  and  water,  to  which  may  be  added 
in  obstinate  cases  a  teaspoonful  or  two  of  glycerin.  Many  of  these  patients 
have  no  constipation  in  the  sense  that  the  ileum  or  colon  is  sluggish;  but, 
on  the  other  hand,  the  sigmoid  flexure  becomes  packed  with  hardened 
feces,  and  mechanical  obstruction  occurs.  The  use  of  purgatives  by  the 
mouth  is  therefore  useless  unless  very  strong  drugs  are  used,  which  are  dan- 
gerous. If  it  is  thought  that  the  bowels  are  really  sluggish  a  little  cascara 
sagrada  (20  to  30  minims  of  the  non-bitter  extract)  may  be  given  each  evening. 

Diarrhoea,  if  excessive — that  is,  more  than  three  or  four  stools  a  day — 
may  be  controlled  by  5  to  10  drop  doses  of  aromatic  sulphuric  acid  in  simple 
elixir  or  by  adding  to  these  two  ingredients  a  half  drachm  of  fluid  extract  of 
hsematoxylon.  If  much  fermentation  is  present,  an  intestinal  antiseptic 
should  be  used,  such  as  zinc  sulphocarbolate  or  acetozone. 

Vomiting  is  to  be  primarily  prevented  by  regulating  the  diet  as  already 
referred  to.  If  it  persists,  as  little  food  and  drink  should  be  given  as  pos- 
sible for  a  few  hours  to  let  the  stomach  rest;  and  if  there  be  much  nervous 
irritability,  60  grains  of  sodium  bromide  in  a  little  starch-water  should  be 
given  by  the  rectum  to  quiet  the  vomiting  centre.  Counterirritation  should 
be  applied  over  the  epigastrium  in  the  form  of  a  mustard  plaster  or  turpentine 
stupe.  If  alcohol  is  being  used  as  a  stimulant  its  use  must  be  stopped,  or, 
if  this  is  impossible,  then  a  very  old  brandy  or  wine  should  be  substituted 
for  the  whiskey  and  given  in  very  small  quantities. 


TYPHOID  FEVER  57 

For  tympanites  a  turpentine  stupe  is  to  be  placed  over  the  belly,  if  possible, 
before  the  gas  accumulates  in  any  amount,  and  if  it  persists  a  rectal  injec- 
tion of  the  emulsion  of  asafoetida,  with  or  without  a  drachm  or  two  of  tur- 
pentine, should  be  given.  The  efficiency  of  this  injection  may  be  much 
increased  in  the  way  of  expelling  gas,  and  if  marked  adynamia  is  present, 
by  adding  half  an  ounce  of  Hoffmann's  anodyne  to  the  injection.  Turpen- 
tine in  the  dose  of  10  drops,  in  emulsion  or  capsule,  may  also  be  given  by 
the  mouth  for  this  condition.  When  the  gas  fails  to  come  away,  its  passage 
may  be  aided  by  the  introduction  of  a  long  rectal  rubber  tube. 

Hemorrhage  from  the  bowel  does  not  offer  very  much  opportunity  for 
direct  rational  treatment.  In  the  majority  of  instances  the  best  we  can  do 
in  the  way  of  real  benefit  to  the  patient  is  the  maintenance  of  body  heat 
by  the  application  of  hot  bottles;  and  if  the  circulation  becomes  markedly 
feeble,  the  employment  of  normal  salt  solution  by  hypodermoclysis,  a  pint 
of  it  being  given  once,  twice,  or  thrice  in  the  succeeding  twenty-four  hours, 
according  to  the  needs  of  the  patient.  Bandages  may  be  applied  to  the 
limbs  to  limit  the  circulation  to  the  vital  parts,  and  the  foot  of  the  bed 
be  raised  for  a  similar  purpose.  The  large  number  of  remedies  which 
have  been  suggested  for  the  direct  control  of  the  hemorrhage  indicate  how 
feeble  they  all  are.  There  is  no  more  reason  for  supposing  that  astringents 
given  by  the  mouth  can  check  hemorrhage  from  an  ulcerated  vessel  in  the 
bowel  than  that  they  can  check  a  hemorrhage  from  a  branch  of  the  anterior 
tibial  artery;  and  when  they  are  given  and  hemorrhage  ceases,  the  arrest 
is  due  more  to  coincidence  than  to  the  effect  of  any  drug.  If  any  remedy 
of  this  type  is  of  value,  it  is  probably  Monsel's  salt  (ferri  subsulphas), 
which  should  be  given  in  a  hard  pill  or  compressed  tablet  enclosed  in  a  cap- 
sule, with  the  hope  that  it  will  escape  from  the  stomach  into  the  intestine 
without  being  dissolved,  and  thereby  exert  its  styptic  influence.  Of  course, 
if  it  is  dissolved  in  the  stomach,  its  chemical  characteristics  are  altered. 
Many  physicians  apply  a  small  ice-bag  over  the  centre  of  the  belly  to  influ- 
ence the  circulation  in  the  small  intestine,  with  the  hope  that  in  that  way 
hemorrhage  will  be  controlled.  There  is  no  objection  to  this  plan  of  treat- 
ment, and  the  author  often  resorts  to  it;  but  it  should  be  used  with  caution, 
if  the  hemorrhage  is  severe,  lest  it  aid  in  devitalizing  the  patient  by  abstract- 
ing heat.  Simultaneously  with  the  application  of  the  ice-bag  to  the  belly, 
hot  bottles  should  be  applied  to  the  other  parts  of  the  body,  for  it  is  to  be 
remembered  that  the  loss  of  bodily  heat  is  an  important  factor,  not  only 
because  the  vital  processes  can  not  be  well  performed  at  a  low  temperature, 
but  also  because  the  sudden  reduction  of  temperature  caused  by  the  hemor- 
rhage deprives  the  heart  and  other  organs  of  the  stimulating  effect  of  the 
fever  which  has  been  present  for  days.  Another  popular  method  of  treat- 
ment is  the  administration  of  a  pill  containing  a  grain  of  opium  and  a  grain 
of  acetate  of  lead;  the  opium  being  expected  to  diminish  peristalsis  and  so 
aid  clotting,  and  the  lead  to  act  as  a  styptic.  The  opium  is  probably  of 
value,  but  it  is  doubtful  if  the  lead  ever  reaches  the  bleeding  spot  without 
becoming  altered  by  the  gastric  and  intestinal  juices.  When  there  seems 
to  be  continued  oozing  of  blood  from  a  large  intestinal  ulcer  without  free 
hemorrhage,  the  administration  of  turpentine  and  the  use  of  adrenalin 


58  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

chloride  is  to  be  seriously  considered,  as  there  is  reason  to  believe  that  they 
both  control  capillary  hemorrhage.  Wright  and  his  co-laborers  have 
shown  that  the  hypodermic  use  of  calcium  lactate  and  the  internal  use 
of  calcium  chloride  increase  the  coagulability  of  the  blood  and  these  salts 
may  be  used.  (See  Purpura.)  After  the  hemorrhage  has  ceased,  particularly 
as  convalescence  is  begun,  small  doses  of  iron  should  be  administered  to 
combat  the  anaemia. 

The  treatment  of  perforation  of  the  bowel  from  a  medical  point  of  view 
consists  in  giving  opium  to  relieve  pain,  and  employing  heat  and  stimulants 
to  combat  shock.  If  a  skilled  abdominal  surgeon  can  be  obtained,  all 
such  cases  should  be  operated  upon  at  once,  since  the  mortality  under 
operation  is  less  than  with  no  operation.  Statistics  seem  to  show  a  mor- 
tality of  about  80  per  cent,  with  operation  and  95  per  cent,  without  it.  My 
colleague,  Dr.  Keen,  has  published  158  cases,  which  were  all  he  and  Dr. 
Tinker  could  find  in  literature  up  to  January  1,  1900.  They  gave  a  recovery 
percentage  of  23.41.  I  have  collected  54  cases  which  have  been  reported 
since  January  1,  1900,  and  find  that  35  of  the  number  were  followed  by 
recovery.  This  gives  a  recovery  percentage  of  61.54,  which  is  far  too  high 
for  the  general  run  of  cases.  Harte  and  Ashhurst  place  the  recovery  after 
operation  at  26  per  cent.  Among  children  the  results  have  been  excel- 
lent. Out  of  25  cases  collected  by  Elsberg  16  recovered,  a  postoperative 
mortality  of  only  36  per  cent.  These  figures  are  of  value  as  showing 
that  recovery  may  take  place,  but  they  do  not  give  the  real  percentage 
of  deaths,  for  most  of  the  cases  that  are  operated  upon  and  die  are  not  re- 
ported. I  have  seen  3  of  these  within  a  year.  To  be  successful  the 
operation  ought  to  be  performed  at  the  earliest  possible  moment  after 
perforation,  although  if  the  patient  when  seen  is  profoundly  shocked 
it  may  be  necessary  to  rally  him  by  stimulation  before  the  operation  is  com- 
menced or  even  postpone  operation  until  suflScient  time  has  elapsed  to  allow 
him  to  rally. 

Statistics  clearly  prove  that  the  prospect  of  recovery  from  perforation 
treated  by  operation  steadily  diminishes  with  each  hour  that  passes  after 
the  accident  occurs.  Cases  are  on  record,  however,  and  I  have  seen  more 
than  one,  in  which  perforation  took  place  and  recovery  occurred  without 
operation. 

Persistent  insomnia  is  rarely  a  troublesome  symptom  in  typhoid  fever. 
Although  patients  complain  of  wakefulness  at  night,  careful  observation 
will  usually  show  that  they  get  sufficient  sleep  in  twenty-four  hours.  In 
some  cases,  however,  when  they  are  wakeful,  largely  because  of  active 
delirium,  and  are  rapidly  exhausting  their  vital  forces  by  continued  nervous 
activity,  life  can  be  saved  by  the  hypodermic  injection  of  j  grain  of 
morphine,  to  which  may  be  added  y^  grain  of  nitroglycerin  to  prevent 
secondary  nausea  and  depression. 

The  application  of  an  ice-bag  to  the  head  throughout  the  attack  will 
usually  prevent  ordinary  delirium  from  becoming  excessive. 

Bed-sores  are  usually  prevented  by  the  friction  applied  to  all  portions  of 
the  skin  in  the  baths  which  are  given  every  few  hours.  If  they  appear  over 
the  sacrum,  the  patient  should  he  as  much  as  possible  on  his  sides,  all  bony 


PARATYPHOID  FEVER  59 

prominences  on  which  the  patient  rests  being  protected  from  contact  with 
the  bed  by  circular  air-cushions.  When  the  skin  first  reddens  the  irritation 
may  be  allayed  by  painting  it  with  a  solution  of  nitrate  of  silver,  20  grains 
to  the  ounce.  If  the  bed-sore  has  begun  to  form,  a  useful  dressing  consists 
in  equal  parts  of  powdered  chloretone  and  boric  acid.  If  the  slough  becomes 
large,  all  that  portion  which  is  actually  dead  should  be  cut  away,  the  part 
thoroughly  sprayed  with  peroxide  of  hydrogen,  dried  by  the  gentle  application 
of  soft  lint,  and  then  dressed  with  the  dusting-powder  just  named. 

The  treatment  of  the  other  complications  of  typhoid  fever  will  be  found 
under  the  headings  of  the  respective  diseases,  such  as  Pneumonia,  etc. 

During  convalescence  the  patient  should  be  fed  with  increasing  quantities 
of  nutritious,  easily  digested  food,  but  stimulants  if  possible  should  be 
avoided.  If  the  patient  is  out  of  bed  care  should  be  taken  that  food  is 
not  ingested  until  after  he  has  lain  down  to  rest,  in  order  that  he  may  not  be 
tired  and  so  lack  nervous  energy  during  the  progress  of  the  digestive 
processes. 

As  already  pointed  out  when  discussing  the  prevention  of  typhoid  fever, 
urotropin  or  uritone  should  be  given  in  doses  of  5  grains  three  times  a  day 
in  water,  to  destroy  the  bacilli  which  are  usually  present  in  the  urine. 

The  ordinary  diet  should  not  be  restored  until  from  two  to  three  weeks 
after  all  fever  has  ceased.  The  author  has  often  been  impressed  with  the 
fact  that  the  use  of  green  vegetables,  such  as  lettuce,  spinach,  asparagus, 
and  similar  substances,  seem  to  exercise  a  most  valuable  influence  in  con- 
valescence in  typhoid  fever,  perhaps  because  they  antagonize  scorbutic 
tendencies. 

PARATYPHOID  FEVER. 

Paratyphoid  fever  is  a  disease  caused  by  infection  with  paratyphoid 
bacilli,  and  presents  a  symptom-complex  closely  resembling  or  indistin- 
guishable from  that  of  typhoid  fever. 

Bacteriology. — The  paratyphoid  bacilli  belong  to  a  group  of  organisms 
intermediate  between  the  Bacillus  typhosus  and  Bacillus  coli  communis. 
Buxton  has  shown  that  by  appropriate  methods  organisms  occupying  this 
position  may  be  divided  into  several  groups;  one  resembling  the  colon 
bacillus,  for  which  he  proposes  to  use  the  name  paracolon;  another  group 
closely  allied  to  the  typhoid  bacillus,  called  the  paratyphoid,  and  pro- 
ducing the  condition  termed  paratyphoid  fever.  The  last-named  group 
may  by  appropriate  cultural  methods  be  further  divided  into  a  species  cul- 
turally unlike  the  paracolon  type,  and  a  second  distinct  species  resembling 
the  paracolon  group. 

Pathology. — Differing  anatomically  from  typhoid  fever  in  essential 
details,  this  disease  possesses  no  characteristic  morbid  anatomy,  resembling 
in  this  respect  the  other  forms  of  septicaemia.  The  most  constant  change 
is  splenic  enlargement,  which  was  present  in  all  of  the  cases  coming  to 
autopsy.  In  3  cases  ulcers  were  present  in  the  intestine,  but  they  resem- 
bled the  ulcers  of  dysentery  more  than  those  of  typhoid;  in  2  cases  the 
ulcers   were   numerous;   in  1  case   with  abundant   hemorrhage   the   most 


60  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

extensive  ulceration  was  observed.  The  patches  of  Peyer  and  the  soHtary 
follicles  are  but  slightly  if  at  all  changed.  The  mesenteric  glands  are  but 
slightly  altered;  focal  necroses,  not  containing  endothelial  cells,  occur  in 
the  liver.  The  proliferative  and  phagocytic  endothelial  changes  of  typhoid 
are  practically  absent.  There  are  no  constant  changes  found  in  other 
organs,  although  toxaemia  in  severe  cases  may  induce  its  usual  anatomical 
changes.  Giitig  examined  the  blood  of  six  paratyphoid  patients  and  found 
that  the  neutrophiles  are  diminished  during  the  early  stages  of  the  disease. 
The  lymphocytes  also  are  diminished  at  first,  but  become  increased  later 
in  the  disease,  and  in  convalescence  they  constitute  more  than  half  the 
entire  number  of  white  cells.  The  eosinophiles  disappear  from  the  blood 
during  the  fever,  but  reappear  just  before  or  shortly  after  the  temperature 
becomes  normal. 

The  bacilli  have  been  found  in  the  heart's  blood,  in  a  cardiac  thrombus, 
in  the  liver,  lungs,  spleen,  adrenal  bodies,  cerebral  cortex,  and  in  the  fluid 
of  pericardial  and  pleuritic  effusions. 

Cases  have  been  reported  from  France,  Germany,  Holland,  Roumania, 
England,  the  United  States,  and  the  Philippine  Islands.  The  disease 
affects  chiefly  young  adults,  and,  like  typhoid  fever,  is  more  prevalent  in 
autumn  than  at  other  seasons  of  the  year.  V.  Sion  and  V.  Negal  and 
De  Feyfer  and  Keyser  found  that  the  epidemics  under  their  observation  were 
produced  by  drinking  infected  water.  Hunermann  traced  several  cases 
occurring  among  children  to  one  of  their  number  who  had  suffered  from  a 
mild  infection.  Of  the  other  recorded  cases  nothing  definite  concerning 
the  mode  of  infection  is  known. 

Symptoms. — The  disease  may  be  mild  or  severe.  The  onset  is  gradual,  and 
the  symptoms  of  invasion  are  the  same  as  those  met  with  in  typhoid  fever, 
namely,  headache,  lassitude,  and  slight  bronchitis.  During  the  course  of 
the  disease  the  spleen  becomes  enlarged,  rose  spots  may  appear,  and  the 
patient  develops  the  typhoid  state.  In  Cushing's  case  a  relapse  occurred. 
Johnston  states  that  diarrhoea  and  termination  of  the  fever  by  crisis  are  of 
more  frequent  occurrence  than  in  typhoid  fever.  Brion  found  diarrhoea 
in  18  per  cent,  of  the  recorded  cases.  In  uncomplicated  cases  no  leuko- 
cytosis has  been  observed.  Hemorrhage  from  the  bowel  occurred  in  5 
per  cent. 

Complications. — Pratt  has  published  a  list  of  complications  which  includes 
all  that  have  occurred  in  the  84  recorded  cases.  He  divides  them  into  three 
categories,  viz.:  1.  Those  occurring  in  cases  caused  by  Bacillus  para- 
typhosus  a.  2.  Those  occurring  in  cases  caused  by  Bacillus  paratyphosus  ^. 
3.  Those  occurring  in  cases  in  which  the  species  of  the  causative  organism 
was  not  determined.  He  has  shown  that  the  complications  of  paratyphoid 
fever  are  of  about  the  same  character  and  frequency  as  those  of  true  typhoid 
fever. 

Diagnosis. — The  diagnosis  depends  upon  the  isolation  and  cultivation 
of  a  paratyphoid  bacillus  from  the  patient's  blood,  urine,  or  feces,  or  from 
a  localized  lesion.  Bacilli  thus  obtained  should  be  agglutinated  by  the 
patient's  blood  serum,  and  the  latter  should  agglutinate  known  paratyphoid 
bacilli.    In  case  an  organism  cannot  be  recovered  Pratt  thinks  a  diagnosis 


TYPHUS  FEVER  61 

of  paratyphoid  is  justifiable  if  the  patient's  blood  serum  agglutinates  known 
strains  of  paratyphoid  bacilli.  While  the  Widal  reaction  is  usually  nega- 
tive, or  positive  only  in  very  low  dilution,  Johnston  believes  that  all  cases  in 
which  it  is  negative  must  not  be  regarded  as  cases  of  paratyphoid  rather  than 
true  typhoid  fever. 

Prognosis. — The  prognosis  would  seem  to  be  favorable,  as  only  3  deaths 
have  occurred  in  83  undoubted  cases  of  the  disease,  and  1  of  these  was  a 
mixed  infection  with  the  Bacillus  typhosus. 

Treatment. — ^This  is  identical  with  that  of  true  typhoid  fever. 


TYPHUS  FEVER. 

Definition. — Typhus  fever  is  an  acute,  infectious,  self-limited  disease  of 
sudden  onset  which  is  characterized  by  fever,  mental  apathy,  and  the  develop- 
ment of  a  rash  which  does  not  recur  in  crops  as  does  the  rose  rash  of  typhoid 
fever.  It  is  particularly  prone  to  attack  large  numbers  of  persons  in  unhealthy 
surroundings,  and  is  distinctly  a  disease  of  starvation  or  overcrowding.  The 
period  of  incubation  of  typhus  fever  as  a  rule  varies  from  eight  to  fourteen 
days,  but  there  can  be  no  doubt  that  many  cases  have  been  attacked  within 
seven  days  after  exposure.  A  few  cases  are  said  to  have  developed  as  early 
as  the  fourth  day.  Typhus  fever  is  one  of  the  most  contagious  of  the  acute 
infectious  maladies. 

Some  confusion  has  arisen  in  the  past  between  typhus  and  typhoid  fever, 
but  at  present,  they  are  clearly  differentiated,  although  it  is  worthy  of  note 
that  the  symptoms  of  enteric  fever  are  so  much  like  typhus  fever  in  their 
degree  of  adynamia  that  it  is  called  "typhoid"  or  like  typhus,  while  German 
writers  of  the  present  day  still  call  typhoid  fever  "  ileotyphus." 

Typhus  fever  is  sometimes  called  Spotted  Fever,  Ship  Fever,  Putrid 
Fever,  or  Hunger  Typhus. 

The  infection  probably  reproduces  itself  solely  in  the  body  of  the  infected 
patient,  and  is  spread  by  direct  contact  with  the  patient  or  by  his  garments 
or  discharges.     It  is  not  transmitted  any  great  distance  through  pure  air. 

History. — Typhus  fever  was  first  described  as  occurring  in  1083  by  Corradi, 
but  it  was  not  fully  recognized  as  a  distinct  malady  till  1546,  when  Fracas- 
torius  wrote  of  the  affection  as  he  had  seen  it  in  Verona  in  1505  and  1508. 
Several  epidemics  are  reported  as  having  occurred  during  the  last  half  of 
the  sixteenth  century,  in  the  eighteenth  century,  and  in  the  early  part  of  the 
nineteenth  century  in  various  parts  of  Europe;  a  most  virulent  epidemic 
ravaging  Ireland  and  England  in  1846.  In  America  it  first  appeared  in 
the  New  England  States  in  1807,  and  in  Philadelphia  in  1812,  where  it  is 
said  to  have  existed  in  isolated  cases  until  1836. 

Distribution. — Typhus  fever  seems  to  occur  in  all  parts  of  the  world  if  the 
conditions  favorable  to  its  development  are  present  in  the  sense  of  unhealthy 
surroundings  and  provided  the  necessary  germ  is  introduced.  Because  of 
its  intimate  association  with  unsanitary  conditions  it  has  been  epidemic  in 
great  armies,  during  famine,  and  on  ships  in  which  the  crew  or  passengers 
often  were  huddled  together  for  long  periods  of  time.     On  the  continent 


62  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

of  Europe  it  spreads  usually  from  east  to  west  and  is  disseminated  chiefly 
by  the  poorest  classes  when  they  travel  from  place  to  place.  Persia, 
China,  Hungary,  and  Turkey  are  never  free  from  typhus  fever,  and  small 
epidemics  occasionally  arise  from  these  sources.  Sometimes  small  epidemics 
or  sporadic  cases  arise  without  it  being  possible  to  find  any  source  of  infec- 
tion. The  disease  is  exceedingly  rare  in  the  United  Stares,  but  the  possi- 
bility of  its  occurrence  must  always  be  borne  in  mind  by  quarantine  officers 
and  physicians  in  charge  of  large  hospitals  in  crowded  cities. 

Etiology. — As  already  stated,  typhus  fever  is  a  malady  which  depends  upon 
a  specific  cause  and  the  presence  of  unsanitary  conditions  for  its  develop- 
ment. The  specific  contagion,  whatever  it  may  be,  retains  its  virulence  for 
long  periods  of  time  in  garments  and  in  furniture.  Much  difference  in  its 
infectiousness  also  exists,  for  in  some  epidemics  nearly  everyone  exposed  is 
taken  ill,  whereas  in  others  but  few  are  affected.  Kelsch  has  advanced 
the  theory  that  the  micro-organism  of  the  disease  is  one  which  is  usually 
benign,  but  may  become  malignant  under  favorable  states.  The  specific 
micro-organism  has  never  been  isolated,  although  several  investigators 
have  claimed  its  discovery. 

Exposure  for  a  considerable  period  of  time  to  the  atmosphere  of  a  room 
which  is  poorly  ventilated  and  which  contains  typhus  patients  is  the  most 
effective  way  of  contracting  the  disease,  whereas  if  ventilation  is  good  and 
the  exposed  person  in  perfect  health  there  is  much  less  danger  of  infection. 
When  a  large  number  of  cases  of  typhus  fever  are  grouped  together  in 
a  ward,  the  infection  becomes  very  virulent  and  both  the  attendants  and  the 
physicians  are  extremely  prone  to  contract  the  disease.  Now  that  vaccination, 
antidiphtheritic  serum,  and  antiplague  inoculations  protect  the  physician 
and  nurse  from  these  infectious  diseases,  there  is  no  malady  so  apt  to 
attack  them  and  against  which  there  is  so  little  prophylactic  aid  as  typhus. 

The  most  infectious  period  of  the  disease  is  in  the  early  stages  and  at  the 
height  of  the  fever,  although  Moore  asserts  that  it  is  most  contagious  during 
convalescence.  It  is  also  infectious  even  during  the  stage  of  incubation. 
Mild  cases  are  probably  as  capable  of  spreading  the  infection  as  severe  ones. 
After  the  febrile  condition  has  passed  away  there  is  reason  to  believe  that 
the  patient  ceases  to  be  a  direct  source  of  infection,  and  if  an  attendant 
who  comes  in  contact  with  him  for  the  first  time  now  contracts  the  disease, 
it  must  be  from  the  poison  which  has  found  lodgement  in  the  clothing  of 
the  patient  during  his  illness.  So  far  as  we  know,  the  most  common 
means  by  which  infection  gains  access  to  the  body  is  by  the  organs  of  res- 
piration and  perchance  by  the  skin.  Indeed,  some  clinicians  of  experience 
assert  that  actual  contact  between  the  body  of  the  patient  and  that  of  the 
attendant  is  necessary  for  infection  to  take  place,  but  this  is  not  generally 
conceded.  Certain  it  is  that  a  very  brief  period  of  exposure  is  sufficient  for 
the  transmission  of  the  .disease.  The  infectious  agent  or  agents  of  typhus 
fever  is  rarely  if  ever  carried  by  water  or  other  liquid  media.  Lowered 
vitality  of  the  individual  naturally  increases  his  susceptibility.  The  influ- 
ence of  age  and  sex  is  very  slight,  for  all  ages,  after  early  infancy,  seem 
equally  susceptible,  the  greater  predominance  of  the  malady  between  twenty 
and  forty  probably  being  due  to  increased  opportunities  for  exposure. 


TYPHUS  FEVER  63 

The  influence  of  climate  and  season  upon  the  spread  of  typhus  fever  is 
only  an  indirect  one,  in  that  the  poor  ventilation  of  the  houses  of  the  lower 
classes  during  the  winter  months  aids  in  the  dissemination  of  the  disease 
among  the  occupants,  whereas  in  summer  the  better  supply  of  fresh  air 
and  the  greater  amount  of  out-door  life  tends  to  diminish  the  danger  of 
infection. 

Prevention. — There  is  no  disease  in  the  prevention  of  which  fresh  air 
plays  so  large  a  part  as  it  does  in  typhus  fever.  Indeed,  it  may  be  stated 
that  if  a  healthy  man  be  supplied  with  plenty  of  fresh  air  while  in  the  pres- 
ence of  the  sick  he  will  have  a  fair  chance  of  escape,  whereas  if  the  air  of  the 
room  be  impure  infection  is  almost  certain,  for,  as  already  stated,  typhus  fever 
is  a  malady  of  darkness  and  poor  ventilation.  Practical  experience  seems  to 
indicate  that  the  various  disinfectants  usually  employed  have  little  value  in 
preventing  its  spread  unless  they  are  used  in  concentrated  form  upon  the 
garments  which  have  been  infected.  By  far  the  best  means  of  preventing  the 
spread  of  typhus  fever  are  the  admission  of  a  plentiful  supply  of  fresh  air  and 
sunshine,  the  application  of  steam  or  scalding  water  to  all  woodwork  and 
clothing,  or  the  use  of  dry  heat  if  steam  heat  cannot  be  employed.  The 
bed-clothing  and  mattresses  should  be  destroyed  by  fire.  The  value  of 
formaldehyde  gas  as  a  disinfectant  is  still  undecided  for  preventing  the 
spread  of  this  disease. 

Pathology  and  Morbid  Anatomy. — Typhus  fever,  unlike  typhoid  fever,  has 
no  peculiar  morbid  anatomy,  and  it  is  therefore  impossible  from  autopsy 
findings  alone  to  determine  that  the  cause  of  death  has  been  typhus.  The 
skin,  it  is  true,  may  show  very  soon  after  death  numerous  petechia?,  and 
early  decomposition  constantly  occurs  after  death  from  this  disease.  The 
body  is  usually  not  greatly  emaciated  because  the  disease  lasts  so  short  a 
time.  The  muscles,  which  are  somewhat  dry,  may  also  show,  when  exam- 
ined under  the  microscope,  signs  of  granular  or  fatty  degeneration  just  as 
they  do  in  typhoid  fever. 

The  respiratory  passages  may  be  inflamed  or  congested.  Thus  there 
may  be  laryngeal  ulceration  as  in  typhoid  fever  and  a  considerable  degree 
of  bronchitis.  Often  hypostatic  congestion  of  the  lungs  is  present.  In 
other  instances  a  true  lobar  pneumonia  occurs.  Indeed,  Curschmann  says 
it  occurred  in  15  per  cent,  of  his  cases.  The  heart  muscle  is  friable  and 
suffers  from  the  form  of  myocarditis  seen  in  afl  infectious  diseases,  and 
the  blood  is  found  to  be  darker  and  more  liquid  than  normal.  It  is  a  note- 
worthy fact  that  the  intestines  show  no  lesions  whatever  either  in  Peyer's 
patches  or  in  the  solitary  glands.  If  such  lesions  are  present  the  disease  is 
typhoid,  not  typhus,  fever.  The  liver  is  usually  swollen  and  is  found  to  be 
the  seat  of  cloudy  swelling,  while  the  spleen  is  also  enlarged  to  some  degree 
but  very  soft.  It  may  contain  infarcts.  The  kidneys  are  also  the  seat  of 
cloudy  swelling. 

Symptoms. — The  symptoms  of  typhus  fever  are  quite  characteristic. 
Unlike  those  of  typhoid  fever,  the  invasion  is  usually  abrupt,  the  patient 
suddenly  feeling  ill  about  twelve  days  after  exposure,  and  being  seized  by  a 
chill  or  series  of  chills,  with  headache,  backache,  and  general  prostration. 
The  fever  rises  rapidly,  reaching  its  acme  it  may  be  as  early  as  the  second 


64  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

day,  but  as  a  rule  it  rises  steadily  during  the  first  four  or  five  days,  and 
during  this  period  of  rise  the  characteristic  morning  remissions  of  typhoid 
fever  do  not  occur  to  so  marked  a  degree.  By  the  fifth  day  the  temperature 
often  reaches  105°  or  even  107°,  but  when  the  infection  is  not  severe  it 
may  not  go  above  103°.  After  having  reached  its  highest  point  it  remains 
fairly  constant  with  a  slight  decrease  each  morning,  the  evening  tem- 
perature, however,  remaining  high  until  the  period  of  crisis,  at  about  the 
fourteenth  day.  In  cases  characterized  by  severe  infection  the  tempera- 
ture may  continue  to  rise  until  it  reaches  as  high  as  109°,  when  death  usually 
occurs.  To  those  cases  in  which  the  temperature  reaches  this  very  high 
point  within  the  first  few  days  of  the  illness  the  term  Typhus  Siderans  is 
usually  applied. 

The  pulse  is  full  and  rapid,  but  usually  not  so  feeble  as  in  the  early 
stages  of  typhoid  fever.  The  face  is  deeply  flushed  the  conjunctiva  con- 
gested, and  the  expression  one  of  apathy,  although  in  some  cases  delirium 
varying  from  mild  wandering  to  actual  maniacal  violence  may  be  met  with. 
Sometimes  the  delirium  is  wild  (delirium  ferox),  sometimes  it  is  like  that 
of  delirium  tremens,  and  sometimes  it  is  low  and  muttering — the  typho- 
mania  of  Galen.  If  the  toxaemia  is  severe  extreme  prostration  and  feeble- 
ness may  ensue  by  the  tenth  day. 

In  from  three  to  five  days  the  eruption  appears  upon  the  abdomen  and 
chest,  and  soon  spreads  to  the  legs,  arms,  and  face.  It  possesses  two  pecu- 
liar characteristics.  In  the  first  place  it  is  papular,  as  in  typhoid  fever,  but 
the  spots  are  rarely  as  rosy  as  they  are  in  that  disease,  and  may  finally 
become  as  dark  as  actual  petechiee,  which  indeed  they  really  are.  The 
second  peculiarity  is  that  there  seems  to  be  a  subcuticular  eruption  or  area 
of  congestion,  or  mottling,  so  that  the  skin  is  marbled  or  mottled.  Unlike 
the  rash  of  typhoid  fever,  that  of  typhus  does  not  disappear  on  pressure, 
and  is  distinctly  manifest  after  death.  Even  if  the  case  is  mild  the  petechial 
character  of  the  rash  is  present.  In  some  instances  the  skin  is  said  to  give 
off  a  peculiar,  musty  or  mouse-like  odor.  In  children  the  rash  may  be  so 
profuse  as  to  resemble  an  attack  of  malignant  measles. 

As  the  disease  advances  to  the  second  week  the  evidences  of  toxaemia 
become  more  marked.  The  active  delirium  which  perchance  was  present 
at  first  is  replaced  by  stupor  and  coma  vigil  with  subsultus  tendinum,  the 
tongue  is  dry  and  heavily  coated,  the  teeth  covered  with  sordes,  and  the 
heart's  action  rapid  and  feeble.  The  respirations  are  quickened  but  shallow, 
and  diarrhoea  may  be  marked.  This  stage  is  called  the  "putrid,"  "malig- 
nant," or  "typhoid"  stage  of  the  malady.  It  is  essentially  one  of  profound 
toxaemia,  and  the  patient  lies  in  a  state  of  deep  prostration,  indifferent  to 
all  sounds  and  objects  in  the  immediate  vicinity,  mumbling  a  few  disjointed 
sentences,  his  tongue  being  so  coated  and  dry  that  it  is  almost  impossible 
for  him  to  move  it.  The  pupils  are  often  strongly  contracted  and  the  ten- 
dons twitch,  while  there  may  also  be  carphologia,  or  picking  at  the  bed- 
clothes. Finally,  if  the  illness  becomes  more  severe,  the  patient  lies  with 
open  eyes,  gazing  into  space,  with  dilated  pupils,  a  thready,  imperceptible 
pulse,  and  a  cold,  clammy  skin,  which  heralds  the  approach  of  death,  which 
is  due  to  the  toxaemia,  asthenia,  and  hypostatic  pulmonary  congestion. 


TYPHUS  FEVER 


65 


If  the  patient  survives  the  early  stages  of  attack,  the  fever  usually  ends 
by  the  twelfth  or  fourteenth  day  and  the  temperature  undergoes  much  more 
rapid  defervescence  than  it  does  in  typhoid  fever.  Indeed,  it  is  generally 
thought  that  the  fever  ends  by  crisis;  so  that  the  patient  passes,  during  a 
prolonged  sleep,  from  a  state  of  severe  illness  with  a  clouded  mind  to  early 
convalescence  with  a  clear  mind,  a  critical  fall  of  temperature  taking  place. 
This  remarkable  change  in  the  aspect  of  the  case  has  been  alluded  to  by 
some  authors  as  quite  pathognomonic  of  typhus  fever,  but  the  statement  that 
the  fall  of  the  temperature  is  always  by  crisis  is  not  universally  conceded 
to  be  correct.  Thus,  Moore,  of  Dublin,  states  that  the  end  is  by  crisis; 
while  Curschmann  asserts  that  in  the  great  majority  of  cases  it  ends  by 
lysis,  although  he  admits  that  a  critical  fall  occasionally  takes  place,  covering 
a  period  of  from  two  to  three  days.  This  is  hardly  a  crisis  in  the  usual 
acceptation  of  the  term. 

Whatever  may  be  the  true  method  of  the  fall  of  temperature,  it  is  certainly 
a  fact  that  convalescence  is  rapidly  established;  so  that  the  patient  pro- 
ceeds to  complete  recovery  more  rapidly  than  after  typhoid  fever,  health 
being  completely  restored,  it  may  be,  by  the  end  of  a  month. 

Relapse  in  typhus  fever  very  rarely  takes  place,  and  in  the  vast  majority 
of  cases  one  attack  produces  immunity  against  further  infection. 

The  complications  of  typhus  fever  are  those  which  we  would  expect  to 
meet  with  in  the  presence  of  any  severe  infection.  Bronchopneumonia  or 
lobar  pneumonia  may  occur.  In  very  poorly  nourished  individuals  noma 
may  develop,  and  symptoms  of  generalized  paralysis  develop  as  the  result 
of  neuritis.  So,  too,  septic  arthritis  and  infection  of  the  parotid  glands  may 
occur. 

Diagnosis. — Several  characteristics  of  typhus  fever  have  already  been 
emphasized.  The  most  noteworthy  of  these  are:  the  sudden  accession  of 
the  disease,  the  rapid  rise  of  temperature  without  morning  remission,  the 
development  of  a  peculiar  rash  between  the  third  and  fifth  day,  the  dusky 
appearance  of  the  face,  the  musty  odor  of  the  skin,  and  the  early  appear- 
ance of  active  delirium  or  profound  apathy.  All  these  symptoms  are  quite 
different  from  those  met  with  ordinarily  in  typhoid  fever,  but  it  is  not  to 
be  forgotten  that  sometimes  typhoid  fever  begins  suddenly  and  presents 
manifestations  closely  resembling  those  of  typhus;  so  that  during  the  pres- 
ence of  an  epidemic  of  typhus  or  typhoid  fever  cases  of  either  one  of  these 
diseases  may  readily  be  overlooked.  In  the  differentiation  the  early  devel- 
opment of  the  rash  (third  to  fifth  day)  in  typhus  fever  is  of  great  practical 
value,  and  the  distribution  of  the  rash  is  still  more  helpful  in  aiding  a 
decision;  for  the  rash  of  typhus  fever,  if  profuse,  involves  the  extremities 
as  well  as  the  trunk,  whereas  that  of  typhoid  fever  is  chiefly  limited  to  the 
body;  a  profuse  and  dusky  rose  rash  on  the  hands  and  legs  is  therefore 
distinctly  in  favor  of  typhus  fever.  Again,  the  rash  of  typhus  fever  is  con- 
stant, whereas  that  of  typhoid  fever  fades  and  recurs  in  crops.  Sometimes 
however,  the  rash  of  typhus  fever,  like  that  of  typhoid  fever,  is  very  scant, 
only  a  few  rose  spots  being  present.  Indeed,  the  disease  may  occur  without 
any  exanthema  being  manifest. 

As  the  illness  progresses  much  additional  differential  information 
5 


66  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

can  be  gained  if  the  case  be  one  of  typhoid  fever  by  the  discovery  of 
the  Widal  reaction,  the  recovery  of  the  Bacillus  typhosus  in  the  blood  and 
in  the  rose  spots.  Then,  too,  typhoid  fever  does  not  end  so  abruptly  nor 
so  early  as  does  typhus  fever.  Malignant  measles  and  variola  may  in 
their  earliest  stages  resemble  typhus,  but  their  later  course  clearly  separates 
them. 

Relapsing  fever  is  separated  from  typhus  fever  by  the  clear  mental  con- 
dition of  the  patient  notwithstanding  his  high  temperature,  by  the  lack  of 
petechise,  and  the  absence,  as  a  rule,  of  severe  initial  symptoms. 

Prognosis. — The  prognosis  in  typhus  fever  varies  greatly  with  the  pre- 
vious condition  of  the  patient,  and  also  to  some  degree  with  the  severity  of 
the  epidemic.  Usually  the  mortality  rate  varies  from  10  to  20  per  cent,  in 
young  adults,  but  in  children  it  is  often  much  less  than  this.  In  advanced 
years  the  mortality  is  very  high. 

Curschmann  has  stated  that  "old  age  makes  itself  felt  as  early  as  the 
fortieth  year  and  that  after  fifty  almost  50  per  cent,  die."  The  accompanying 
chart.  Fig,  14,  made  from  the  statistics  of  JMurchison,  Guttstadt,  and 
Curschmann  indicates  further  the  influence  of  age  on  the  prognosis. 

Death  in  typhus  fever  rarely  occurs  before  the  second  week.  After  the 
end  of  the  second  week  it  seldom  takes  place  except  as  the  result  of  some 
untoward  complication. 

Treatment. — The  treatment  of  typhus  fever  is  in  many  respects  identical 
with  that  now  recognized  as  useful  in  typhoid  fever.  The  patient  should 
be  isolated,  of  course,  and  provided  with  an  abundance  of  light  and  air. 
As  already  stated,  in  no  disease  are  these  aids  to  health  more  essential  for 
recovery.  As  the  course  of  the  malady  is  one  toward  profound  asthenia, 
easily  assimilated  or  predigested  foods  should  be  given  as  freely  as  the 
patient  can  utilize  them.  Milk  to  which  is  added  a  little  pancreatin  and 
sodium  bicarbonate,  barley-  and  rice-gruel  in  which  is  placed  some  taka- 
diastase,  and  copious  draughts  of  water  to  flush  the  kidneys  and  aid  in  the 
elimination  of  poisons  are  to  be  administered.  The  fever  is  to  be  treated 
by  cool  or  cold  bathing  as  the  patient  lies  in  bed,  according  to  the  directions 
given  under  typhoid  fever,  and  cold  is  to  be  kept  applied  to  the  head  con- 
tinuously. The  coal-tar  antipyretics  are  not  to  l^e  used  if  they  can  be 
avoided.  When  signs  of  cerebral  and  pulmonary  hypostatic  congestion 
manifest  themselves  the  patient  may  be  immersed  in  a  bath  of  about  90°, 
and  cold  water  at  60°  poured  over  his  head  and  shoulders  as  a  douche, 
active  friction  of  the  body  and  limbs  being  performed  by  the  nurse  for 
several  minutes  before  the  sick  man  is  returned  to  his  bed.  Should  the  cir- 
culation fail,  alcohol  in  the  form  of  whiskey  or  brandy,  well  diluted  with 
water,  is  to  be  employed  for  the  purpose  of  supporting  the  heart  and  nervous 
system.  Camphor  in  ^  grain  doses  is  useful  for  this  purpose.  If  the  nervous 
restlessness  of  the  patient  is  sufficient  to  endanger  life  by  the  resulting 
exhaustion,  a  hypodermic  injection  of  morphine  may  be  given  to  produce 
sleep  or  nervous  quiet. 

The  bowels  should  be  kept  open  by  the  use  of  gentle  laxatives,  or  be 
evacuated  by  a  sajine  purge  if  obstinately  confined.  The  activity  of  the 
kidneys  must  also  be  maintained  by  the  use  of  alkaline  diuretics  and  sweet 


TYPHUS  FEVER 


67 


spirit  of  nitre  and  by  the  free  administration  of  a  pure  drinking  water. 
As  retention  of  urine  often  occurs,  the  state  of  the  bladder  must  be  care- 
fully watched. 


Fig.  14 


H            BETWEEN             BETWEEN 

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Showing  the  decreasing  morbidity  and  increasing  mortality  percentage  of  typhus  fever  with  advanc- 
ing years.  Solid  line  represents  morbidity  from  Murchison's  statistics.  Broken  line,  mortality  percent- 
age from  the  statistics  of  Murchison,  Guttstadt,  and  Curschmann. 


68  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


RELAPSING  FEVER. 

Definition. — Relapsing  fever,  as  its  name  indicates,  is  characterized  by 
an  attack  of  fever  which  lasts  about  six  days,  this  in  turn  is  followed  by  a 
period  in  which  fever  is  absent,  and  this  again  by  a  recurrence  of  a  period 
of  fever.  These  alternating  periods  may  be  repeated  three  or  four  times. 
It  is  due  to  a  specific  micro-organism,  the  so-called  spirillum  or  spirochsete 
of  Obermeier.  Sometimes  it  is  called  Febris  Recurrens,  "Seven  Days' 
Fever,"  and  "Famine  Fever." 

History.- — The  history  of  relapsing  fever  is,  when  compared  to  some  other 
infectious  diseases,  fairly  modern,  for  the  first  descriptions  of  it  occurred 
in  medical  literature  about  1729,  although  it  was  not  until  1739  that  Rutty 
gave  a  clear  description  of  its  course.  After  this  for  nearly  a  century  no 
reports  of  its  existence  are  to  be  found,  but  between  1842  and  1852  it 
appeared  over  a  wide  area,  occurring  in  England,  Ireland,  Scotland,  Ger- 
many, and  finally  in  America,  to  which  country  it  was  brought  by  a  ship- 
load of  immigrants  who  came  from  Liverpool  and  landed  in  Philadelphia 
in  1844.  It  became  epidemic  in  the  United  States  in  the  decade  from  1861 
to  1870,  and  it  is  interesting  to  note  that  as  the  American,  Gerhard,  first 
aided  in  the  differentiation  of  typhoid  fever  from  typhus  in  Philadelphia,  so 
Pepper,  Rhoads,  and  Parry,  of  the  same  city,  have  contributed  to  medical 
literature  the  best  account  of  the  disease  as  it  has  appeared  in  this  country, 
havino-  observed  a  larger  number  of  cases  than  any  other  clinicians. 

Distribution. — Relapsing  fever  has  occurred  in  almost  all  parts  of  the 
civilized  world. 

Etiology. — It  has  been  claimed  that  filthy  surroundings  and  bad  food 
are  active  in  the  development  of  relapsing  fever,  but  they  probably  exercise 
a  general  influence  by  lowering  vitality  rather  than  by  directly  aiding  infec- 
tion. Sex,  age,  and  nationahty  exercise  no  influence,  and  it  is  doubtful  if 
any  one  season  of  the  year  increases  the  prevalence  of  the  disease.  The 
actual  cause  of  relapsing  fever,  as  already  stated,  is  a  spirillum  known  as 
the  spirillum  of  Obermeier,  which  is  constantly  found  in  the  blood  of  patients 
suffering  from  the  disease  during  the  stage  of  fever.  It  is  absent  from  the 
blood  in  the  intermissions,  although  small,  glistening  bodies,  said  to  be 
spores,  can  be  seen.  The  disease  is  contagious,  that  is  it  requires  contact 
with  the  patient  or  with  his  garments  for  the  infection  to  be  spread.  Patients 
may  be  infected  by  insects,  for  example  by  bed-bugs  which  have  previously 
bitten  patients  suffering  from  relapsing  fever.  That  the  disease  is  ever 
conveyed  by  the  air  is  doubtful. 

Pathology  and  Morbid  Anatomy. — The  changes  produced  in  the  body  by 
relapsing  fever  are  not  only  not  marked,  but  not  at  all  characteristic.  The 
spleen  and  liver  are  swollen  and  engorged,  as  in  nearly  all  febrile  infectious 
diseases,  and  the  voluntary  muscles  may  undergo  granular  degeneration. 
Similar  changes  may  be  found  also  in  the  heart  muscle.  Sometimes  multiple 
infarctions  and  hyperplasia  of  the  bone-marrow  are  present  and  ecchymotic 
spots,  which  are  found  ante-mortem,  are  seen  in  the  skin  and  subcutaneous 
tissues. 


RELAPSING  FEVER 


69 


Symptoms. — As  a  rule  about  six  or  seven  days  after  exposure  to  the  dis- 
ease the  infected  person  is  abruptly  seized  by  a  severe  chill,  or  more  rarely  by 
headache  and  vomiting.  The  face  becomes  flushed,  but  the  expression  is 
not  dull  and  apathetic  as  it  is  in  typhus  or  typhoid  fever,  unless  the  infection 


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is  very  severe,  when  typhoid  symptoms  may  soon  develop.  A  moderate 
degree  of  jaundice  also  is  present  in  many  cases.  No  characteristic  eruption 
appears  on  the  skin,  although  small  petechise  or  ecchymotic  spots  may 


70  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

occur  in  severe  cases.  Many  observers  have  recorded  the  presence  of  a 
disagreeable,  musty  odor  about  the  patient. 

The  febrile  movement  is  the  most  notable  manifestation  of  the  disease. 
The  fever  begins  to  rise  while  the  stage  of  chill  is  still  young,  and  reaches 
102°  or  103°  in  the  first  twenty-four  hours  and  104°  or  106°  in  the  next 
twenty-four  hours.  During  the  febrile  stage  of  about  six  days  this  level 
of  temperature  is  fairly  constantly  maintained,  although  irregular  remis- 
sions of  1°  or  2°  may  occur.  Sometimes  the  fever  reaches  108°.  In  some 
cases  the  primary  febrile  period  lasts  only  two  days.  While  the  febrile 
movement  just  described  is  characteristic,  its  ending  is  more  so,  for  a  crit- 
ical fall  of  temperature  takes  place  with  a  suddenness  and  completeness 
which  is  rarely  met  with  in  any  other  disease  unless  it  be  croupous  pneu- 
monia (Fig.  15).  Not  rarely  it  falls  6°  in  three  hours,  although  a  fall  of 
1°  an  hour  is  more  common.  The  rapid  fall  may  carry  the  temperature 
a  little  below  normal.  After  a  few  days  of  no  fever  the  relapse  takes 
place  with  the  same  sudden  onset  as  occurred  with  the  primary  attack. 
It  runs  a  course  in  all  respects  like  the  original  seizure,  but  it  more  com- 
monly ends  by  lysis  than  does  the  first  paroxysm.  The  third  and  fourth 
attacks,  if  they  occur,  are  usually  milder  than  the  first  two.  The  duration 
of  the  period  of  intermission  varies  from  one  to  ten  days,  although 
it  is  usually  six  days  or  a  week,  and  the  duration  of  the  entire  illness 
may  vary  from  eighteen  to  ninety  days,  according  to  the  number  of 
relapses. 

The  pulse  during  the  early  attacks  is  rapid,  and  it  may  be  bounding, 
but  if  the  patient  be  enfeebled  by  prolongation  of  the  illness  it  may  be 
small  and  compressible.  Severe  frontal  and  occipital  headache  is  often 
experienced  by  the  patient  in  the  first  attack,  but  delirium  is  rare  except  it 
be  due  to  serious  complications  or  to  very  high  fever. 

Prognosis. — ^The  prognosis  as  to  ultimate  recovery  is  quite  good,  the 
mortality  of  the  disease  usually  being  about  4  per  cent. 

Treatment. — There  is  no  specific  treatment  for  relapsing  fever.  Good 
nursing,  careful  feeding,  and  the  use  of  stimulants,  if  the  patient  is  feeble, 
are  of  course  needful.  The  action  of  the  bowels  and  kidneys,  as  in  all  infec- 
tious diseases,  should  be  carefully  attended  to.  No  results  from  the  use  of 
hydrotherapy  in  relapsing  fever  have  been  published  so  far  as  the  writer  is 
aware,  but  the  course  of  the  febrile  movement  scarcely  indicates  this  plan 
of  treatment. 

VARIOLA. 

Definition. — Variola,  or  smallpox,  is  an  acute  infectious  disease  affecting 
the  entire  body,  but  manifesting  itself  chiefly  by  the  development  upon  the 
skin,  more  particularly  that  of  the  face  and  forearms,  of  an  exanthem  which 
is  at  first  macular,  then  papular,  then  vesicular,  pustular,  and  finally 
umbilicated. 

History. — Smallpox  is  one  of  the  ancient  diseases,  for  records  exist  which 
show  it  to  have  occurred  many  centuries  before  the  time  of  Christ.  The 
first  authentic  medical  record  of  the  malady  did  not  appear,  however, 


VARIOLA  71 

before  the  tenth  century,  v/hen  Rhazes,  of  Bagdad,  wrote  his  Treatise  on 
Smallpox  and  Measles.  It  is  generally  considered  that  smallpox  did  not 
gain  entrance  to  Europe  till  about  a.d,  710,  when  the  Arabs  conquered 
the  Spaniards.  It  reached  Germany  about  the  tenth  century,  at  which  time 
it  also  appeared  in  England.  At  times  since  the  tenth  century  it  has  swept 
away  thousands  of  persons  in  a  single  epidemic,  and  very  few  escaped 
its  ravages.  Indeed,  a  large  part  of  the  population  of  I^ondon  were  at  one 
time  pock-marked.  It  was  first  introduced  into  Mexico  in  1520,  and  into 
Massachusetts  in  1633.  Until  the  introduction  of  vaccination  it  was  one 
of  the  most  death-dealing  maladies  known  to  man.  (For  the  influence  of 
vaccination  in  diminishing  smallpox  see  article  on  Vaccinia.) 

Distribution. — Smallpox  has  occurred  in  all  parts  of  the  civilized  world, 
from  the  Arctic  to  the  Tropics,  and  is  of  equal  virulence  in  very  cold  and 
in  very  warm  climates. 

Etiology. — Variola  is  believed  by  some  to  be  due  to  a  parasite  named  by 
Guarnieri,  in  1892,  the  Cytoryctes  varioloe,  and  carefully  studied  by  Wasie- 
lewski  in  1901.  Its  evolution  has  been  more  fully  known  by  the  labors 
of  Councilman,  Magrath,  and  Brinckerhoff  in  1903  and  Brinckerhoff  and 
Tyzzer  in  1905,  the  latter  being  an  extensive  investigation  of  experimental 
variola  and  vaccine  in  Philippine  monkeys.  These  in  every  respect  con- 
firm the  previous  findings  in  human  beings.  Basing  his  views  upon  pre- 
viously accomplished  work,  but  especially  upon  the  study  of  Councilman 
and  his  students,  Calkins  has  attempted  to  formulate  the  different  stages 
in  the  life  history  of  the  parasite.  A  full  review  of  these  and  previous 
inquiries  into  the  nature  of  the  specific  organism  of  variola  and  vaccinia 
will  be  found  in  the  Journal  of  Medical  Research,  February,  1904,  vol. 
xi..  No.  1,  pp.  8-360  and  January,  1906,  vol.  xiv.,  No.  2,  pp.  209-359.  (For 
the  process  of  the  development  of  this  organism  see  Pathology  and  Morbid 
Anatomy.) 

The  disease  affects  persons  who  may  be  exposed  to  it  at  all  ages, 
and  remarkably  few  people  who  are  unvaccinated  are  able  to  resist  the 
infection,  not  more  than  from  1  to  5  per  cent.  The  negro  race  is  peculiarly 
susceptible,  and  in  this  race  the  rate  of  mortality  from  the  disease  is 
usually  very  high.  Smallpox  affects  males  more  frequently  than  females. 
It  is  more  common  in  the  winter  and  spring  than  in  the  summer,  per- 
haps because  of  the  crowding  in  the  homes  of  the  poor  during  the  cold 
months. 

The  contagion  of  smallpox  is  spread  in  several  ways — viz.,  directly,  that 
is,  by  contact  with  the  patient's  body  and  his  clothing;  and  indirectly,  by 
the  air.  Stokes  has  recently  published  a  paper  indicating  that  the  infec- 
tion usually  enters  the  body  through  the  lungs.  A  nurse  may  convey  the 
disease  from  a  patient  to  a  healthy  individual,  and  rats,  mice,  and  flies 
may  do  likewise.  The  patient  ill  of  smallpox  is  capable  of  infecting  a 
healthy  person  from  the  initial  stage  of  the  disease  to  the  moment  when, 
recovery  having  occurred,  every  particle  of  pustule  or  desquamating  skin 
has  been  cast  off.  The  most  contagious  periods  are,  however,  those  of 
vesication,  pustulation,  and  exfoliation. 

The  fact  that  the  disease  is  spread  by  aerial  convection  is  never  to  be 


72 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


forgotten,  and  it  may  be  carried  in  this  way  from  a  few  feet  to  several  yards 
(Fig.  16) .  Much  difference  of  opinion,  however,  exists  among  those  who 
have  studied  the  question  of  aerial  convection.  Power,  of  Fulham,  and 
Barry,  of  Sheffield,  England,  found  a  noticeable  influence  exercised  by  the 
propinquity  of  a  smallpox  hospital,  but  Savill,  from  investigations  carried 
on  at  Warrington,  came  to  the  conclusion  that  aerial  currents  influenced  the 
spread  of  the  disease  but  little.  It  must  be  remembered,  moreover,  that 
before  we  accept  these  figures  as  to  aerial  convection  we  must  be  sure  that 
the  contagion  was  actually  carried  by  the  air  and  not  by  insects  or  animals. 
I  know  of  one  smallpox  hospital  from  which  flies,  mice,  rats,  and  cats 
passed  freely,  and  surrounding  which  smallpox  was  almost  constantly 
present. 

Fig.  16 
4000  feet. 


0.02  per  cent. 
Diagram  showing  the  percentage  of  aerial  convection  of  smallpox.     (Moore.) 

Bodies  dead  of  smallpox  can  also  spread  the  disease  among  those  who 
handle  them. 

The  severity  of  the  infection  depends  not  so  much  upon  the  violence  of 
the  disease  in  the  giver  as  in  the  susceptibility  of  the  receiver  of  the  malady. 
A  mild  case  may  therefore  be  provocative  of  most  virulent  epidemic. 

Incubation. — The  period  of  incubation  of  smallpox  varies  from  five  to 
twenty  days,  but  as  a  rule  it  is  about  twelve  days.  Cases  occurring  in  less 
than  five  days  after  exposure  are  very  rare. 


VARIOLA  73 

Prevention. — There  is  one  measure  above  all  others  to  be  used  in  the 
prevention  of  smallpox,  and  that  is  vaccination,  which  by  its  beneficent 
influence  has  changed  smallpox  from  a  common  and  fearful  scourge  of  man- 
kind to  a  disease  so  rare  that  many  physicians  practice  a  lifetime  without 
seeing  a  case.     (See  Vaccine  and  Vaccination). 

It  is  very  important  to  bear  in  mind  the  clinical  fact  that  vaccination 
not  only  protects  the  patient  who  may  be  subsequently  exposed  to  small- 
pox, but  also  that  it  protects  the  patient  who,  having  been  so  exposed,  is 
subsequently  vaccinated.  Even  if  the  vaccination  be  performed  so  long 
after  the  exposure  that  smallpox  nevertheless  develops,  the  severity  of  the 
disease  will  be  modified,  the  degree  of  modification  being  in  direct  ratio  to 
the  length  of  time  between  vaccination  and  the  appearance  of  the  variola. 

A  most  interesting  illustration  of  this  has  been  sent  me  most  kindly  by 
Dr.  Allan  Warner,  of  the  Borough  Isolation  Hospital,  Leicester,  England. 
The  history  of  the  cases  is  as  follows: 

A  boy,  aged  fourteen  years,  un vaccinated,  sickened  with  smallpox  on 
April  14.  He  was  removed  to  the  hospital  on  April  18,  where  he  had  a 
severe  confluent  attack.  The  father  consented  to  his  wife  and  three  children 
being  vaccinated,  stating  that  personally  he  would  not  be  vaccinated,  but 
would  be  a  "test,"  to  see  if  there  was  anything  in  it.  Ten  days  later  his 
daughter,  aged  three  years,  developed  a  smallpox  eruption;  she  had  less 
than  one  hundred  spots  and  never  appeared  ill.  No  other  person  in  the 
house  suffered  from  smallpox  except  the  father,  vaccinated  in  infancy,  his 
eruption  appearing  fourteen  days  after  the  son  had  been  removed  to  the 
hospital.  A  photograph  of  the  father  and  daughter,  taken  on  the  twelfth  day 
of  the  father's  eruption,  may  be  seen  in  Fig.  17,  and  requires  no  comment. 

In  cases  of  urgency  it  is  generally  held  that  humanized  virus  is  more  valu- 
able than  calf  virus,  but  as  humanized  virus  is  often  diflficult  to  obtain  it 
is  better  to  vaccinate  the  patient  in  different  places  with  glycerinated  vac- 
cine made  by  different  manufacturers,  since  in  this  way  there  is  little  doubt 
but  that  one  will  surely  take. 

The  second  preventive  measure  of  importance  is  the  absolute  isolation  of 
the  patient,  and  the  third  the  complete  disinfection  or  destruction  of  all 
garments  and  bed-clothing  which  have  been  about  the  sick  person,  includ- 
ing those  worn  by  his  attendants.  Finally,  all  individuals  exposed  to  the 
contagion  should  be  quarantined  for  a  period  of  twenty-one  days,  in 
order  that  the  physician  may  be  sure  ihat  they  are  not  going  to  be  attacked 
and  so  spread  the  infection. 

Frequency. — Smallpox  is  so  constantly  present  in  the  poorer  part  of  large 
cities  that  it  may  be  said  to  be  almost  endemic  in  all  of  them,  but  to  a  very 
moderate  degree.  Occasionally  when  a  considerable  number  of  unvac- 
cinated  persons  have  accumulated  in  a  city  or  country  district,  the  disease 
bursts  out  in  a  small  epidemic,  and  sometimes,  without  any  such  apparent 
cause,  certain  districts  seem  to  be  affected,  many  unvaccinated  persons 
being  attacked.  During  the  winter  of  1901  and  1902  smallpox  appeared 
almost  all  over  the  United  States  in  scattered  localities.  It  can,  however, 
always  be  stamped  out  by  house-to-house  vaccination,  and  its  spread 
depends  upon  imperfect  quarantine  and  ineflScient  vaccination. 


74 


DISEASES  DUE   TO  A  SPECIFIC  INFECTION 


As  an  illustration  of  the  extraordinary  effect  of  vaccination  and  sanitation 
upon  this  malady  it  is  interesting  to  note  that  during  the  eighteenth  century 
fully  two-thirds  of  all  children  born  in  Europe  were  sooner  or  later  attacked 


Fig. 17 


^,:y;^*  ■;{■;. 

f      ^.            .              '    .;*'lk 

1/  ;    ■'  \://#": 

'^H 

,l^^'  -^ 

\  ■  '  ^'  '  :                 '■ 

■•,*#'S| 

^^^H 

h  :  >     ^  /  ^;  '*:^ 

Father  and  child  suffering  from  smallpox.     The  child  was  vaccinated  in  the  incubation  period. 

(Allan  Warner's  cases.) 

by  smallpox,  and  an  average  of  one-twelfth  died  of  the  disease.  On  the 
other  hand,  the  death  rate  from  smallpox  in  the  latter  part  of  the  nine- 
teenth century  in  London  was  98.5  per  cent,  less  than  one  hundred  years 
before.     To  put  it  differently,  the  death  rate  from  smallpox  in  1838  was 


VARIOLA  75 

1064  per  million,  while  in  1889  it  was  1  per  million,  and  in  1890  nil  per 
million. 

During  1904  the  disease  was  totally  eradicated  from  New  York  and 
Philadelphia  by  vaccination  and  quarantine. 

Pathology  and  Morbid  Anatomy. — The  most  noteworthy  lesion  produced 
by  smallpox  takes  place  in  the  skin.  The  dermal  papillae  become  hyper- 
jemic,  the  cells  of  the  rete  Malpighii  swell  and  so  raise  the  epiderm,  and 
under  this  epiderm  serum  exudes  and  pushes  the  stratum  still  farther 
upward.  The  cells  of  the  rete  are  more  or  less  elongated,  pigmented,  and 
form  fibrils  extending  from  the  epiderm  to  the  base  of  the  inflamed  zone  in 
the  derma,  constituting  the  vacuolar  focal  degeneration  described  by  Coun- 
cilman, Magrath,  and  Brinckerhoff.  In  this  reticulum  still  further  serous 
exudation  occurs,  and  so  forms  a  vesicle  which  increases  at  its  margin, 
where  the  exudation  takes  place  very  rapidly,  while  degenerative  and 
necrotic  changes  progress  in  the  epithelium  of  the  area  involved.  As  a 
result  the  area  under  and  around  the  vesicle  becomes  indurated  and  we 
have  the  characteristic  hard  pock  of  variola.  The  persistence  of  this  free 
exudation  at  the  margin  of  the  pock  and  the  greater  density  of  the  centre 
lead  to  depression  of  the  latter,  giving  rise  to  umbilication.  Wright  has 
shown  that  the  central  depression  in  the  pock  may  be  due  to  diphtheroid 
degeneration.  It  may  also  be  due  to  retraction  by  a  hair  or  small  gland. 
Councilman,  Magrath,  and  Brinckerhoff  do  not  believe  that  the  pock  is 
always  produced  by  the  same  cause,  but  that  a  number  of  factors  enter 
into  its  formation. 

Following  this  stage,  the  serum  in  the  pock  is  infiltrated  with  leuko- 
cytes, and  these  becoming  great  in  number,  the  contents  of  the  pock 
become  opaque  or  turbid,  and  finally  resemble  pus.  Sometimes  if  the 
inflammation  in  the  adjoining  pocks  is  very  severe  the  deeper  layers  of 
the  skin  become  involved,  undergo  necrosis,  and  so  great  local  destruction 
of  tissue  takes  place.  After  this  stage  epithelial  regeneration  progresses 
beneath  the  scab,  which  dries  up  and  ultimately  falls  off,  leaving  a  red  or 
pink  depression  in  the  skin,  which  depends  for  its  depth  upon  the  degree 
of  pustulation  or  necrosis  present  during  the  acute  stage.  Not  only  do 
vesicles  form  on  the  skin,  but  upon  the  mucous  membrane  of  the  mouth, 
pharynx,  tongue,  and  even  the  rectum,  anus,  vagina,  penis,  and  conjunctiva 
in  some  cases. 

The  changes  just  noted  probably  arise  from  the  minute  organism  recently 
studied  by  Councilman  and  his  assistants.  He  has  described  its  development 
in  the  following  words:  "In  the  lower  layers  of  skin  epitheha,  before  there  is 
present  any  anatomical  evidence  of  vesicle  formation,  there  are  found 
small,  structureless  bodies  from  one  to  four  microns  in  diameter.  The  cells 
present,  at  this  time,  little  or  no  evidence  of  degeneration.  The  bodies, 
one  or  more  in  number,  lie  in  vacuoles  in  the  cells.  The  vacuoles  are,  at 
first,  but  little  larger  than  the  enclosed  bodies.  The  bodies  increase  in 
size,  and  evidence  of  structure,  consisting  of  granules  more  distinctly 
stained,  and  lying  in  definite  spaces,  begin  to  appear.  With  the  increase 
in  size  of  the  body,  the  vacuole  of  the  cell  enlarges  until  a  large,  central 
space  around  the  nucleus  is  formed.    At  this  time   there  is  but  little  evi- 


76  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

dence  of  degeneration  of  the  nucleus.  The  body  continues  to  increase 
and  becomes  granular,  the  granules  lying  in  a  reticular  structure.  The 
form  of  the  larger  bodies  is  irregular  and  suggests  an  amoeboid  character. 
They  may  become  as  large  as,  or  larger  than,  the  nucleus  of  an  epithelial 
cell.  A  definite  nucleus  has  not  been  made  out  in  them,  unless  the 
reticular  structure  which  stains  more  intensely  than  the  rest  of  the  body 
be  so  considered.  At  this  time  segmentation  takes  place,  leading  to  the 
formation  of  small,  round  bodies  about  one  micron  in  diameter.  All  this 
is  best  seen  in  the  acute  hemorrhagic  cases.  It  may  also  be  seen  in  the 
advancing  edge  of  a  young  vesicle,  the  bodies  becoming  larger  and  more 
definite  in  structure  as  the  formation  of  the  vesicle  advances.  The 
bodies  in  the  cells  we  regard  as  living  organisms,  and  the  gradual 
growth  and  final  segmentation  as  a  cycle  in  its  hfe  history.  Up  to  this 
time  the  nuclei,  although  showing  such  evidences  of  degeneration  as  the 
massing  of  chromatin  in  the  periphery,  are  not  greatly  altered. 

"At  the  period  of  segmentation,  and  when  most  of  the  intracellular 
bodies  have  disappeared,  small,  round  or  oval,  ring-like  bodies  appear  in 
the  nucleus.  These  increase  in  size  and  acquire  a  definite  structure,  con- 
sistino;  of  a  series  of  vacuoles  around  a  large,  central  vacuole.  The  rim  of 
the  central  vacuole  stains  more  distinctly  than  do  other  parts  of  the  body. 
One  or  more  of  these  bodies  may  appear  in  a  single  nucleus.  When  several 
are  present  they  are  smaller,  but  have  the  same  structure.  The  bodies 
become  larger;  the  nuclear  rim  grows  less  distinct,  and  finally  disappears, 
and  the  body  lies  in  a  completely  degenerated  cell,  or  this  breaks  down, 
setting  free  the  body.  With  the  growth  and  development  of  the  intranuclear 
body  the  vacuolar  structure  becomes  less  evident,  and  finally  a  structure 
is  formed  which  contains  numerous  fine  vacuoles.  At  this  time  small,  cir- 
cular bodies  begin  to  appear  in  it,  and  groups  of  these  are  surrounded  by 
a  faint  ring,  which  probably  represents  the  remains  of  the  body  in  which 
they  were  formed." 

Myocardial  degeneration  is  present  in  most  cases,  and  a  variolous  myo- 
carditis has  been  described. 

In  general  the  cardiovascular  changes  of  smallpox  resemble  similar 
alterations  occurring  in  other  infectious  diseases. 

Proliferative  changes  occur  in  hsematopoietic  organs  (spleen,  lymph 
nodes,  and  marrow),  associated  with  the  production  of  basophilic  mono- 
nuclear cells  which  enter  the  circulation  and  also  phagoc}i:ic  endothelial 
elements.  The  basophilic  mononuclear  cells  infiltrate  the  testicle  and  usually 
the  kidney,  liver,  and  adrenals. 

Cloudy  swelling  occurs  in  the  glandular  viscera  and  a  diffuse  toxic 
degeneration  takes  place  in  the  liver,  kidneys,  adrenals,  and  testicles. 

Pharyngitis  and  fatal  bronchopneumonia  occur;  less  commonly  croupous 
pneumonia  and  pulmonary  abscess  or  gangrene  develop. 

Endocarditis,  pleurisy,  and  empyema  are  infrequent. 

The  kidneys  are  more  or  less  altered  in  all  cases;  in  milder  degrees 
this  may  amount  to  little  more  than  intense  cloudy  changes,  but  in  other 
cases  acute  diffuse,  glomerular,  or,  less  commonly,  suppurative  nephritis 
occurs. 


VARIOLA  77 

Many  of  the  lesions  produced  in  the  internal  organs  in  smallpox  are  the 
result  of  the  secondary  infection  from  the  skin  and  respiratory  tract,  and 
this  usually  depends  upon  the  presence  of  the  Streptococcus  pyogenes. 

As  in  most  of  the  acute  infectious  diseases,  bronchitis  is  present  in  many 
cases  of  variola,  and  the  secretion  of  the  bronchial  mucous  membrane  may 
be  profuse  and  mucopurulent. 

Bronchopneumonia  may  also  develop. 

When  hemorrhagic  smallpox  takes  place  we  have  transudations  of  blood 
into  the  pocks  and  into  the  conjunctiva,  the  retina,  the  muscles,  the  sub- 
pleural  tissues,  into  all  the  abdominal  organs,  and  into  the  kidneys  and 
the  perirenal  fat. 

Submucous  extravasations  also  take  place  in  all  the  organs  of  the  body 
lined  with  mucous  membrane. 

Symptoms. — After  an  incubation  period  of  about  twelve  days  the  symp- 
toms develop.  As  in  many  acute  infections,  headache  and  backache  are  the 
predominant  initial  symptoms  of  smallpox,  but  they  are  peculiar  in  their 
severity  in  this  disease,  so  that  their  very  intensity  possesses  diagnostic 
significance.  Sometimes  the  pain  in  the  back  extends  down  the  posterior 
portions  of  the  legs.  Rigors  also  occur  and  pain  in  the  epigastrium  and 
vomiting  may  come  on.  Sometimes  drowsiness  and  sleep  with  muscular 
twitching  develops  as  a  prominent  initial  sign  in  children.  The  urine  is 
often  scanty,  loaded  with  urates,  and  usually  contains  some  albumin.  The 
tempercture  in  smallpox  is  usually  high  from  the  onset,  so  that  it  may 
reach  104°  as  early  as  the  latter  part  of  the  first  day,  and  105°  or  106°  by 
the  end  of  the  first  forty-eight  hours.  It  maintains  this  high  degree  with 
very  slight  remission  until  the  eruption  is  developed.  The  pulse  is  rapid 
often  as  high  as  120  per  minute,  in  adults,  and  unless  profound  depression 
is  very  early  manifested  it  is  fairly  strong.  The  abdominal  organs  present 
no  signs  of  any  importance,  but  constipation  is  more  frequently  present  than 
is  diarrhoea. 

The  true  variolous  eruption  makes  its  appearance,  in  the  majority  of 
cases,  on  the  third  day,  although  many  writers  state  that  it  appears  most 
commonly  on  the  fourth  day,  while  others  insist  that  it  appears  on  the 
second.  The  facts  are  that  the  time  of  the  appearance  of  the  rash  varies 
materially  in  different  cases,  for  it  is  delayed  in  mild  attacks  and  develops 
early  in  severe  ones.  Sydenham  said  of  the  confluent  form  of  this  disease: 
"This  kind  usually  comes  out  on  the  third  day,  sometimes  earlier,  but 
scarcely  ever  later;  whereas  the  distinct  (discrete)  form  appears  on  the 
fourth  day  or  later,  but  rarely  before."  Boerhaave  said:  "The  slower  the 
small  pocks  come  out,  the  milder  they  prove  and  the  better  they  ripen.  Those 
appearing  on  the  first  day  of  the  illness  are  esteemed  the  worst  kind;  those 
on  the  second,  milder;  those  on  the  third,  still  more  gentle,  and  on  the  fourth 
the  most  favorable."  Very  rarely  indeed  the  rash  may  be  delayed  till  the 
fifth  day,  but  this  is  an  unfavorable  sign. 

It  must  be  borne  in  mind  that  the  first  signs  of  the  eruption  may  be  very 
scanty.  But  one  or  two  papules  may  be  present  on  the  face  or  hand  or 
forearm.  In  other  instances  the  papules  are  very  numerous  on  the  face, 
the  extensor  surfaces  of  the  forearms,  and  then  on  the  trunk,  these  being 


7S 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


the  parts  which  are  particularly  prone  to  present  the  first  sign  of  the  erup- 
tion. In  still  other  cases  the  entire  surface  of  the  body  is  speedily  covered 
and  the  mucous  membrane  of  the  mouth,  pharynx,  and  vulva  also  are 
involved.  The  portion  of  the  skin  least  affected  in  most  cases  is  that 
of  the  anterior  part  of  the  thorax,  the  abdomen,  and  the  flexor  surfaces  of 
the  extremities. 

The  eruption  of  smallpox  proceeds  through  the  following  five  stages  of 
development  with  considerable  rapidity:  For  the  first  few  hours  minute 
bright-red  macules  are  present,  which  disappear  on  pressure.     They  soon 

Fig.  18 


Well-developed  variola, 

become  hard  and  elevated — that  is,  the  macules  become  papules.  By  the 
end  of  the  first  twenty-four  hours  of  the  eruption  the  papule  begins  to  show 
at  its  apex  a  tiny  vesicle,  which  rapidly  develops  so  that  by  the  fourth  or 
fifth  day  of  the  rash  the  vesicular  stage  has  reached  its  full  development. 
This  vesicle  is,  as  a  rule,  less  than  a  sixth  of  an  inch  in  diameter,  contains 
fairly  pearly  looking  fluid  (lactescent),  and  is  surrounded  by  a  narrow 
areola  of  red.  A  peculiarity  of  the  vesicle  of  smallpox  is  that  though  some 
serum  may  escape  when  it  is  pinched,  it  never  empties  itself  or  collapses 
because  of  the  fibrilla  which  are  present  in  the  cavity  of  the  vesicle,  as  already 


VARIOLA  79 

described.  With  the  advent  of  the  fifth  or  sixth  day  the  centre  of  the  vesicle 
is  seen  to  be  sHghtly  depressed,  showing  the  beginning  of  the  stage  of  umbil- 
ication. 

The  fluid  in  the  vesicle  now  rapidly  becomes  cloudy  and  purulent,  the 
surface  of  the  pock  gradually  loses  its  umbilication,  and  by  the  seventh 
or  eighth  day  of  the  eruption  the  eruption  exists  as  a  pustule,  which  by  the 
tenth  day  is  dome-like  and  surrounded  by  an  areola.  This  pustule,  when 
it  is  punctured  and  pressed  upon,  discharges  pus  and  cloudy  serum.  If 
the  pustule  is  not  meddled  with  it  ruptures  in  about  twenty-four  to  forty- 
eight  hours  and  the  pus  escapes,  dries,  and  forms  a  dirty-looking  scab,  so 
that  by  the  eleventh  or  twelfth  day  of  the  eruption  the  primary  macule  has 
advanced  through  its  stages  of  maturation  to  the  ruptured  pustule.  These 
scabs  produce  a  disgusting  odor.  Sometimes  the  pustule  does  not  rupture, 
but  simply  dries  up;  when  the  scab  falls  off  it  leaves  under  its  former  site  a 
red  or  pink  depression  in  the  skin,  the  future  pockmark.  This  stage  of 
desiccation  or  drying,  followed  by  exfoliation,  may  last  in  severe  cases  for 
several  weeks,  and  it  is  followed  by  a  period  of  desquamation  of  fine  scales 
of  epidermis,  during  which  time  the  reddened  pockmark  gradually  heals  and 
cicatrizes.  This  desquamation  rarely  takes  place  earlier  than  the  sixteenth 
and  often  about  the  eighteenth  day. 

The  eruption  on  the  mucous  membranes  runs  a  much  more  rapid  course 
than  that  on  the  skin,  so  that  as  early  as  the  fifth  day  the  pustule  ruptures, 
leaving  an  ulcerated  surface,  which,  if  the  eruption  on  the  mucous  mem- 
brane of  the  mouth  has  been  confluent,  may  resemble  the  ragged,  dirty- 
looking  exudate  of  diphtheria. 

There  are  two  additional  facts  of  importance  in  connection  with  the 
eruption  not  yet  named — viz.,  a  peculiarity  of  the  papule  of  smallpox  is  that 
when  the  finger  is  drawn  over  it  it  feels  indurated  as  if  a  shot  were  under 
or  in  the  skin.  The  second  point  is,  that  the  rash  does  not  all  appear  at  once, 
but  different  parts  of  the  body  are  affected,  one  after  the  other,  so  that  one 
part  may  present  vesicles  while  another  is  beginning  to  show  pustules. 

Another  point  of  interest  from  a  diagnostic  standpoint  is  the  characteristic 
course  of  the  fever.  Primarily  high  till  the  eruption  begins,  it  speedily  falls 
to  99°  in  moderate  cases,  or  to  100°  in  confluent  ones,  and  remains  low  until 
pustulation  begins,  when  the  so-called  secondary  fever  develops,  which 
rises  to  102°  or  even  104°.  This  fever,  unlike  the  primary  fever,  has  morn- 
ing remissions  of  1°  to  2°,  and  gradually  ends  by  lysis,  so  that  at  about  the 
twelfth  day,  which  is  the  period  at  which  the  pustules  rupture  or  become 
dry,  the  temperature  reaches  normal. 

As  would  be  expected  from  the  severity  of  the  eruption  the  skin  during 
the  active  stage  of  the  disease  is  deeply  inflamed  and  so  greatly  swollen 
that  the  features  of  the  patient  may  be  unrecognizable.     (See  Fig.  17.) 

In  many  cases  the  mind  is  clear  throughout  the  illness,  but  in  others  it  is 
clouded,  and  active  delirium,  which  may  be  violent,  is  met  with  in  severe 
cases. 

In  the  earliest  stages  of  variola  initial  rashes  may  precede  the  true  erup- 
tion and  mislead  the  physician  if  he  be  not  on  his  guard.  In  some  instances 
an  erythema,  like  that  of  early  scarlet  fever,  is  present,  and  in  still  others 


80  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

a  rash  appears  which  strongly  resembles  the  early  stages  of  the  eruption 
of  measles.  These  rashes  may  last  from  a  few  hours  to  a  few  days,  and 
usually  appear  on  the  trunk  and  limbs  and  but  slightly  on  the  face.  The 
scarlatiniform  rash  is  to  be  separated  from  that  of  scarlet  fever  by  the 
fact  that  it  is  not  so  punctate,  nor  so  bright  in  hue,  and  is  not  associated 
with  the  presence  of  the  sore  throat  of  that  disease.  The  rash  which  resem- 
bles measles  is  scarcely  raised  at  all,  as  is  the  real  rash  of  that  disease;  it 
develops  much  more  rapidly,  covering  the  entire  body  in  a  few  hours,  and 
disappears  with  a  speed  equal  to  that  of  its  onset,  rarely  lasting  over  thirty- 
six  hours. 

In  some  cases  both  the  scarlatiniform  and  morbilliform  rashes  appear 
in  very  small  patches  on  the  wrists  or  about  other  joints.  These  initial 
rashes  possess  a  considerable  degree  of  prognostic  importance,  since  they 
usually  appear  in  mild  cases. 

Fig.  19 


Variola  in  a  child  with  scant  eruption.    (Schamberg.) 

Still  another  initial  skin  lesion,  of  some  importance  because  of  its  prog- 
nostic features,  is  an  intensely  red  rash,  which  appears  on  the  second  day 
of  the  illness  and  spreads  over  the  entire  body  so  that  the  surface  may  after 
a  few  hours  look  as  if  it  were  affected  by  a  generalized  erysipelas  in  its 
early  stages.  Such  a  rash  is  said  to  indicate  the  future  development  of  the 
hemorrhagic  or  malignant  type  of  the  disease. 

Petechial  rashes  also  occur  as  initial  or  preliminary  lesions.  They  usually 
involve  the  suprapubic  or  inguinal  regions,  but  sometimes  they  appear  in 
the  infraclavicular  areas.  The  individual  petechise  may  be  bright  red,  or 
dull  red,  or  purple  in  appearance.  In  still  other  cases  an  eruption  which 
closely  resembles  that  of  true  purpura  develops.  In  very  malignant  cases 
death  may  occur  before  any  typical  eruption  of  smallpox  appears. 


VARIOLA  81 

Something  more  must  be  said  in  regard  to  the  variations  which  occur  in 
the  eruption  of  smallpox.  In  the  first  place,  it  is  possible  for  smallpox  to 
occur  without  eruption,  although,  of  course,  such  instances  are  exceedingly 
rare.  In  all  probability,  careful  examination  of  such  patients  will  reveal  one 
or  two  papules  which  otherwise  might  be  overlooked.  Indeed,  this  type 
of  smallpox  may  be  considered  as  belonging  to  so-called  varioloid,  and 
to  occur  in  those  patients  who  have  been  imperfectly  protected  by  early 
vaccination. 

Councilman,  Magrath,  and  Brinckerhoff  describe  secondary  vesicles 
usually  formed  pn  the  surface  of  the  primary  vesicle,  but  occasionally 
seen  in  the  base. 

Confluent  smallpox,  as  its  name  implies,  may  be  localized  or  general; 
that  is  to  say,  the  confluence  of  the  various  pocks  may  occur  only  in  certain 
portions  of  the  body,  while  in  other  instances  all  portions  of  the  body  may 
be  covered  by  a  coalescence  of  the  eruption.  In  these  cases  there  is  always 
an  extensive  dermatitis.  There  is  usually  great  restlessness,  delirium, 
marked  circulatory  disturbance,  and  death  very  frequently  occurs  from  the 
ninth  to  the  eleventh  day.  It  is  in  this  type  of  case,  too,  that  the  greatest 
degree  of  the  oedema  of  the  subcutaneous  tissues  appear,  and  the  tempera- 
ture usually  maintains  a  high  degree.  Sometimes,  however,  in  confluent 
smallpox,  the  vesicles  do  not  seem  to  reach  as  great  a  degree  of  fulness  as  in 
ordinary  cases,  and  there  is  not  the  same  degree  of  swelling  of  the  subcu- 
taneous tissues,  although  the  skin  is  apt  to  be  harsh  and  thickened.  Curiously 
enough,  this  form  of  confluent  smallpox  is  considered  by  experts  to  be  more 
frequently  followed  by  death  than  that  form  in  which  the  eruption  seems  to 
be  more  completely  matured. 

Very  rarely  in  the  pustular  stage,  the  epiderm  at  the  base  of  a  pustule 
may  be  displaced  by  the  formation  of  a  bulla,  or  bleb,  which  contains  a 
clear,  straw-colored  serum,  and  which  holds  in  its  centre  the  pustule. 

Under  the  name  of  hemorrhagic  or  black  smallpox,  which  is  by  no  means 
rare,  and  which  takes  place  both  in  sporadic  and  epidemic  cases,  a  form  of 
the  disease  occurs  in  which  the  initial  symptoms  are  always  very  severe,  and 
in  which  hemorrhages  into  the  skin  occur  early.  Not  only  do  the  spots 
become  purpuric  by  extravasations  of  blood  into  the  skin,  particularly  about 
the  joints,  but  the  hemorrhages  also  occur  on  the  eyelids  under  the  conjunc- 
tiva, and  even  on  the  tongue,  the  palate,  the  fauces,  and  the  vagina.  Bleed- 
ing also  frequently  takes  place  from  the  gums,  and  nose-bleed,  bloody  vomit, 
and  bloody  stools  may  occur.  Sometimes  hsematuria  also  develops.  In  these 
instances  the  temperature  usually  does  not  rise  above  100°,  and  the  mind 
remains  clear  and  unclouded,  but  they  are  distinctly  typhoid  in  type,  and 
death  often  occurs,  sometimes  as  early  as  the  third  day,  but  more  commonly 
between  the  third  and  sixth  day,  as  the  result  of  the  profound  toxaemia  and 
associated  cardiac  failure. 

Under  the  name  variola  pustulosa  hemorrhagica,  a  form  of  the  disease  is 
described  in  which  the  eruption  does  not  become  hemorrhagic  until  the 
stage  of  pustulation  is  reached.  This  type  is  not  so  severe  as  that  just 
described. 

Under  the  name  of  variola  fulminans,  an  exceedingly  fatal  form,  with 
6 


82  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

a  high  temperature  of  105°,  delirium,  coma,  and  collapse  occur.  In  these 
cases  death  comes  on  within  a  few  hours  after  the  onset  of  the  disease,  and, 
while  no  hemorrhages  are  manifest  in  the  skin,  since  the  eruption  is  as  yet 
scarcely  developed,  internal  hemorrhages  are,  nevertheless,  found  at  autopsy. 
It  is  much  more  apt  to  occur  in  unvaccinated  than  in  vaccinated  persons. 

While  the  symptoms  detailed  up  to  this  point  may  be  considered 
as  those  of  ordinary  smallpox  which  runs  a  natural  course,  it  is  not  to  be 
forgotten  that  a  modified  form  of  the  disease  quite  frequently  occurs,  in 
which  by  reason  of  vaccination  many  years  before,  or  natural  immunity, 
the  manifestations  of  the  affection  are  quite  markedly  modified.  To  this 
type  of  the  disease  the  term  varioloid  is  applied. 

The  whole  of  the  eruption  may  appear  within  half  a  day  after  the 
first  papule  is  developed.  The  vesicles  which  in  an  ordinary  case  reach 
their  maturity  by  the  fourth  or  fifth  day  in  these  cases  become  fully 
developed  in  seventy-two  hours,  and  they  are  often  very  small.  Instead  of 
the  fluid  in  the  pock  becoming  cloudy  on  the  fifth  day  this  change  develops 
as  early  as  the  third  or  fourth  day,  and  many  of  the  vesicles  never  become 
pustules  but  dry  up.  Those  that  do  develop  into  pustules  reach  this  con- 
dition by  the  fifth  or  sixth  day  instead  of  as  late  as  the  seventh  or  eighth 
in  the  unmodified  form  of  the  disease.  It  is  evident,  therefore,  that,  as 
most  persons  have  been  vaccinated  in  all  civilized  countries,  physicians 
will  often  meet  with  a  modified  type  of  smallpox  rather  than  the  severe 
form. 

The  temperature  in  these  cases  runs  a  very  mild  course,  often  remain- 
ing at  the  normal  point  as  soon  as  the  rash  develops,  and  never  partaking  of 
a  secondary  rise.  Indeed,  the  entire  symptom-complex  of  the  illness  may 
be  of  the  mildest  possible  type  as  to  objective  symptoms,  suffering,  or 
discomfort.  The  appetite  is  good,  the  patient  sleeps  well,  no  complications 
develop,  and  convalescence  is  rapid. 

The  important  fact  to  be  remembered  concerning  these  mild  or  modified 
cases  is  that  they  are  quite  as  competent  to  spread  the  disease  as  are  the 
more  severe  types  of  variola,  and  they  require  as  strict  quarantine  as  any 
severe  cases  of  the  disease  that  may  occur.  There  is  therefore  every  reason 
why  a  case  of  varioloid  should  be  quarantined  most  strictly. 

Even  in  some  cases  of  modified  smallpox,  coalescence  or  confluence  takes 
place  with  associated  oedema.  In  these  instances  the  confluence  is  not  to 
be  regarded  as  a  very  grave  omen,  since  the  pocks  mature  early,  frequently 
do  not  rupture,  and  convalescence  may  begin  as  early  as  the  eighth  or  ninth 
day  of  the  illness. 

Smallpox  almost  never  occurs  a  second  time  in  the  same  individual. 
In  nearly  every  instance  where  a  second  attack  is  stated  to  occur,  there 
has  been  an  error  in  diagnosis,  either  at  the  time  of  the  first  or  second 
illness. 

Complications  and  Sequelae. — When  the  severity  of  variola  as  an  infectious 
disease  is  considered,  it  is  remarkable  that  it  has  so  few  severe  complications, 
and,  aside  from  the  state  of  the  skin,  so  few  serious  sequelae.  In  some 
instances  where  the  infection  of  the  skin  seems  to  be  very  severe,  multiple 
abscesses  may  develop,  varying  in  size  from  a  small  bean  to  a  large  slough. 


VARIOLA  83 

They  usually  do  not  appear  until  after  the  eruption  has  passed  on  to  the  stage 
of  desiccation,  but  they  may  persist  for  a  long  period  of  time  and  so  prolong 
the  illness.  Moore  speaks  of  a  case  in  which  a  patient  who  suffered  from  this 
condition  could  not  be  discharged  from  the  hospital  until  after  a  period  of 
nine  months  and  nine  days,  because  he  had  forty-two  large  abscesses  follow- 
ing confluent  smallpox.  The  most  common  seat  for  these  abscesses  is  upon 
the  extremities  and  about  the  buttocks  and  shoulders,  and  occasionally  on 
the  scalp.  Much  more  rarely  abscesses  which  are  more  deeply  situated 
form,  as,  for  example,  ischiorectal  abscess.  Such  abscesses  may  produce 
marked  systemic  symptoms,  but  ordinarily  evidences  of  septicaemia  are  not 
severe. 

Occasionally  erysipelas  occurs  as  a  late  complication  of  the  disease, 
either  upon  the  face  and  scalp  or  on  the  scrotum.  Under  these  circum- 
stances it  is  a  most  serious  malady,  and  frequently  destroys  the  patient, 
since  he  has  not  the  vital  resistance  to  withstand  the  new  infection. 

Bed-sores  are  rare  if  proper  nursing  has  been  carried  out,  but  boils  may 
occasionally  occur,  and  are  caused  most  frequently  by  the  Staphylococcus 
pyogenes  aureus. 

Gangrene  of  the  skin  complicating  smallpox  is  almost  unknown.  But 
when  it  occurs  it  usually  affects  the  scrotum.  The  eyelids  sometimes  become 
the  seat  of  abscesses,  or  more  rarely  slough,  as  the  result  of  the  swelling  and 
oedema,  but  actual  disease  of  the  eyeball  complicating  smallpox  is  not 
common.  The  ears,  on  the  other  hand,  are  not  rarely  affected,  and  deafness 
occurs  in  a  certain  proportion  of  cases.  When  earache  is  complained  of,  the 
possibility  of  an  extension  of  the  suppurative  process  to  the  mastoid  should 
be  borne  in  mind,  as  this  sometimes  occurs  with  serious  results. 

So  far  as  the  respiratory  organs  are  concerned,  it  is  important  to  note 
that  smallpox  sometimes  produces  laryngitis,  varying  in  severity  from  a 
catarrhal  to  an  ulcerative  type.  As  in  typhoid  fever,  the  developm.ent  of 
aphonia,  due  to  ulcerative  laryngitis,  is  an  exceedingly  serious  complication, 
since  the  cartilages  of  the  larynx  may  become  eroded.  Bronchitis  and 
bronchopneumonia  may  develop,  and  occasionally  pleurisy  results  from  an 
extension  of  the  infection  from  the  lung  or  by  direct  involvement  of  the 
pleura  by  pyogenic  organisms. 

The  circulatory  system  does  not  suffer  with  anything  like  the  degree  of 
severity  which  we  would  expect. 

Pericarditis  and  endocarditis  are  exceedingly  rare  complications. 

Myocarditis,  on  the  other  hand,  is  more  frequently  met  with  as  a 
result  of  the  infection,  as  it  is,  indeed,  in  all  of  the  acute  infectious 
diseases. 

The  kidneys,  aside  from  the  ordinary  albuminuria  of  all  acute  infectious 
maladies,  usually  escape,  as  does  also  the  nervous  system.  That  there  is 
irritation  of  the  kidneys  is  evident  from  the  fact  that  Arnaud,  in  1898,  found 
albuminuria  in  95  per  cent,  of  his  cases. 

Septic  arthritis  occasionally  occurs. 

The  occurrence  of  smallpox  in  a  pregnant  woman  very  frequently  results 
in  abortion,  but  if  the  mother  goes  to  term,  the  child  is  to  some  extent  pro- 
tected from  smallpox,  although  cases  are  on  record  in  which  children  have 


84  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

apparently  had  smallpox  in  utero,  and,  extraordinary  to  relate,  there  are 
instances  reported  in  which  the  child  bore  the  eruption  at  birth,  although 
the  mother  seemingly  did  not  have  smallpox.  INIacCombie  even  states  that 
one  case  is  recorded  in  which  the  mother  contracted  smallpox  from  her 
newborn  infant. 

Diagnosis. — In  the  later  stages  of  well-developed  smallpox  there  is  little 
difficulty  in  maldng  a  positive  diagnosis ;  but  in  the  early  stages,  when  the 
initial  skin  lesions  which  have  been  named  are  present,  the  diagnosis  may 
be  for  a  time  impossible.  Indeed,  great  difficulty  may  be  experienced  in 
expressing  a  positive  opinion  as  to  the  presence  of  smallpox,  even  when  the 
papular  stage  is  in  its  early  development.  The  unusually  severe  headache 
and  backache,  with  chills,  and  pain  in  the  epigastrium,  are  strongly  in  favor 
of  smallpox,  particularly  if  there  is  a  history  of  exposure  to  this  disease 
within  the  incubation  period  already  named.  The  absence  of  throat  symp- 
toms, of  enlargement  of  the  cervical  and  submaxillary  glands,  and  of  the 
peculiar  coating  of  the  tongue  of  scarlet  fever  may  enable  us  to  determine 
that  the  initial  scarlatiniform  rash  sometimes  seen  is  probably  to  be  fol- 
lowed by  smallpox,  and,  furthermore,  as  has  already  been  pointed  out, 
this  scarlatiniform  rash  lacks  the  punctated  appearance  of  true  scarlet 
fever. 

On  the  other  hand,  it  is  to  be  borne  in  mind  that  in  persons  in  whom  the 
protective  effect  of  an  early  vaccination  is  waning,  it  not  rarely  happens 
that  true  smallpox,  or  varioloid,  develops  in  so  mild  a  manner  as  to  present 
but  a  few  pocks  and  very  mild  systemic  symptoms,  A  similar  state  may 
also  be  present  in  those  who  possess  a  natural  immunity  even  if  they  have 
never  been  vaccinated,     (See  Symptoms,) 

When  the  measles-like  rash  is  present,  the  absence  of  the  characteristic 
catarrhal  symptoms  of  that  disease,  with  its  cough,  running  at  the  nose,  and 
puffiness  of  the  face,  should  cause  the  physician  to  hesitate  in  making  a  diag- 
nosis until  a  sufficient  time  has  elapsed  for  the  eruption  to  be  well  developed. 
The  papules  which  form  in  measles,  while  they  are  often  confluent,  do  not 
possess  the  shot-like  feeling  so  typical  of  the  early  papular  stage  of  smallpox. 
Finally  the  measles-like  rash  preceding  smallpox  disappears  in  twelve  to 
twenty-four  hours,  leaving  no  stain  on  the  skin,  while  that  of  true  measles 
pursues  a  course  lasting  several  days,     (See  ^Measles.) 

Chickenpox  is  one  of  the  diseases  which  is  most  frequently  confused  with 
smallpox.  In  this  disease,  however,  the  initial  symptoms  are  always  mild, 
and  the  temperature  does  not  rise  as  rapidly  as  it  does  i  i  variola.  Then,  too, 
in  variola,  the  eruption  occurs  on  the  arms  and  face;  whereas,  in  chickenpox 
it  is  most  abundant  on  the  trunk,  and  sometimes  on  the  scalp.  It  is  always 
discrete,  and  it  appears  in  successive  groups.  The  vesicles  of  varicella,  when 
punctured,  collapse,  since  they  are  unilocular;  while,  as  has  already  been 
pointed  out,  those  of  smallpox  are  multilocular,  and  so  do  not  completely  dis- 
charge their  contents  when  punctured.  The  vesicles  in  chickenpox  also  reach 
their  full  development  in  twenty-four  hours,  after  the  appearance  of  the 
papule;  whereas,  in  smallpox  they  are  not  completely  developed  for  five 
days. 

Next  to  varicella,  syphilis  may  be  considered  as  the  disease  which  most 


VARIOLA  85 

frequently  produces  confusion  in  diagnosis,  for  variola  must  be  separated 
from  that  form  of  pustular  syphiloderm  which  is  sometimes  called  variola- 
form  syphilide.  In  most  instances  pustular  syphiloderm  is  preceded  by 
macular  or  papular  syphilitic  eruptions,  but  in  certain  instances  a  history 
of  these  previous  eruptions  may  not  be  present.  Pustular  syphiloderm  is 
more  frequently  met  with  in  negroes  than  in  the  white  race,  and  occurs,  as  a 
rule,  somewhere  between  the  sixth  month  and  the  second  year  of  the  syphil- 
itic infection.  Important  points  in  the  differentiation  are  that  in  pustular 
syphiloderm,  the  patient  does  not  present  the  well-marked  prodromal  symp- 
toms of  smallpox,  such  as  intense  backache,  although  there  may  be  a 
moderate  fever  and  some  pain  and  aching.  Again,  in  syphiloderm  there 
is  no  marked  remission  of  the  temperature  such  as  occurs  when  the  erup- 
tion appears  in  smallpox,  and  syphilitic  patients  presenting  such  an  eruption 
do  not,  as  a  rule,  appear  very  ill  or  have  to  take  to  their  beds.  Further 
than  this,  the  syphilitic  eruption  comes  out  in  successive  crops,  is  often 
profuse  upon  the  trunk,  and  the  individual  pustules  never  become  so  large 
and  deep  seated  as  do  tliose  of  variola.  Again,  they  are  practically  always 
non-confiuent.  Many  cases  of  syphilitic  eruption  have  associated  with  the 
vesicles  copper-colored  papules,  which  should  render  the  diagnosis  easy. 

Drug  eruptions,  which  are  sometimes  papular  and  pustular,  are  differ- 
entiated by  the  absence  of  fever  and  of  constitutional  symptoms. 

Prognosis. — The  prognosis  of  smallpox  differs  greatly  in  different  epi- 
demics and  in  different  individuals.  The  greatest  difference,  of  course, 
exists  between  those  who  are  vaccinated  and  those  who  are  not  vaccinated. 
The  mortality  present  in  the  unvaccinated  may  be  said  to  amount  to  nearly 
45  per  cent.,  and  in  the  vaccinated  to  about  8  per  cent.  If  a  patient  has 
been  vaccinated  more  than  once,  the  mortality  of  the  disease  is  wonder- 
fully decreased.  Thus,  while  among  those  who  have  been  vaccinated  once 
the  mortality  may  be  8  per  cent.,  those  who  have  been  vaccinated  twice  have 
a  mortality  of  less  than  4  per  cent.  If  the  mark  of  both  vaccinations  is  a 
satisfactory  one,  the  prognosis  is  exceedingly  favorable,  for  death  very  rarely 
occurs  unless  the  patient  is  already  suffering  from  some  serious  disease 
which  has  undermined  his  constitution  and  therefore  aids  materially  in 
causing  death.  In  most  of  the  instances  in  which  smallpox  has  occurred 
after  even  a  single  vaccination,  the  vaccination  mark  has  been  so  unsatisfac- 
tory that  there  has  been  grave  doubt  as  to  whether  the  patient  has  been 
protected  at  all. 

The  age  of  the  patient  influences  the  prognosis  materially.  It  is  much 
more  grave  in  early  infancy  and  after  thirty  years  of  age,  and  best  at  about 
the  end  of  the  second  decade  of  life. 

Chronic  alcoholism  and  the  presence  of  any  antecedent  disease  in  the 
heart,  lungs,  or  kidneys  makes  the  prognosis  more  grave. 

Marked  severity  of  onset  is  an  evil  prognostic  sign,  but  a  mild  onset  does 
not  necessarily  promise  recovery,  for  in  many  instances  cases  which  seem 
mild  afterward  become  severe  and  fatal.  Petechial  rashes  are  always  of  evil 
import,  whereas  early  maturation  of  the  eruption  or  an  aborted  maturation, 
so  that  it  does  not  go  on  to  pustulation,  is  a  favorable  omen.  Confluent 
smallpox,  if  it  has  not  been  modified  by  previous  vaccination,  is  more  dan- 


86  DISEASES  DUE  TO   A    SPECIFIC  IXFECTION 

gerous  than  the  discrete  form,  and  varies  in  its  mortahty  with  the  age  of  the 
patient.  Young  cliildren  almost  invariably  die  from  it.  Older  children  and 
adults  often  recover,  and  it  may  be  said  that  prognosis  is  favorable  in  con- 
fluent cases  in  direct  proportion  to  the  age  of  the  patient  until  after  the 
third  decade. 

Great  swelling  of  the  hands  and  feet,  associated  with  salivation  and  swell- 
ing of  the  face,  in  confluent  smallpox  has  long  been  regarded  by  physicians, 
who  have  had  a  large  experience,  as  possessing  considerable  prognostic  value, 
since  if  the  eruption  fails  to  appear  the  patient  very  frequently  dies.  The 
swelling  is,  of  course,  due  to  non-maturation  of  the  pustules. 

Hemorrhagic  smallpox,  if  at  all  well  developed,  always  ends  in  death. 

When  death  takes  place  from  smallpox,  it  most  commonly  occurs  about 
the  twelfth  or  sixteenth  day,  as  the  result  of  pneumonia,  hypostatic  conges- 
tion of  the  lungs,  or  from  the  profound  exhaustion  and  septicemia. 

Treatment. — As  in  most  infectious  diseases,  the  treatment  of  smallpox 
consists  chiefly  in  good  nursing  and  the  maintenance  of  vitality  by  the  use 
of  proper  nourishment  and  care.  The  air  of  the  room  should  be  fresh  and 
cool,  and  frequently  changed.  Draughts  should  be  avoided,  and  food  should 
be  given  frequently  in  small  quantities.  Water  should  be  given  freely  for 
the  purpose  of  allaying  thirst  and  flushing  the  kidneys,  and  there  is  no 
objection  to  the  patient  receiving  a  small  quantity  of  ice  to  relieve  the 
dry  condition  of  the  mouth.  If  the  urine  is  scanty  5  grain  doses  of 
citrate  of  potassium  or  citrate  of  lithium  should  be  given  every  six  hours. 
Stimulants  are  not  needed,  unless  there  are  evidences  of  circulatory  feeble- 
ness, when  alcohol  is  considered  by  most  practitioners  of  experience  to  be 
valuable.  Good  brandy  and  whiskey  are  the  best  forms  of  alcohol  to 
employ.  For  the  relief  of  intense  nervous  irritation,  opium  or  morphine 
may  be  administered  in  small  doses,  particularly  if  the  condition  of  the 
skin  seems  to  be  the  chief  cause  of  the  patient's  suffering.  These  drugs 
are  also,  perhaps,  the  best  for  the  purpose  of  allaying  excessive  delirium, 
since  they  do  not  irritate  the  kidneys  as  do  some  of  the  newer  hypnotics. 
Wliere  the  delirium  is  active  and  threatens  to  exhaust  the  patient,  a  hypo- 
dermic injection  of  i  to  J  grain  of  morphine  will  often  produce  several  hours 
of  restful  sleep,  with  benefit. 

For  the  relief  of  the  intense  irritation  of  the  skin  all  over  the  body,  a  very 
useful  dressing  is  ordinary  carron  oil — that  is,  hme-water  and  olive  oil  mixed 
in  equal  parts.  To  this  may  be  added  1  per  cent,  of  carbolic  acid  for  its 
local  antiseptic  and  anaesthetic  properties,  and  where  great  pain  is  expe- 
rienced, because  of  the  occurrence  of  the  eruption  in  the  thick  skin  of  the 
hands  and  feet,  prolonged  hand-baths  and  foot-baths  of  lukewarm  water 
may  be  employed,  or  hot  poultices  used.  An  ointment  of  aristol  of  the 
strength  of  one  drachm  to  the  ounce  may  also  be  used. 

It  seems  to  be  generally  considered  that  local  applications  to  the  eruption 
are  of  little  value  in  the  sense  of  modifying  its  severity,  although  certain 
parts  of  the  skin  vvhich  seem  to  suffer  from  an  excessive  degree  of  irritation 
may  be  relieved  by  cool  compresses  or  by  the  application  of  antiseptic 
poultices.  MacCombie  states  that  the  best  dressing  for  the  face  is  a  mask 
with  holes  cut  for  the  eyes,  nose,  and  mouth.  Upon  this  mask  is  smeared  on 


VARIOLA  87 

its  inner  surface  a  small  linseed  poultice,  over  which  is  placed  some  vaselin 
which  contains  iodoform.  This  poultice  should  be  changed  every  two 
hours.  It  aids  materially  in  separating  the  crusts,  and  so  leaves  the  skin 
free  for  the  application  of  the  dressings,  which  tend  to  prevent  ulceration 
and  the  formation  of  scars.  The  local  use  of  antiseptic  drugs  to  the 
surface  of  the  entire  body  has  not  met  with  favor. 

The  mucous  membrane  of  the  mouth  should  be  kept  cleansed  by  mouth- 
washes of  boric  acid  or  chlorate  of  potassium  and  myrrh.  When  the  mouth 
is  exceedingly  dry,  flaxseed-tea,  sweetened  with  a  little  white  sugar  and 
acidulated  with  lemon-juice,  may  be  used. 

The  primary  fever  of  smallpox  does  not  last  long  enough  to  require  treat- 
ment, but  the  secondary  fever  may  be  sufficiently  high  to  demand  relief. 
Cold  compresses  may  be  applied  to  the  head,  and  sponging  the  body 
with  cool  or  tepid  water  may  be  employed,  but  the  cold-bath  treatment, 
so  successfully  employed  in  typhoid  fever,  has  not  apparently  given  good 
results  in  smallpox,  and  it  is  practically  never  employed. 

Should  any  irritation  or  inflammation  of  the  eyes  appear,  they  should  be 
carefully  washed  every  few  hours  with  boric  acid  solution,  and,  if  necessary, 
cold  wet  compresses  should  be  applied,  great  care  being  taken  that  the 
warmth  of  the  body  does  not  speedily  change  the  cool  compress  into  a  hot 
poultice. 

During  the  suppurative  stage,  it  is  exceedingly  important  that  the  nutri- 
tion and  vitality  of  the  patient  be  preserved  by  the  frequent  administra- 
tion of  easily  digested  and  predigested  food. 

In  considering  the  general  condition  of  a  patient  who  is  suffering  from 
smallpox,  it  must  be  borne  in  mind  that  the  disease  is  essentially  one  which 
is  prone  to  produce  profound  toxaemia,  since  it  is  incredible  that  such  wide- 
spread infection  can  take  place  all  over  the  body  without  simultaneously 
resulting  in  septic  absorption  on  the  one  hand,  or  profound  exhaustion  on  the 
other.  For  this  reason  the  degree  of  suppuration  should  be  controlled  as 
far  as  possible,  measures  should  be  introduced  to  aid  in  the  escape  of  pus, 
and  the  treatment  should  be  stimulating  and  supporting. 

Finally,  mention  should  be  made  of  the  so-called  red-light  treatment  of 
smallpox,  in  which  patients  are  kept  in  rooms  to  which  no  light  is  allowed 
to  enter  save  through  red  glass,  it  being  claimed  by  advocates  of  this  method 
that  the  severity  of  the  eruption,  and  so  indirectly  the  severity  of  the  disease, 
is  greatly  modified,  and,  further,  that  scarring  of  the  skin  is  diminished. 
Suffice  it  to  state,  that  while  certain  European  clinicians  have  claimed  to 
have  obtained  excellent  results  from  this  method,  Welch  and  Schamberg  in 
Philadelphia,  and  others,  have  found  it  entirely  useless. 

There  are  several  points  in  the  treatment  of  variola  which  should  be  care- 
fully avoided.  For  the  relief  of  the  severe  backache  and  headache,  counter- 
irritation  is  sometimes  employed  in  the  early  stages  of  the  disease.  Such 
treatment  frequently  results  in  severe  ulceration  or  sloughing  of  the  part 
to  which  the  irritation  is  applied.  Again,  the  application  of  powders,  anti- 
septic or  otherwise,  is,  as  a  rule,  disadvantageous.  The  opening  of  individual 
pocks  by  means  of  a  needle  or  the  fine  blade  of  a  knife  is  not  advisable. 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


VACCINIA  AND  VACCINATION. 

History. — Little  is  known  of  the  history  of  vaccinia,  save  that  it  has  been 
recognized  for  many  years  as  a  disease  which  affects  heifers  and  cows,  and 
that  it  causes  an  eruption  to  appear  on  the  teats  and  udder  or  neighboring 
parts.  Although  it  was  known  among  those  persons  who  milked  these 
animals,  or  otherwise  handled  them,  that  the  disease  could  be  transmitted 
from  the  cow  to  the  human  being,  and  although  many  of  these  persons  also 
knew  that  this  transmission  protected  the  human  being  from  smallpox,  it 
was  not  until  Jenner,  on  May  14,  1796,  first  inoculated  a  patient  with  the 
contents  of  a  cow-pock  that  the  preventive  influence  of  vaccination  was  first 
tried  in  a  scientific  manner.  Two  years  before  this  an  English  farmer,  by 
the  name  of  Benjamin  Jesty,  inoculated  his  wife  and  two  children  in  a  similar 
manner,  but  at  the  time  no  report  of  the  procedure  was  made.  From  this 
small  beginning  so-called  vaccination,  or  the  inoculation  of  human  beings 
with  vaccine  virus,  has  spread  all  over  the  world,  and  is  a  well-recognized 
procedure,  by  which  millions  of  lives  have  been  saved.  There  are  a  few 
persons,  not  medical  men  as  a  rule,  who  still  express  doubt  as  to  its  efficacy, 
but  they  are  not  worthy  of  credence,  and  the  statistics  of  every  civilized  land 
prove  that  vaccination  is  one  of  the  greatest  blessings  yet  discovered  for 
mankind.  It  is  only  necessary  here  to  state  that  vaccination  is  now  ob- 
ligatory in  most  civilized  lands,  and  that  the  frequency  of  smallpox  is  in 
direct  ratio  to  the  laxity  with  which  vaccination  laws  are  enforced.  Im- 
mense statistics  as  to  its  protective  value  are  to  be  found  in  all  works  on 
public  health. 

Vaccination,  when  properly  performed,  and  when  an  active  vaccine  is  used, 
may  be  said  to  be  a  sure  preventive  of  smallpox  for  a  very  considerable  space 
of  time,  if  not  for  the  lifetime  of  the  individual;  but  it  is  safer  to  be  vaccinated 
every  few  years,  and  every  year  if  exposed  during  an  epidemic.  Not  only 
does  vaccination  protect  the  individual  for  a  long  period  of  time,  but  it  also 
modifies  the  severity  of  smallpox  if  the  patient  contracts  this  disease  before 
the  vaccinia  can  completely  protect  him.  This  has  been  proved  by  practical 
experience  so  often  that  it  is  a  fact  beyond  all  doubt,  and  it  bears  this  impor- 
tant truth  with  it,  namely,  that  when  a  person  who  has  not  been  recently 
vaccinated  is  exposed  to  smallpox  he  should  be  re  vaccinated  at  once,  since 
if  the  vaccine  fails  to  confer  complete  immunity  it  will  modify  the  disease 
if  it  develops.  The  degree  of  immunity,  or  the  degree  of  modification,  if 
smallpox  develops,  depends  upon  the  space  of  time  elapsing  between  ex- 
posure to  the  smallpox  and  the  vaccination.  Further  than  this,  if  the  patient 
contracts  smallpox  many  years  after  a  vaccination,  the  severity  of  the  disease 
is  usually  modified.  Thus  in  58,278  cases  of  variola  collected  from  various 
sources,  occurring  in  individuals  who  had  been  vaccinated,  but  in  whom 
the  "takes"  were  not  known  to  be  good,  there  were  4872  deaths,  a  percentage 
of  8.35;  whereas  in  23,360  cases  of  variola,  occurring  in  individuals  who  had 
not  been  vaccinated,  there  were  8682  deaths,  a  percentage  of  32.88. 

Method  of  Vaccination. — The  skin  on  the  arm  or  calf  of  the  leg,  having  been 
cleansed  by  washing  it  with  soap  and  water,  is  scarified  or  scratched  by  a 


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VACCINIA   AND   VACCINATION  89 

needle  or  knife-blade  in  such  a  manner  as  to  remove  the  epiderm  and  expose 
the  true  skin  over  an  area  of  about  an  eighth  of  an  inch  in  all  directions.  Care 
should  be  taken  that  the  spot  is  not  so  deeply  scratched  as  to  cause  free 
bleeding.  Upon  this  area  is  now  deposited  the  vaccine,  which  is  then  gently 
rubbed  into*  the  part  and  allowed  to  dry  before  any  clothing  comes  in  contact 
with  it.  Several  forms  of  vaccine  are  used,  but  that  most  commonly  employed 
at  present  is  known  as  "  glycerinated  vaccine  lymph,"  prepared  from  the 
contents  of  the  vaccine  vesicles  as  they  have  developed  on  the  belly  of  a  heifer. 
This  glycerinated  lymph  is  put  up  in  small  glass  tubes,  which  are  her- 
metically sealed  at  the  ends,  so  that  it  may  not  be  contaminated  before  it 
is  used. 

Primary  Vaccinia  in  Man. — Three  or  four  days  after  vaccination  has  been 
performed  the  infected  area  begins  to  be  slightly  reddened,  and  this  red- 
dening increases  while  at  the  same  time  a  reddish  papule  develops  which 
by  the  fifth  day  begins  to  look  like  a  vesicle,  particularly  if  the  margin  of 
the  area  inoculated  be  examined.  This  vesicle  increases  in  size,  becomes 
filled  with  thin,  clear  lymph,  and  by  the  eighth  day  reaches  its  greatest 
development.  At  this  time  the  contained  fluid  begins  to  be  more  opaque 
and  yellow  and  the  top  of  the  vesicle  is  seen  to  be  slightly  sunken — that  is, 
the  early  stage  of  its  umbilication  has  been  reached.  The  skin  surrounding 
the  vesicle  is  now  surrounded  by  a  zone  or  areola  of  red  which  by  the  ninth 
or  tenth  day  becomes  very  well  developed,  so  that  it  extends  for  a  consider- 
able distance  in  all  directions;  the  spot  inoculated  is  painful  and  the  neigh- 
boring lymphatic  glands  may  be  swollen  and  tender.  At  this  time,  too— that 
is,  about  the  tenth  day — constitutional  symptoms  may  come  on  and  the 
patient  suffer  from  moderate  chills,  a  slight  rise  of  temperature,  and  malaise. 
Sometimes  roseola  (roseola  vaccinosa)  may  develop  over  the  body.  By  the 
eleventh  or  twelfth  day  these  symptoms  are  modified,  the  vesicle  begins 
to  desiccate,  and  by  the  end  of  the  fifteenth  day  it  is  completely  dried  up, 
although  the  scab  may  not  fall  off  till  the  twenty-first  or  twenty-fifth  day. 
The  crust  or  scab  is  dark  red  in  color  and  thin  at  its  centre  and  at  its  edges, 
but  there  is  a  thickened  area,  or  ridge,  between  the  centre  and  the  periphery. 
After  the  crust  falls  off  it  leaves  a  pink  spot  which  gradually  fades  and 
leaves,  after  some  months,  a  foveated  or  pitted  mark  from  which  small  scars 
may  radiate.  It  is  to  be  borne  in  mind  that  in  some  cases  the  constitutional 
symptoms  are  so  mild  as  not  to  be  worthy  of  note,  while  in  others  they  may 
be  quite  severe.  To  be  a  true  "take,"  the  full  development  of  the  pock  by 
the  stages  named  is  essential,  but  it  is  possible  for  the  "take"  not  to  ensue 
for  a  month  after  inoculation.     (See  Plate  II.) 

Secondary  Vaccinia  in  Man. — Very  few  persons  who  have  once  been 
successfully  vaccinated  present  the  conditions  just  described  when  inocu- 
lated a  second  time.  It  is  this  variation  from  the  appearance  of  true  primary 
vaccination  that  has  led  to  much  misunderstanding  in  secondary  cases. 
In  other  words,  the  secondary  vaccination  of  a  person  who  has  lost  the  pro- 
tective effect  of  the  primary  attempt  may  in  its  effects  be  very  like  primary 
vaccination,  but  usually  it  is  so  greatly  modified  as  to  be  very  dift'erent  in 
its  appearance.  The  difference,  however,  is  one  of  degree,  not  one  of  kind, 
and  vesiculation  and  umbilication  should  appear  in  all  cases. 


90  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

It  is  a  point  worthy  of  note  that  the  so-called  "raspberry  excrescence" 
which  sometimes  follows  vaccination  on  the  fourth  or  fifth  day,  looking 
like  a  small  nsevus,  is  not  a  vaccine  pock  and  confers  no  immunity  to  small- 
pox upon  the  patient— that  is,  it  is  not  to  be  considered  as  a  "take."  Care 
must  be  taken,  too,  that  the  sore  or  mark  produced  by  the  injury  of  the 
operation  be  not  taken  for  the  specific  lesion  of  vaccinia. 

Children  should  always  be  vaccinated  during  the  first  year  of  life,  or 
immediately  after  birth,  if  exposed  to  smallpox.  Vaccination  should  be 
repeated  through  life  every  five  years  and  oftener  if  smallpox  is  prevalent. 
If  one  inoculation  fails  it  should  be  repeated  at  least  three  times,  since 
sometimes  primary  failure  is  due  to  poor  vaccine  or  to  an  error  in  technique. 
If  after  three  attempts  no  "take"  is  produced  the  patient  may  be  considered 
as  immune,  at  least  for  a  time. 


VARICELLA. 

Definition. — Varicella  is  usually  called  chickenpox.  It  is  an  acute  infec- 
tious disease  which  usually  occurs  in  children  under  ten  years  of  age,  and 
rarely  attacks  individuals  after  puberty.  In  adults  it  is  still  more  uncom- 
mon, although  Tyzzgr  reports  38  cases  occurring  in  adult  male  Filipinos 
and  states  that  at  the  time  of  the  last  observation  300  cases  had  been  re- 
corded. The  men  were  prisoners,  and  this,  together  with  race  and  climate, 
are  considered  possible  factors  in  increasing  susceptibility.  In  all  proba- 
bility one  of  the  reasons  for  its  rarity  in  those  of  mature  years  is  that  it 
affects  so  large  a  proportion  of  all  children  that  most  adults  are  rendered 
immune  by  an  attack  in  childhood.  The  most  marked  characteristic  of  the 
disease  is  the  appearance  within  the  first  twenty-four  or  forty-eight  hours  of 
fever  and  malaiss  and  of  papules,  followed  by  vesicles,  upon  the  skin  of 
the  forehead  and  face  or  upon  the  chest  and  back.     (vSee  Fig.  20.) 

Etiology. — Like  all  acute  infectious  diseases,  chickenpox  is  produced  by 
a  micro-organism,  but  as  yet  it  has  not  been  isolated.  Tyzzer  found 
specific  nuclear  and  cytoplasmic  inclusions  in  all  the  lesions,  but  obtained 
no  evidence  favoring  the  hypothesis  that  they  are  parasites.  It  also  resembles 
the  other  acute  infectious  eruptive  diseases  in  that  it  occurs  in  epidemics, 
although  at  times  isolated  cases  take  place  that  cannot  be  traced  to  any 
source  of  contagion.  While  the  eruption  in  its  peculiarities  resembles  to 
some  extent  that  caused  by  smallpox,  chickenpox  bears  absolutely  no  rela- 
tion to  that  malady  and  in  no  way  protects  a  patient  from  developing  a 
typical  attack  of  variola.      (See  Variola.) 

Symptoms. — At  a  time  varying  from  ten  to  fifteen  days  after  exposure 
to  varicella  the  child  usually  manifests  some  evidence  of  a  beginning  illness. 
If  very  young  it  may  be  unusually  restless  and  fretful,  there  may  be  some 
disorder  of  the  digestive  apparatus,  and  vomiting  may  occur.  Fever  is  an 
early  symptom  and  it  may  be  moderately  high — that  is,  about  103°  or  even 
104°.  Often,  however,  it  fails  to  reach  such  a  height.  If  the  child  is  old 
enough  to  describe  its  sensations,  some  aching  in  the  back  or  in  the  limbs 
may  be  complained  of. 


VARICELLA 


91 


After  about  twenty-four  hours  the  erwption  appears  in  the  form  of  red 
papules,  which  speedily  become  vesicles  containing  clear  or  turbid  serum. 
The  vesicle  is  superficial,  it  is  not  surrounded  by  a  zone  of  induration,  as 
it  is  in  smallpox,  and  it  does  not  become  umbilicated,  although  the  top  of 
the  vesicle,  when  it  is  ripe,  may  be  flattened.  By  the  end  of  thirty-six  to 
forty-eight  hours  the  vesicle  becomes  a  true  pock,  the  previously  clear  serum 


Fig.  20 


Chickenpox.    (Schamberg.) 

becoming  opaque  but  not  purulent  unless  it  is  denuded  by  scratching,  and 
then  infected.  These  pocks  speedily  shrivel  and  by  the  fourth  day  form 
crusts,  which  readily  fall  off  and  rarely  leave  a  scar  unless  the  skin  be 
scratched  by  the  child  so  that  the  deeper  layers  become  infected.  Many 
individuals  bear  scars  of  this  sort  upon  the  face,  and  they  are  particularly 
well  marked  in  women  with  a  fair  skin. 


92  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

The  eruption  of  chickenpox  develops  in  a  series  of  crops,  or,  to  speak 
more  accurately,  it  continues  to  develop  in  new  areas  as  those  which  were 
affected  first  begin  to  pass  into  the  stage  of  crusts.  An  examination  of  the 
patient  on  the  third  day  may  therefore  reveal  the  eruption  in  all  stages  of 
development. 

It  is  a  noteworthy  fact  that  the  eruption  of  varicella  is  always  discrete 
and  never  confluent.  It  is  never  profuse  as  in  smallpox.  Rarely  the  vesicles 
appear  on  the  mucous  membranes. 

The  severity  of  the  fever  and  of  the  signs  of  general  illness  vary  greatly 
in  children  affected  by  varicella.  In  some  cases  the  disease  runs  so  mild 
a  course  that  the  child  is  not  kept  in  bed,  in  others  it  causes  a  considerable 
degree  of  illness ;  but  in  the  majority  of  instances  it  is  a  very  mild  malady. 
In  children  who  are  weakened  by  previous  disease  it  sometimes  develops 
into  a  dangerous  malady  in  that  the  associated  digestive  disturbance  still 
further  impairs  vitality,  or  because  the  lesions  of  the  skin  become  infected 
and  sloughing  or  gangrene  appears.  Sometimes  erysipelas  is  developed 
in  this  manner  in  poorly  nourished  children.  Rarely,  if  the  child  is  exposed 
to  cold,  nephritis  develops.  Allaire  reports  peripheral  neuritis  cf  the  left 
arm  following  an  attack  of  varicella  in  a  child  aged  eight  years,  the  pocks 
having  suppurated. 

Diagnosis. — The  eruption  of  chickenpox  must  be  separated  from  that 
of  modified  or  mild  smallpox.  The  most  important  factors  in  this  separa- 
tion are  the  superficial  character  of  the  pock,  the  lack  of  the  sense  of  indura- 
tion when  it  is  taken  between  the  thumb  and  finger,  the  early  appearance 
of  the  rash  on  the  chest  rather  than  on  the  forearms,  as  in  smallpox,  and 
the  mild  character  of  the  general  symptoms,  combined  with  the  brief  course 
of  the  disease  and  the  speedy  completion  of  the  illness. 

Additional  diagnostic  factors  are  the  presence  of  a  good  vaccination 
mark  which  largely  excludes  variola.  Again,  the  onset  of  varicella  is  usually 
devoid  of  prodromes,  whereas  smallpox  presents  for  some  days  backache, 
vertigo,  fever,  nausea,  and  chills.  The  mere  fact  that  the  eruption  is  scanty 
does  not,  however,  exclude  smallpox.  The  vesicles  of  varicella  do  not  become 
umbilicated  as  do  those  of  variola,  but  they  rapidly  dry  up  and  make  a 
dark-colored  scab.  The  eruption  of  smallpox  comes  out  in  one  crop,  that 
of  varicella  in  several  crops ;  that  of  smallpox  lasts  from  ten  to  twelve  days 
in  typical  cases,  never  less  than  six  days,  whereas  chickenpox  lasts  but 
from  two  to  four  days. 

Prognosis. — The  prognosis  is  always  favorable  unless  the  unfavorable 
preliminary  states  just  noted  are  present. 

Treatment. — Medicinal  treatment  of  varicella  is  usually  unnecessary. 
Careful  nursing  that  prevents  exposure  to  cold  and  wet,  regulation  of  the 
diet,  and  the  use  of  a  few  drops  of  sweet  spirit  of  nitre  in  a  teaspoonful  of 
liquor  potassii  citratis  every  four  hours,  to  keep  the  kidneys  active,  are  all 
that  is  needed  in  most  cases.  The  fever  runs  so  brief  a  course  that  anti- 
pyretic measures  are  not  necessary. 


SCARLET  FEVER 


SCARLET  FEVER. 


93 


Definition. — Scarlet  fever  is  an  acute  infectious  disease  which  chiefly 
affects  children  under  fifteen  years  of  age.  It  is  characterized  by  the  devel- 
opment of  an  intensely  scarlet,  punctated  rash  on  the  second  day  of  the  ill- 
ness, accompanied  by  a  marked  febrile  movement.  It  is  sometimes  called 
"  scarlatina,"  and  it  is  to  be  clearly  understood  that  this  word  is  synonymous 
with  scarlet  fever  and  that  it  does  not  describe  a  modified  or  diminutive 
form  of  the  malady,  although  the  laity  often  employ  the  term  in  this 
manner. 

History. — Hirsch  states  that  the  oldest  reference  to  an  epidemic  of  scarlet 
fever  dates  from  Sicily  in  1543,  but  Sydenham,  of  London,  first  differen- 
tiated it  from  measles.  Prior  to  his  time  it  had  been  considered  a  form  of 
measles. 

Distribution. — Like  almost  all  of  the  acute  infectious  maladies,  scarlet  fever 
occurs  in  all  parts  of  the  world,  although  it  seems  to  be  much  more  prevalent 
in  the  temperate  zone  than  elsewhere.  In  the  United  States  it  occurs  less 
frequently  in  the  Southern  States  than  in  the  Northern  States.  It  did  not 
develop  in  the  United  States  until  1735,  nor  in  South  America  until  1830. 
In  Australia  and  in  Polynesia  the  disease  first  appeared  in  1848,  assuming  a 
mild  type  but  a  severe  epidemic  occurred  in  Melbourne  in  1876.  It  is  said 
that  only  imported  cases  are  met  in  India,  and  only  one  case  has  been  reported 
in  Greenland.  It  does  not  occur  nearly  so  frequently  as  does  measles,  and 
very  many  persons  reach  adult  life  without  having  suffered  from  it.  This 
is  in  part  due  to  the  fact  that  it  is  not  so  readily  transmitted  as  some  of  the 
other  acute  infectious  fevers,  and  also  because  a  large  number  of  persons 
seem  to  be  resistant  to  the  disease.  Johannessen  states  that  of  185  children 
exposed  only  28  per  cent,  developed  scarlet  fever,  and  out  of  314  adults 
exposed  only  5  suffered  from  the  malady.  If  the  same  number  of  cases 
had  been  exposed  to  the  infection  of  measles,  very  few  of  the  children 
would  have  escaped. 

Scarlet  fever  is  more  apt  to  occur  in  the  winter  months  than  at  any  other 
time,  but  statistics  differ  as  to  the  winter  months'  frequency.  Thus,  White- 
legge  from  his  statistics  based  upon  cases  occurring  in  nine  English  towns, 
found  in  the  first  quarter  219  cases;  second  quarter,  194;  third  quarter,  327; 
fourth  quarter,  460;  and  Reece  has  supported  his  conclusions  by  the  accom- 
panying chart.     (See  Fig.  21.) 

On  the  other  hand,  Seibjrt,  of  New  York,  gives  a  statistical  table  which 
shows  that  the  last  winter  months  are  those  of  greatest  frequencv.  (See 
Fig.  22.) 

August  Hirsch  gives  the  following  statistics  based  on  an  analysis  of  435 
epidemics  occurring  in  all  parts  of  Europe  and  North  America:  178  epi- 
demics occurred  in  winter;  157  in  spring;  173  in  summer;  213  in  autumn. 

The  frequency  and  mortality  of  scarlet  fever  have  greatly  decreased  in  the 
last  sixty  years.     (See  Fig.  23.) 

Etiology. — Scarlet  fever  does  not  disseminate  itself  through  the  air  as  does 
measles;  direct  contact  or  near  association  with  the  infected  person,  or  with 


94 


DISEASES  DUE   TO   A   SPECIFIC   INFECTION 


the  desquamated  scales  from  his  skin,  being  needful  for  the  transmission  of 
the  disease.  The  disease  can  be  transmitted  by  the  nasal  mucus,  clothing, 
and  other  articles  which  have  been  in  contact  with  the  patient.  Thus  books, 
cards,  letters,  and  pets,  such  as  dogs  and  cats,  and  other  means  of  convey- 


Per  cent 
+  70 
+  C0 
+  50 
+  40 
+  30 
+  20 
+  10 
Mean  0 

-  10 

-  20 

-  30 

-  iO 

-  50 


Jan. 

Feb. 

3Iar. 

Apr. 

May 

June 

July 

Aug. 

Sept. 

Oct. 

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Pec. 

r^ 

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Showing  seasonal  mortality  of  scarlet  fever  in  all  ages  and  both  sexes  in  England 
and  Wales.     (Eeece.) 

ance  may  assist  in  spreading  the  infection.  The  clothing  of  the  nurse  and 
physician  may  convey  the  disease,  and  cases  are  very  numerous  in  which 
physicians  have  so  communicated  scarlet  fever  to  their  own  children  after 
visiting  patients  ill  with  this  malady. 


JAN.        FEB.       MAR.      A 

PRIl|    MAY       JUNE     JULY       AUG. 

SEPT. 

OCT.       NOV.      DEC. 

se&  ^SiSig  siSiSis  sssgssssis 

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.d- 5  5^5  .*  ^  ^  "d- "     Tj-inioS 

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^ 

Frequency  of  scarlet  fever,  by  weeks,  throughout  the  year.     (Seibert.) 

The  persistence  of  the  infection  in  articles  of  clothing  is  very  remarkable. 
No  other  acute  disease  renders  the  surroundings  of  the  patient  a  source  of 
danger  for  so  long  a  period.     Instances  in  which  clothing  or  upholstered 


SCARLET  FEVER 


95 


goods  have  transmitted  the  disease  to  heaUhy  children  two  years  after 
recovery  of  the  first  patient  are  recorded. 

The  breath  of  the  patient  and  the  air  of  the  bed-room  are  probably  incap- 
able of  transmitting  the  infection,  unless  the  latter  is  laden  with  the  dust 
containing  the  micro-organism.  It  is  noteworthy  that  nurslings  are  not 
as  susceptible  as  children  of  from  two  to  five  years,  at  which  period  of 
life  the  disease  most  often  occurs.  The  age  incidence  is  well  shown  in 
Fig.  24. 

A  patient  who  is  a  sufferer  from  the  infection  of  scarlet  fever  is  not  capable 
of  transmitting  the  disease  until  the  rash  develops.  At  the  fourth  or  fifth 
day  of  the  disease  the  infectiousness  of  the  case  is  perhaps  at  its  height, 
and  the  ability  to  transmit  the  malady  exists  as  long  as  the  skin  of  the 
patient  continues  to  desquamate,  which  is  often  for  as  long  a  period  as 
six  weeks.  It  is  important  to  remember  that  not  only  the  desquamating 
skin,  but  the  nasal  mucus,  the  discharge  from  a  purulent  otitis  media  or 


Fig.  23 


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Showing  the  decreasing  mortality  of  scarlet  fever  in  England  and  Wales.     Deaths  per  100,000 
population.     (Modified  from  Wilson  and  Eeece.) 

from  a  chronic  consecutive  scarlatinal  pharyngitis  are  also  active  sources 
of  infection,  and  until  all  these  parts  are  entirely  healthy  the  danger  of 
spreading  the  disease  exists.  Indeed,  numerous  instances  are  recorded 
m  which  children  with  such  mild  consecutive  pharyngitis  as  to  escape 
notice  have  conveyed  the  disease  several  weeks  after  apparent  complete 
recovery  from  scarlet  fever. 

Articles  of  food  may  also  convey  the  infection.  Thus  Ekholm  has 
recently  reported  an  instance  in  which  six  families  who  partook  of  milk 
from  a  dairy  in  which  there  was  a  milkmaid  who  had  a  phlegmonous 
pharyngitis,  suffered  from  scarlet  fever. 

Many  investigators  have  endeavored  to  isolate  the  specific  micro- 
organisms of  scarlet  fever,  but  without  success.  Loeffler,  Fraenkel,  and 
other  German  physicians  first  demonstrated  the  presence  of  streptococci 
in  cultures  prepared  from  secretions  taken  from  the  throats  of  scarlet  fever 


96 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


patients,  but  their  observations  were  limited  to  a  small  number  of  cases 
and  are  of  interest  from  an  historical  rather  than  a  practical  standpoint. 
Tlie  same  statement  may  be  made  concerning  the  researches  of  Klein  in 
connection  with  an  epidemic  of  scarlet  fever  (1885)  caused  by  contaminated 
milk  from  a  farm  at  Hendon,  in  England,  for  although  Klein  cultivated  a 
micro-organism  from  lesions  on  the  udders  and  teats  of  cows  on  this  farm, 
which  apparently  was  identical  with  one  he  found  in  the  blood  of  scarlet  fever 
patients,  and  although  this  latter  organism  when  injected  into  calves  pro- 
duced a  lesion  resembling  the  one  with  which  the  Hendon  cows  were  affected, 
the  inquiry  instituted  by  the  Medical  Society  of  Edinburgh  and  the  investiga- 


FlG.  24 


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Showing  age  incidence  of  scarlet  fever  based  on  7470  cases,  and  representing  the  combined 
statistics  of  Whitelegge,  Ballard,  and  Keen. 


tion  of  Dr.  Crookshank,  of  London,  proved  that  the  disease  from  which  the 
cows  suffered  was  a  modified  form  of  cowpox,  and,  moreover,  that  the  persons 
who  milked  the  cows  did  not  contract  scarlet  fever.  A  similar  history  as 
to  cows  and  patients  has  recently  been  recorded  in  Lincoln,  England.  Li 
1891  Kurth  found  in  the  throats  of  scarlet  fever  patients,  in  pus  from  the 
cervical  abscesses  and  in  the  viscera  of  persons  who  had  died  from  scarlet 
fever,  a  streptococcus  wliich  formed  a  twisted,  gelatinous  mass  Avhen  grown 
in  broth.  This  organism,  called  by  Kurth  Streptococcus  conglomeratus,  was 
subsequently  studied    hy   IMervyn   Gordon,   who  found   it  present   in   the 


SCARLET  FEVER  97 

throats  of  twenty  out  of  twenty-seven  scarlet  fever  patients,  in  tlie  internal 
organs  of  most  patients  who  died  from  the  disease,  and  in  the  fluid  of  a 
scarlatinal  pleural  effusion.  Baginsky  and  Sommerfield,  who  published 
the  results  of  their  investigations  at  about  the  same  time  as  Gordon,  found 
a  streptococcus,  having  virulent  properties  and  generating  a  toxin,  in  all 
cases  of  scarlatinal  angina,  and  in  cultures  made  from  the  viscera,  bone- 
marrow,  and  blood  of  one  hundred  and  forty-two  children  in  whom  the 
disease  terminated  fatally.  This  streptococcus  they  considered  to  be  the 
specific  organism  of  scarlet  fever. 

Of  the  work  done  by  American  bacteriologists  that  of  Class,  of  Chicago, 
should  be  mentioned.  In  1899  Class  noticed  the  frequent  presence  of  a 
diplococcus  in  cultures  made  from  the  throats  of  patients  having  different 
forms  of  angina,  and  upon  further  investigation  he  found  that  the  organism 
invariably  occurred  in  cases  of  scarlatinal  angina.  He  then  made  cultures 
from  the  blood  of  scarlet  fever  patients  and  from  desquamated  epidermal 
scales,  and  found  the  same  diplococcus.  Gradwohl,  of  St.  Louis,  and 
Calvin  Page,  of  Boston,  have  also  found  an  organism  identical  with  the 
one  described  by  Class,  but  their  observations  were  confined  to  a  small 
number  of  cases. 

From  this  brief  resumS  of  the  bacteriology  of  scarlet  fever,  it  is  apparent 
tliat  streptococci  are  generally  present  in  the  throat  of  scarlet  fever  patients, 
and  that  they  are  often  found  in  the  blood  and  internal  organs;  but  when 
we  come  to  consider  that  streptococci  have  been  found  in  healthy  throats, 
that  cases  of  streptococcic  angina  exist  independent  of  scarlet  fever,  and 
that  streptococci  are  found  in  the  blood  in  other  diseases,  it  is  not  justifiable 
to  assume  that  any  one  of  the  forms  thus  far  described  is  the  specific  organism 
of  scarlet  fever.  Closely  associated  with  the  specific  germ  of  scarlet  fever, 
whatever  it  may  be,  we  always  find  a  variety  of  the  streptococcus,  and  it 
has  been  claimed  by  some  that  this  is  the  cause  of  the  disease.  There  can 
be  no  doubt  that  it  is  responsible  for  a  large  number  of  the  symptoms  and 
complications  of  the  disease. 

Mallory  has  recently  described  a  parasite  of  the  animal  group — a  pro- 
tozoon — which  he  suggests  may  be  the  cause  of  the  disease.  He  suggests 
the  name  Cyclasterion  Scarlatinalis  for  it. 

Prevention  or  Prophylaxis. — Every  case  of  scarlet  fever  should  be  promptly 
isolated  and  every  attendant  of  the  patient  should  also  be  prevented  from 
mingling  freely  with  the  inmates  of  the  house.  The  food  should  if  possible 
be  placed  in  an  outer  room  and  from  there  obtained  by  the  nurse  for  the 
patient.  If  the  nurse  is  to  leave  the  room  her  clothes  should  be  changed. 
Before  she  leaves  the  convalescent  patient  to  take  care  of  other  cases  she 
should  take  a  hot  bath  and  have  her  hair  shampooed.  The  clothing  she 
has  worn  in  the  sick-room  should  be  sterilized  by  boiling.  The  physician 
should  always  change  his  clothes  on  entering  and  leaving  the  room,  or  at 
least  wear  over  his  street  dress  a  long  operating  gown  to  protect  him  from 
the  infection.  If  he  is  attending,  or  about  to  attend,  a  case  of  confinement 
he  should  refuse  to  take  charge  of  a  case  of  scarlet  fever.  The  same  rule 
holds  true  as  to  operative  cases. 

All  clothing  and  bed-clothing  should  be  immersed  in  boiling  water,  or  in 
7 


98  DISEASES  DUE   TO   A    SPECIFIC  INFECTION 

a  disinfectant  solution ^  before  they  are  taken  from  the  sick-room,  and  books 
and  cards  which  have  been  in  the  patient's  room  should  be  burned.  If 
possible  it  is  better  to  burn  the  pillows  and  mattress  than  to  attempt  to 
disinfect  them.  If  they  are  disinfected,  steam  should  be  used  for  this 
purpose.  The  hanging  of  sheets  saturated  with  disinfectant  fluids  over 
doorways  and  the  placing  of  pans  of  disinfectants  about  the  house  are 
utterly  useless  except  that  their  presence  constantly  reminds  the  inmates 
or  visitors  that  an  infectious  disease  is  present  and  so  aids  in  the  main- 
tenance of  caution.  An  amount  of  disinfectant  in  the  air  sufficient  to 
destroy  the  contagium  will  destroy  the  patient  and  nurse.  After  the  illness 
is  over  and  the  patient  has  left  the  room,  it  should  be  carefully  disinfected 
by  an  adequate  formaldehyde  generator,  the  floors  and  walls  being  first 
moistened  with  water  to  aid  in  the  efficiency  of  this  gas.  Afterward  the 
floors  and  walls  should  be  scrubbed  with  1 :  2000  bichloride  solution  or  one 
of  chlorinated  lime. 

No  case  should  be  isolated  less  than  four  weeks,  and  no  case  should  be 
allowed  to  mingle  with  other  persons  as  long  as  desquamation  or  nasal, 
aural,  or  pharyngeal  discharges  exist.  Before  the  patient  is  discharged  he 
should  receive  at  least  three  hot  baths,  after  each  of  which  he  should  be 
scrubbed  with  carbolic  acid  and  water  (1 :  100)  or  with  bichloride  solution 
(1 :  4000).  Particular  attention  should  be  paid  to  the  scalp  and  hair.  Sleeping 
with  other  children  is  to  be  prohibited  for  several  months. 

After  exposure  a  child  should  be  placed  in  quarantine  for  at  least  a  week 
to  discover  if  the  disease  is  to  develop.  When  an  epidemic  is  present  all 
schools  should  be  closed. 

There  can  be  no  doubt  that  the  use  of  inunctions  of  carbolized  oil  or 
vaselin  is  an  active  agent  in  diminishing  the  spread  of  the  disease,  particu- 
larly during  desquamation,  but  great  care  must  be  taken  that  the  acid  is 
not  too  freely  used,  lest  it  be  absorbed  and  increase  or  produce  renal  irrita- 
tion.    In  many  instances  ordinary  olive  oil  is  equally  useful. 

Pathology  and  Morbid  Anatomy. — A  point  of  primary  importance  to  be 
borne  in  mind  in  considering  the  pathology  of  scarlet  fever  is  that  the  organs 
of  the  body  suffer  from  a  multiple  not  a  single  infection.  Whether  a  special 
form  of  streptococcus  is  the  cause  of  the  disease,  or  whether  an  entirely 
distinct  organism  is  the  cause,  the  fact  is  that  the  disease  is  accompanied 
by  streptococcus  infection  in  all  cases  and  not  rarely  by  other  forms  of 
infection  as  well. 

The  organic  changes  produced  in  the  body  by  an  attack  of  scarlet  fever 
are  marked,  but  none  of  them  can  be  said  to  be  characteristic  of  the  disease. 
Alterations  in  the  skin  and  inflammation  of  the  mucous  membrane  of  the 
mouth  and  pharynx  are  the  most  constant  changes,  but  even  these  may 
escape  notice.  The  skin  is  the  seat  of  a  very  acute  inflammatory  process 
involving  to  a  varying  degree  all  its  layers  and  terminating,  even  in  mild  cases, 
in  exfoliation  of  the  superficial  cells,  often  in  large  flakes.  The  pharyngeal 
mucosa  is  inflamed,  the  inflammation  varying  in  degree  from  a  mild  acute 
attack  to  extensive  necrosis  involving  the  deeper  strata  of  the  uvula  and 
tonsils.  This  inflammation  in  a  modified  form  extends  at  times  all  the 
way  down  the  cesophagus  and  by  way  of  the  Eustachian  tube  into  the 


SCARLET  FEVER  99 

middle  ear,  where  it  not  infrequently  causes  so  destructive  a  change  as  to 
produce  permanent  deafness;  or  if  the  infection  be  severe  and  no  vent  for 
the  pus  is  afforded  the  mastoid  cells  become  involved  and,  finally,  a  second- 
ary meningitis,  or  abscess  of  the  brain,  is  produced.  This  is  a  rare  sequel. 
In  still  other  instances  the  inflammatory  process  extends  into  the  nasal 
cavities  and  from  them  proceeds  to  an  infection  of  the  antrum  of  High- 
more  or  even  the  frontal  sinus.  Extension  of  the  pharyngeal  lesions  to 
the  lymphatics  of  the  submucosa  may  cause  infection  of  the  cervical 
and  submaxillary  lymph  nodes,  so  that  there  is  developed  great  swelling 
under  the  jaw,  and  in  some  instances  suppuration,  the  so-called  "collar 
of  brawn." 

Equal  in  frequency  with  these  changes,  and  of  more  importance,  are  those 
which  take  place  in  the  kidneys.  These  changes  not  only  endanger  the  life 
of  the  patient  during  the  illness,  but  occasionally  leave  him  with  kidneys 
structurally  so  impaired  that  complete  restoration  to  health  may  never  take 
place.  The  renal  changes  are  primarily  those  of  an  acute  diffuse  nephritis 
involving  the  whole  texture  of  the  kidney,  particularly  the  cortex,  and  accom- 
panied by  marked  albuminuria,  intertubular  cellular  infiltration  and  necrosis, 
and  desquamation  of  the  epithelium  lining  the  tubes.  Areas  of  necrosis 
and  infarction  and  even  acute  suppurative  nephritis  occur,  although  infre- 
quently. 

When  the  infection  with  the  streptococcus  is  particularly  severe  and  the 
evidences  of  toxaemia  are  profound  the  autopsy  reveals  degenerative  changes 
in  the  heart  muscle,  areas  of  necrosis  in  the  liver,  and  bronchopneumonia 
with  swelling  and  softening  of  the  bronchial  glands.  Degenerative  or 
necrotic  changes  in  the  myocardium  and  endocarditis, vegetative  or  ulcerative, 
may  be  present.  Pericarditis  may  be  marked.  As  in  all  septic  infections 
arthritis  may  be  found  in  numerous  joints.  Pleurisy,  if  present,  often 
results  in  empyema. 

With  the  onset  of  scarlet  fever  there  develops  a  hyperleukocytosis 
amounting  according  to  Tileston  and  Locke  to  from  18,000  to  40,000. 
After  the  eighth  day,  if  there  are  no  complications  of  an  inflammatory 
nature,  there  is  a  gradual  decline  to  the  normal,  somewhere  about  6000 
to  8000.     The  increase  is  chiefly  in  the  polymorphonuclear  cells. 

Incubation. — The  period  of  incubation  of  scarlet  fever  is  about  two  to 
six  days,  but  cases  are  recorded  in  which  it  has  been  as  brief  as  twenty-four 
hours  and  as  long  as  twenty-one  days.  Reimer  gives  the  following  figures: 
1  day,  379  cases;  2  days,  928  cases;  3  days,  751  cases.  The  period  of 
incubation  is,  therefore,  the  shortest  of  all  the  acute  exanthematous  fevers. 

Symptoms. — ^The  symptoms  of  an  ordinary  case  of  scarlet  fever  chiefly 
consist  in  sore  throat,  a  moderately  high  fever,  a  scarlet  rash  first  appearing 
on  the  chest,  albuminuria  of  moderate  degree,  and  a  tendency  to  middle-ear 
inflammation. 

The  onset  of  the  symptoms  in  scarlet  fever  is  usually  abrupt  and  the 
severity  and  abruptness  of  these  symptoms  is  often  indicative  of  the 
severity  of  the  attack  which  is  to  follow.  A  child  apparently  in  good  health 
in  the  evening  passes  a  restless  night,  and  in  the  morning  suddenly, 
without  apparent  cause  and  perhaps  without  preliminary  nausea,  vomits 


100  DISEASES  DUE   TO  A   SPECIFIC  INFECTION. 

actively  as  soon  as  its  breakfast  is  swallowed.  If  the  temperature  is  taken, 
it  will  usually  be  found  to  be  101°  or  103°,  the  skin  feels  hot  and  dry,  the 
pulse  is  quick,  the  eyes  bright,  the  expression  listless,  and  the  tongue  and 
mucous  membrane  of  the  mouth  distinctly  reddened.  Sometimes  the  first 
complaint  on  the  part  of  the  patient  is  one  of  sore  throat,  in  other  cases 
no  such  discomfort  is  mentioned;  but  if  the  mouth  be  opened  the  pharyn- 
geal mucous  membrane  is  seen  to  be  angry  and  inflamed,  and  perhaps 
unduly  dry.  The  child  is  manifestly  ailing,  is  peevish,  and  is  anxious  to 
lie  down.  In  from  twelve  to  twenty-four  hours  from  the  manifestation 
of  the  preliminary  symptoms  just  detailed,  and  in  some  cases  in  even 
less  time  than  this,  the  eruption,  or  rash,  develops,  beginning  on  the  neck 
and  upper  part  of  the  chest,  as  a  rule. 

No  one  of  the  eruptive  diseases  is  so  characteristic  in  its  appearance 
as  is  scarlet  fever,  the  skin  of  the  patient  being,  as  the  name  of  the 
disease  indicates,  actually  scarlet  or  as  bright  a  red  as  is  the  shell  of  a 
boiled  lobster.  Again,  in  no  other  one  of  the  eruptive  diseases  does  the 
rash  appear  over  so  wide  a  surface  in  the  first  hours  of  its  appearance  as  in 
scarlet  fever.  Not  rarely  the  entire  body  and  extremities  are  involved  in 
four  or  five  hours. 

There  are  four  peculiarities  about  this  rash  which  are  worthy  of  note : 
first,  it  is  punctate — that  is,  about  each  hair  follicle  in  the  skin  the  color 
is  slightly  deeper  than  elsewhere;  second,  the  rash  is  often  most  marked 
in  the  folds  of  the  joints,  as  about  the  groins;  third,  the  skin  of  the  face 
about  the  mouth  or  in  the  nasolabial  line  is  palhd,  forming  a  marked 
contrast  to  the  scarlet  hue  elsewhere;  and  fourth,  the  rash  on  the  upper 
part  of  the  thorax  is  often  very  profuse. 

When  the  rash  is  developed,  the  sense  of  heat  conveyed  to  the  hand  and 
complained  of  by  the  child  is  notable.  The  eruption  persists  from  three  to 
seven  days  in  the  majority  of  cases,  and  ends  in  desquamation  of  the  epi- 
derm,  which  comes  away  in  large  flakes,  rather  than  in  fine  bran-like  scales. 
The  skin  may  literally  peel  off  the  hands  and  feet.  In  rare  instances  it  may 
be  shed  from  the  hand  in  the  shape  of  an  old  glove.  This  desquamation  lasts 
from  a  week  to  three  weeks,  beginning  about  the  neck  and  continuing  longest 
on  the  palmar  and  plantar  surfaces,  where  the  skin  is  thick.  Indeed,  I  have 
seen  it  continue  between  the  toes  for  six  or  eight  weeks.  The  period  of 
desquamation  is,  however,  greatly  shortened,  as  a  rule,  if  during  the  illness 
the  child  has  been  anointed  by  some  oily  substance  to  allay  dermal  irritation, 
or  if  during  convalescence  it  is  frequently  bathed.  As  long  as  desquamation 
lasts  there  is  danger  of  the  spread  of  the  disease  from  the  patient. 

The  stage  of  invasion,  already  described,  varies  in  certain  cases  to  a  consid- 
erable degree.  It  may  be  so  mild  as  to  lead  to  a  belief  that  the  rash  is  due  to 
indigestion,  and  it  may  be  so  severe  that  the  patient  is  first  convulsed,  and 
then  speedily  overwhelmed  by  toxaemia.  The  eruption  may  not  be  widely 
diffused,  but  appear  for  a  short  time  on  the  chest  and  abdomen,  in  the  groin, 
or  about  the  buttocks  before  it  spreads  elsewhere.  It  may  not  spread  farther 
than  these  areas,  and  may  last  only  one  day.  Such  cases  are  often  given 
the  unfortunate  name  of  "scarlet  rash."  They  are  just  as  capable  of  giving 
scarlet  fever  to  another  child  as  a  more  severe  attack.      In  other  cases,  of  a 


SCARLET  FEVER 


101 


malignant  type,  the  rash  seems  to  be  suppressed,  the  skin  is  mottled,  but  the 
true  rash  fails  to  appear,  or  it  may  appear  in  blotches,  which  may  seem  to 
be  macular,  as  in  measles.  When  doubt  exists  in  such  cases,  the  patient  will 
be  benefited  and  the  diagnosis  cleared  by  a  hot  bath  or  hot  pack  to  stimulate 
the  peripheral  circulation  and  bring  out  the  rash. 

The  temperature  in  scarlet  fever  runs  its  course  side  by  side  with  the 
severity  of  the  disease.  It  reaches  its  acme  within  a  few  hours  from  the 
onset,  and  is  often  as  high  as  105°  within  twelve  hours.  As  a  rule,  this 
height  is  not  maintained,  but  after  twenty-four  hours  to  three  days  it  falls 
gradually  to  about  103°,  and  then  gradually  decreases  daily  by  lysis,  reaching 
normal,  as  desquamation  begins,  about  the  eighth  or  ninth  day  (Fig.  25).  If 
it  remains  high  or  if  a  recrudescence  occurs,  some  secondary  trouble,  such  as 
middle-ear  disease  or  bronchopneumonia,  is  to  be  sought  for. 


Fig.  25 


DAY  OF 
DISEASE 

1 

2 

s 

4 

5 

G 

7 

8 

9 

10 

11 

12 

13 

14 

ir, 

io5° 
104° 
103° 
102° 

lOl' 

100° 
99° 

NORM'L 

M    E 

M   E 

M  E 

M  E 

M  E 

M   E 

M  E 

ME 

M  E 

M  E 

M  E 

M  E 

M  E 

M  E 

M  E 

f\ 

A 

/ 

\^/ 

V 

A 

/ 

M 

/ 

V 

/ 

A 

/ 

1 

/ 

/' 

f\ 

A 

L_ 

-._ 

V- 

/_. 

/■ 

mA 

/\ 

/ 

Chart  of  scarlet  fever. 


In  the  stage  in  which  the  disease  is  fully  developed  the  clinical  picture 
presents  very  great  variations  in  different  cases.  In  some  children  with  a 
well-developed  rash,  the  systemic  symptoms  are  so  mild  that  it  is  difficult  to 
keep  the  patient  in  bed,  and  all  the  manifestations  seem  of  little  moment. 
In  others  the  general  symptoms  are  sufficient  to  show  that  the  child  is  seri- 
ously ill,  and  in  still  others  of  a  severe  type  the  systemic  state  may  be  one 
of  deep  toxaemia,  so  that  the  child  seems  overwhelmed  by  the  infection.  The 
cases  in  which  toxaemia  is  marked  are  not  necessarily  those  in  which  great 
glandular  involvement  is  present,  although  both  sets  of  symptoms  may 
occur  simultaneously. 

Sometimes  the  throat  symptoms  by  their  severity  mask  all  others.  Not  only 
may  the  pharyngeal  and  tonsillar  surfaces  be  ulcerated,  but  they  may  be  cov- 
ered by  a  false  membrane,  which,  in  some  cases,  is  due  to  a  concurrent  diph- 
theria, but  which  may  also  be  due  to  the  streptococcus,  and  is  always  poly- 
microbic in  nature.  Such  cases  often  present  a  horrid  type  of  the  disease, 
for  the  lips  and  teeth  are  covered  with  sordes,  the  tissues  of  the  neck  are 
infiltrated  and  swollen,  and  the  head  thrown  far  back  to  diminish  pressure 
on  the  air-passages  produced  by  the  swelling.  In  such  cases  the  general 
infection  extends  rapidly  into  the  chest,  and  bronchial  or  pulmonary  symp- 
toms develop  with  great  rapidity,  thereby  causing  a  fatal  issue,  although 
even  with  these  grave  complications  recovery  sometimes  takes  place. 

If  to  these  mahgnant  manifestations  are  added  a  tendency  to  suppression 


102  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

of  urine,  because  of  the  intense  nephritis  which  has  been  produced,  the  signs 
of  toxaemia  deepen  into  stupor  and  death  ensues.  Cases  of  this  type  rarelj 
die  before  the  sixth  or  twelfth  day,  since  this  time  is  required  to  develop  the 
condition  described.  There  is,  however,  a  fulminant  form  of  the  disease 
in  which  the  malady,  after  being  ushered  in  by  severe  convulsions, 
speedily  develops  into  deep  stupor,  with  hyperpyrexia  and  death.  In 
some  of  these  cases,  however,  the  infection  is  so  profound  that  a  high 
temperature  does  not  occur,  the  temperature  never  rising  above  101°. 
These  cases  are  very  rare  and  are  described  more  frequently  by  French 
clinicians  than  they  are  seen  by  Anglo-Saxon  practitioners. 

A  few  cases  are  on  record  in  which  no  fever  has  developed,  and  others 
in  which  no  rash  has  been  seen. 

Under  the  name  "surgical  scarlet  fever"  is  described  a  febrile  affection 
which  attacks  persons,  usually  children,  after  surgical  operations  or  injuries. 
The  term  is  an  unfortunate  one,  for  no  such  malady  exists  as  a  distinct 
disease.  The  condition  is  an  erythema  due  to  sepsis  or  else  it  is  an  attack 
of  scarlet  fever  coming  on  during  convalescence  from  the  operation. 

Complications  and  Sequelae. — Scarlet  fever  depends  very  largely  for  its  gravity 
upon  its  complications  and  sequelae,  which  are  not  rarely  met  with.  The 
most  constant  of  these  is  a  certain  degree  of  renal  irritation  or  inflammation. 
The  condition  of  the  kidneys  from  a  time  very  early  in  the  attack  is  such  that 
slight  albuminuria  may  be  considered  a  fairly  constant  symptom.  In  some 
instances  this  febrile  albuminuria  is  the  only  evidence  that  the  kidneys  are 
affected,  but  in  others  the  character  of  the  urine  and  the  general  systemic  con- 
dition render  it  very  plain  that  a  true  nephritis  is  present.  Not  only  does  the 
urine  of  such  patients  show  considerable  quantities  of  albumin  and  casts, 
but  there  is  distinct  puffiness  of  the  eyelids  and  oedema  of  the  ankles,  or  even 
a  generalized  anasarca.  In  such  patients,  if  this  state  persists,  transudation 
may  take  place  into  the  serous  cavities  of  the  body,and  the  patient  suffers  from 
the  pressure  produced  by  the  fluid  upon  the  heart  and  lungs.  He  may  develop 
ursemic  symptoms,  and  these  in  turn  may  cause  death.  In  many  of  these 
cases,  however,  the  acute  nephritis,  responsible  for  these  manifestations, 
speedily  diminishes  with  the  subsidence  of  the  disease  itself,  and  recovery 
follows  with  a  rapidity  which  is  extraordinary.  I  have  seen  recovery  take 
place,  even  after  the  anasarca  was  so  marked  as  to  almost  close  the  eyes  and 
after  repeated  severe  ursemic  convulsions. 

Suppression  of  urine  may  be  the  first  symptom. 

There  is  still  another  type  of  renal  disorder  met  with  in  a  few  cases  of 
scarlet  fever  in  which  the  infection  seems  so  intense  that  the  kidneys  are 
completely  suppressed  in  their  functional  power  very  early  in  the  attack,  and 
in  which  we  find  great  diminution  of  urinary  flow,  hsematuria,  and  copious 
amounts  of  albumin  and  casts.  In  these  cases  the  toxaemia  of  the  disease 
and  that  resulting  from  the  renal  lesions  produces  death  in  a  very  short  time. 

The  renal  changes  of  scarlet  fever  are,  therefore,  to  be  carefully  watched, 
and  the  greatest  care  must  be  taken  that  the  kidneys  are  not  permitted  to  be 
additionally  congested  by  the  patient  being  chilled.  Exposure  during  and 
soon  after  scarlet  fever  may  change  a  mild  renal  state  into  a  most  desperate 
condition. 


SCARLET  FEVER  103 

As  a  sequel,  rather  than  a  comphcation  of  scarlet  fever,  inflammations  of 
the  joints  sometimes  occur.  This  is  not  acute  rheumatism,  but  of  the  nature 
of  a  septic  arthritis.  Rarely  the  joint  suppurates.  The  swelling  does  not 
persist,  as  a  rule,  if  the  effusion  be  simply  serous.  Another  very  rare  sequel  of 
scarlet  fever  is  dislocation  of  the  hip-joint.  In  1804  J.  Franck  reported  a  case 
of  dislocation  of  the  hip  occurring  in  an  attack  of  scarlet  fever.  In  1894 
Champenois  published  anaccount  of  three  other  cases,  which  were  all  he  could 
collect  from  the  literature.  Since  1894  H.  Stanfield  Collier  has  reported  two 
cases.  Robert  Jones,  of  Liverpool,  states  that  one  such  case  has  come  under 
his  observation. 

Much  more  common  than  arthritic  changes  during  or  after  scarlet  fever 
are  those  which  are  met  with  in  the  ears,  due  to  an  extension  of  the  septic 
inflammation  from  the  throat  through  the  Eustachian  tube  to  the  middle  ear. 
These  have  already  been  referred  to  when  considering  the  pathology  of  the 
disease.  The  physician  should  always  be  on  his  guard  for  aural  inflamma- 
tion in  the  course  of  this  malady  and  after  it  has  run  its  course.  Permanent 
deafness  not  rarely  results  from  the  otitis  media  due  to  this  cause. 

Parotitis  sometimes  occurs  as  a  complication. 

Next  to  acute  articular  rheumatism,  scarlet  fever  stands  as  the  most 
common  of  all  the  acute  infections  in  producing  valvular  disease  of  the  heart. 
These  changes  are  in  the  endocardium  and  myocardium,  and  may  be 
acute  and  transient  or  become  permanent.  Very  rarely  does  the  endo- 
carditis become  severe  enough  to  be  called  ulcerative.  Great  responsibility 
rests  upon  the  physician  in  regard  to  the  cardiac  changes  in  this  disease, 
because,  while  it  is  true  that  he  cannot  prevent  them,  he  can,  by  insisting  on 
rest  during  the  attack  and  during  convalescence,  to  a  large  extent,  limit  their 
severity,  both  as  to  their  temporary  and  permanent  character.  This  is  the 
more  important,  since,  as  in  all  acute  infections,  the  heart  is  often  the  seat 
of  a  myocardial  change. 

Bronchopneumonia  develops  in  a  small  proportion  of  cases.  Empyema 
may  be  a  sequel  of  scarlet  fever,  and  is  usually  insidious  in  onset. 

The  induration  of  the  cervical  glands,  which  may  suppurate,  has  already 
been  referred  to. 

Nervous  complications  of  scarlet  fever,  aside  from  delirium  and  convul- 
sions due  to  the  toxaemia,  are  rare.  As  a  sequel,  chorea  may  develop,  or  hemi- 
plegia arise,  caused  by  an  embolus  lodging  in  a  cerebral  vessel.  Very  rarely 
an  acute  ascending  paralysis,  which  is  the  result  of  neuritis,  may  develop  in 
the  lower  limbs. 

An  exceedingly  rare  complication  of  scarlet  fever  is  peritonitis,  due  in  all 
probability  to  a  streptococcus  infection  of  the  peritoneum.  McCollom  and 
Blake,  of  Boston,  have  reported  two  such  cases  in  the  Boston  City  Hospital 
Reports. 

Diagnosis. — While  scarlet  fever  in  its  typical  development  is  not  difficult 
of  diagnosis,  it  not  infrequently  happens  that  mild  attacks  render  a  decision 
as  to  the  exact  nature  of  the  illness  most  difficult  to  determine.  The  chief 
reason  for  this  is  that  children  very  commonly,  and  adults  more  rarely, 
develop  a  roseola  or  rose  rash  as  a  result  of  many  different  causes,  and  if 
the  manifestation  of  scarlet  fever  be  mild,  or  the  rose  rash  be  severe,  the  skin 


104  DISEASES  DUE   TO   A   SPECIFIC  IXFECTION 

lesions  may  not  only  not  aid  in  diagnosis,  but  greatly  impede  the  physician  in 
reaching  a  decision.  The  most  common  of  these  rose  rashes  is  that  pro- 
duced by  certain  types  of  indigestion,  and  particularly  that  which  follows 
eating  fish,  shell-fish  seeming  especially  prone  to  cause  it.  As  active  vomiting 
and  diarrhoea  and  even  fever  may  be  present  in  such  cases,  the  patient  at 
first  sight  quite  markedly  resembles  one  suffering  from  scarlet  fever ;  but  the 
absence  of  sore  throat,  of  enlarged  tonsils,  of  enlarged  cervical  glands,  and 
of  a  history  of  no  exposure  to  the  specific  fever,  all  aid  in  excluding  scarlatina, 
particularly  if  it  can  be  discovered  that  indigestible  food  has  been  ingested. 
Then,  too,  the  rose  rash  of  indigestion  does  not,  as  a  rule,  appear  first  on  the 
chest.  In  some  persons,  with  a  very  sensitive  skin,  contact  with  nettles  or 
other  irritants  may  cause  a  roseola.  In  all  such  cases  the  physician  should 
not  be  hasty  in  making  a  diagnosis,  but  insist  that  enough  time  be  given  to 
permit  him  to  make  a  careful  study  of  the  case  for  several  days  before  express- 
ing an  opinion.  In  such  instances  the  patient  should  be  isolated  until 
the  diagnosis  is  decided. 

The  rose  rash  sometimes  met  with  in  German  measles  is  never  as  scarlet 
as  it  is  in  true  scarlet  fever  and  is  distinctly  maculated.  Further,  it  appears 
on  the  face  before  it  is  seen  on  the  chest,  the  punctation  of  the  rash  of  scarlet 
fever  is  absent,  the  fever  is  slight  and  lasts  but  two  or  three  days,  and  flaky 
desquamation  does  not  occur. 

Roseola  due  to  vaccination  and  that  due  to  the  use  of  diphtheria  antitoxin 
are  easily  diagnosticated  by  the  history  of  the  patient. 

Should  a  rose  rash  with  fever  develop  in  an  adult  there  is  much  more  like- 
lihood of  its  being  due  to  early  secondary  syphilis  than  to  scarlet  fever.  The 
rose  rash  of  syphilis  is  not,  however,  so  bright  a  red  as  that  of  scarlatina.  Such 
a  rash,  when  due  to  syphilis,  disappears  and  reappears,  becomes  dusky,  and, 
finally,  it  is  apt  to  be  circinate. 

Sometimes  in  acute  and  chronic  nephritis  not  due  to  scarlet  fever  a  rose 
rash  develops.  The  absence  of  throat  symptoms  and  the  signs  of  nephritis 
revealed  by  the  urine  aid  in  the  differentiation. 

A  condition  called  "erythema  scarlatiniform"  has  a  sudden  onset  with 
fever,  and  is  characterized  by  a  rash  which  develops  rapidly  over  the 
whole  body,  lasts  for  several  days,  and  ends  in  desquamation.  The  absence 
of  throat  symptoms  in  these  cases  is  once  more  an  important  differential 
point.  Further,  the  other  symptoms  are  by  no  means  so  severe  as  the 
rash  would  lead  one  to  expect.  Such  patients,  too,  usually  have  a  history 
of  repeated  attacks. 

A  factor  of  very  great  value  in  diagnosis  is  the  peculiar  appearance  of 
the  tongue  in  many  cases  of  scarlet  fever.  At  the  time  of  onset  it  may 
have  a  white  coating,  which  soon  diminishes  in  degree  and  becomes  dotted 
with  red  and  enlarged  papillae.  This  has  been  called  the  "strawberry 
tongue"  of  scarlet  fever.        ' 

Another  point  of  some  importance  is  the  time  at  which  desquamation 
appears,  for  the  mere  occurrence  of  desquamation  is  by  no  means  peculiar 
to  scarlet  fever.  In  this  disease  this  symptom  usually  develops  about  the 
fourth  to  the  sixth  day  on  the  face  and  about  the  sixth  day  on  the  chest  and 
neck.     The  hands  do  not  begin  to  desquamate  until  as  late  as  the  twelfth 


SCARLET  FEVER  105 

day,  and  the  feet  some  days  later  than  this.  Other  eruptions  which  resemble 
scarlet  fever  and  desquamate  usually  begin  to  shed  the  skin  in  these  areas 
earlier  than  the  days  just  named. 

In  the  cases  of  scarlet  rash  due  to  sepsis  it  is  noteworthy  that  the 
progress  of  the  malady  is  always  aberrant  or  irregular,  for  the  throat 
symptoms  are  often  absent,  the  temperature  is  rather  that  of  sepsis  than 
scarlatina,  and  the  septic  symptoms  may  be  severe.  These  cases  are  par- 
ticularly interesting  and  worthy  of  the  most  careful  study,  because  anti- 
septics, when  absorbed,  sometimes  produce  a  scarlatiniform  rash,  and 
because  if  the  case  be  one  of  true  scarlet  fever  it  is  a  menace  to  all  other 
children,  sick  or  well. 

As  the  differential  diagnosis  of  such  cases  cannot  be  made  in  some  instances 
till  the  disease  has  lasted  for  some  days  or  until  desquamation  has  begun, 
all  patients  with  such  symptoms  should  be  promptly  isolated.  A  focus  of 
septic  infection  is  to  be  carefully  sought  for. 

Prognosis. — This  varies  greatly  in  different  epidemics  and  depends 
largely  upon  the  severity  of  the  symptoms  in  a  given  case.  The  malady 
is  always  to  be  considered  a  grave  one.  The  actual  mortality  is  shown  in 
the  following  statistics.  Of  26,921  cases  of  scarlet  fever,  3216,  or  11.9  per 
cent.,  were  fatal.  Holt  states  that  the  average  mortality  is  from  10  to  14  per 
cent.,  but  that  for  children  under  five  years  of  age  the  mortality  varies 
from  20  to  30  per  cent.  (See  Fig.  26.)  The  diminution  of  mortality  after 
the  first  decade  of  life  is  noteworthy. 

Treatment. — In  the  treatment  of  scarlet  fever  the  fact  must  never  be  lost 
sight  of  that  the  disease  is  self-limited,  that  it  is  bound  to  run  its  course,  and 
the  most  the  physician  can  do  is  to  guide  his  patient  through  the  illness  with 
the  hope  that  complications  may  be  avoided  and  that  severe  symptoms  may 
be  modified. 

First  and  foremost  in  the  treatment  of  this  malady,  it  is  essential  that 
the  patient  have  hygienic  surroundings,  with  plenty  of  fresh  air  and  careful 
avoidance  of  draughts  and  exposure  to  sudden  changes  of  temperature, 
since  such  exposures  by  chilling  the  surface  of  the  body  are  almost  certain 
to  exaggerate  the  renal  congestion  or  inflammation  which  is  practically 
always  present  during  the  acute  stages  of  this  disease.  Indeed,  it  may  be 
said  that  the  prime  object  of  the  physician  and  nurse,  from  the  beginning 
to  the  end  of  the  attack,  is  to  use  every  effort  to  avoid  sources  of 
irritation  to  the  kidneys,  for  it  cannot  be  doubted  that  many  cases  of  serious 
renal  difficulty  which  arise  in  connection  with  scarlet  fever  depend  upon 
carelessness  in  this  respect.  It  is  also  important  to  remember  that  these 
precautions  in  regard  to  exposure  are  not  only  necessary  during  the  acute 
attack,  but  until  convalescence  has  been  thoroughly  completed  and  until 
the  urine  no  longer  shows  any  evidence  whatever  of  renal  irritation.  As 
these  lines  are  written  I  have  seen  in  consultation  a  boy,  aged  fourteen  years, 
who  apparently  had  recovered  entirely  from  an  attack  of  scarlet  fever,  except 
that  there  was  still  some  desquamation  in  the  palms  of  his  hands.  He  was 
allowed  to  play  ball  out-of-doors,  became  overheated  and  then  chilled,  and 
within  forty-eight  hours  suffered  from  violent  ursemic  convulsions,  which 
nearly  cost  him  his  life. 


106 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


Fig.  26 


Medicinally,  it  is  usually  well  in  cases 
of  scarlet  fever  to  prescribe  from  the 
first  a  mild  alkaline  diuretic,  of  which, 
perhaps,  the  best  is  5  grains  of  citrate 
of  potassium  with  20  drops  of  sweet 
spirit  of  nitre  in  water  three  or  four 
times  a  day  to  a  child  of  eight  years, 
giving  at  the  same  time  copious  quan- 
tities of  such  pure  water  as  the  non- 
sparkling  water  from  Poland  Springs, 
or  any  other  spring  water  which  con- 
tains a  very  small  amount  of  organic  and 
inorganic  matter.  By  these  means  we 
flush  the  kidneys  of  toxic  substances 
which  in  a  concentrated  form  might 
produce  serious  renal  irritation. 

The  second  point  of  therapeutic  im- 
portance is  the  condition  of  the  throat. 
If  the  child  is  old  enough  to  gargle  its 
throat  with  a  weak  solution  of  chlorate 
of  potash  (3  or  5  grains  to  the  ounce) 
four  or  five  times  a  day,  such  a  gargle 
is  useful  from  the  very  beginning  to  the 
end  of  the  attack.  When  the  inflam- 
matory changes  in  the  pharynx  are 
severe,  the  part  may  be  cleansed  with  a 
spray  of  peroxide  of  hydrogen,  or  this 
drug  may  be  applied  by  means  of  a 
cotton  applicator,  the  throat  being  after- 
ward cleansed  by  a  spray  of  Dobell's 
solution.  For  the  pseudomembranous 
pharyngitis  which  sometimes  develops 
a  similar  local  treatment  is  advisable, 
and,  combined  with  this,  both  diph- 
theria antitoxin  and  antistreptococcic 
serum  should  be  given.  If  the  false 
membrane  be  due  to  the  Klebs-Loeffler 
bacillus,  diphtheria  antitoxin  is  cer- 
tainly indicated,  and,  as  the  strepto- 
coccus is  always  present  in  scarlet  fever, 
and  is  probably  responsible  for  the 
formation  of  false  membranes  in  some 
cases,  the  use  of  serums  designed  to 
antagonize  both  of  these  poisons  is 
manifestly  rational. 

For  the  relief  of   the    intense  burn- 

Showing  the  mortality  of  scarlet  fever  accord-    i^g    and     itchiug    of     the     skiu    which    is 
ing  to  age,  based  on  Johannessen's  9855  cases,      present    in    SOmC  CaSCS,  the    cllild     may 


SCARLET  FEVER  107 

be  anointed  with  olive  oil  containing  0.5  to  1  per  cent,  of  carbolic  acid,  or 
weak  carbolized  vaselin  may  be  used.  Sometimes  a  very  distinct  fall  in  tem- 
perature can  be  produced  by  allaying  irritation  of  the  skin  in  this  manner. 

Should  the  fever  become  high  enough  to  deserve  attention — that  is,  if  it 
persistently  remains  above  103°  or  if  it  occasionally  rises  as  high  as  105° — 
the  patient  should  be  sponged  with  tepid  water  and  alcohol,  a  small  ice-bag 
being  simultaneously  applied  to  the  head.  Such  a  sponging,  given  early  in 
the  evening,  will,  by  diminishing  the  irritation  of  the  skin  and  quieting 
the  peripheral  sensory  nerves,  often  cause  the  child  to  pass  a  comfortable 
night.  The  antipyretic  coal-tar  drugs  are  contraindicated  in  these  cases, 
except  under  extraordinary  circumstances. 

If  intense  nervous  irritation  is  present,  5  or  10  grains  of  the  bromide  of 
strontium  or  sodium  may  be  given  several  times  a  day.  Full  doses  of  chloral 
have  been  highly  recommended,  but  they  are  often  contraindicated  because 
of  the  irritant  effects  upon  the  kidneys  and  the  depressant  influence  upon 
the  heart.  Should  evidence  of  circulatory  failure  develop,  small  doses  of  an 
old  brandy  poured  over  shaved  ice,  or  given  in  cool  water,  may  be  admin- 
istered every  two  or  three  hours  with  advantage.  Or,  small  doses,  frequently 
repeated,  of  aromatic  spirit  of  ammonia  may  be  used  in  the  same  manner. 
If  the  circulatory  failure  is  acute  or  sudden,  either  the  aromatic  spirit  of 
ammonia  or  Hoffmann's  anodyne  should  be  used  as  rapidly  acting  diffusible 
stimulants. 

Pain  in  the  ear  should  be  relieved  by  irrigating  the  external  auditory  canal 
with  normal  salt  solution  as  hot  as  the  child  can  bear  it.  In  all  these  cases  a 
careful  examination  of  the  ear-drum  should  be  made  twice  a  day  to  see  whether 
there  is  any  bulging  due  to  accumulated  secretion  or  suppuration  in  the 
middle  ear,  and  if  this  is  present  paracentesis  of  the  tympanum  should  be 
performed  at  once  to  relieve  the  pain  and  avoid  danger  of  infection  of  the 
mastoid  cells. 

If  evidences  of  septicaemia  are  present  and  the  patient  seems  anaemic, 
either  during  the  later  stages  of  the  attack  or  during  convalescence,  the 
tincture  of  the  chloride  of  iron,  in  the  dose  of  5  drops  three  or  four  times  a 
day,  is  advantageous,  since  it  tends  to  combat  the  anaemia  and  the  infection 
and  also  exercises  a  slight  stimulant  influence  upon  the  kidneys.  For  the  relief 
of  persistent  albuminuria  after  the  attack  is  passed,  the  child  should  be 
prevented  from  taking  excessive  exercise,  but,  nevertheless,  should  live  in 
the  sunshine  as  much  as  possible,  and  may  take  either  small  doses  of  the 
tincture  of  chloride  of  iron  or  a  very  minute  dose  of  the  tincture  of  cantharides 
— say,  I  to  1  drop  twice  or  thrice  a  day,  well  diluted ;  but  the  cantharides  is 
contraindicated  if  the  microscope  shows  in  the  urine  the  presence  of  red 
blood  cells,  indicating  that  the  kidneys  are  still  acutely  inflamed. 

In  those  cases  of  scarlet  fever  in  which  the  rash  fails  to  develop  its  full 
eflflorescence  promptly,  and  particularly  in  those  cases  in  which  the  skin  is 
mottled  and  marbled,  indicating  poor  capillary  circulation,  it  is  exceedingly 
useful  to  immerse  the  child  in  a  hot  bath.  In  other  cases  the  cool-warm  pack 
may  be  used.  This  consists  in  stripping  the  child  of  its  night-clothing  and 
rolling  it  in  a  sheet  which  has  been  dipped  in  warm  water,  which,  by  the  time 
it  is  wrapped  around  the  child,  has  become  considerably  cooled  by  evapora- 


108  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

tion.  As  soon  as  the  sheet  is  wrapped  about  the  child,  an  ice-bag  being  in 
the  mean  time  apphed  to  the  head,  it  is  wrapped  in  a  blanket,  and  in  a  few 
moments  the  heat  of  the  child's  body  transforms  the  cool  sheet  into  a  warm 
pack.  The  primary  effect  of  the  cool  sheet  is  to  drive  the  stagnant  blood  out 
of  the  peripheral  capillaries,  and  the  effect  of  the  warm  sheet  is  to  bring  new 
blood  into  these  vessels.  By  these  means  we  are  very  frequently  enabled 
not  only  to  improve  the  circulation  and  develop  the  rash,  but  to  diminish 
the  toxic  symptoms  and  relieve  nervous  stress.  It  is  hardly  necessary  to  add 
that  exposure  for  any  length  of  time  to  the  cool  sheet  is  to  be  avoided.  The 
blanket  is  to  be  placed  tightly  about  the  child  at  the  earliest  possible  moment 
after  the  cool  sheet  comes  in  contact  with  its  body,  so  that  the  chilling  of  the 
surface  will  be  only  instantaneous.  French  therapeutists,  and  some  other 
practitioners,  have  advised  that  in  those  cases  in  which  cerebral  symptoms  are 
very  marked  and  toxsemia  is  evidently  profound,  the  child  should  be  placed 
in  a  warm  bath,  and  that  cool  water  should  be  poured  over  its  head,  neck, 
and  chest  for  a  moment,  in  order  to  produce  a  certain  amount  of  shock  and 
rouse, the  flagging  powers  of  the  body.  This  method  has  been  so  highly 
endorsed  by  excellent  practitioners  that  it  cannot  be  condemned  for  theoret- 
ical reasons,  but  the  author  has  never  been  brave  enough  to  employ  it. 

Within  the  last  few  years  several  attempts  have  been  made  to  produce  an 
antiscarlatinal  serum  without  very  satisfactory  therapeutic  results.  In  the 
cases  in  which  the  author  has  directed  its  use,  it  has  seemed  to  modify 
the  throat  symptoms,  but  otherwise  it  has  not  affected  the  progress  of  the 
disease. 

MEASLES 

Definition. — Measles  is  an  acute  infectious  disease,  usually  epidemic,  which 
most  commonly  attacks  children  and  rarely  occurs  after  the  second  decade 
of  life.  The  skin  during  an  attack  is  covered  more  or  less  profusely  by  a 
dusky  red  eruption  of  a  maculopapular  type.  The  eyes  are  congested  and 
lachrymose,  and  the  nasal  and  pharyngeal  mucous  membranes  swollen  and' 
red.  One  attack  usually  confers  immunity.  Measles  is  sometimes  called 
"Morbilli." 

Distribution. — Measles  is  met  with  in  all  parts  of  the  civilized  world.  If 
by  chance  it  is  carried  to  a  people  who,  by  reason  of  isolation,  have  not  been 
exposed  in  previous  generations  to  its  effects,  it  often  develops  in  a  malignant 
form  and  causes  a  great  mortality.  Perhaps  the  most  noteworthy  example 
of  this  is  the  case  of  the  inhabitants  of  certain  of  the  Fiji  Islands,  who,  being 
exposed  to  the  infection,  fell  ill  and  died  by  thousands,  so  that  it  is  estimated 
that  20,000  deaths  occurred  in  four  months.  The  epidemic  ceased  only  after 
every  person  on  the  islands  had  been  infected. 

The  susceptibility  of  children  in  the  first  ten  years  of  life  to  the  infection 
is  quite  remarkable.  If  a  large  number  who  have  not  been  rendered  immune 
by  a  previous  attack  are  exposed  to  the  infection,  nearly  all  fall  sick.  Smith 
and  Dabney  report  an  instance  in  which  110  children  between  eight  and 
eighteen  years  of  age  were  exposed,  and  only  2  were  not  taken  ill. 

Measles  is  much  more  prevalent  in  the  spring  and  winter  months  than  in 


MEASLES  109 

the  summer  months,  probably  because  the  open-air  Hfe  and  free  ventilation 
of  the  warmer  season  aids  in  preventing  the  exposure  of  susceptible  persons 
to  a  concentrated  form  of  the  contagion. 

Etiology. — Measles  is  in  all  probability  due  to  a  distinct  micro-organism 
but  so  far  it  has  not  been  isolated.  Bacilli  have  been  found  in  the  blood  and 
in  the  pharyngeal  and  nasal  secretions  of  persons  affected  with  the  disease 
but  no  evidence  has  been  adduced  to  show  that  they  are  its  causative  agents. 
The  bacillus  isolated  and  cultivated  by  Canon  and  Pielicke  in  1892  pro- 
duced no  ill  effects  when  injected  into  animals.  CzajkoM^ski  and  Borini 
have  also  obtained  bacilli  from  the  blood.  A  micrococcus  which  Lesage 
found  in  1900,  although  highly  virulent  for  rabbits,  did  not  reproduce  the 
disease.  Protozoa  have  been  found  by  Doehle  and  Pfeiffer  (1892)  in  the 
blood  of  patients  suffering  from  measles.  Rosenberger  and  Wilson  (1906) 
found  in  the  blister  fluid  of  39  out  of  41  cases  a  small  hyaline  body, 
containing  a  motile  granule.     Its  relation  to  the  disease  is  not  yet  clear. 

The  disease  spreads  with  great  readiness  through  the  air  and  contact  with 
the  patient  or  his  garments  is  not  necessary  for  its  transmission,  although 
such  contact,  of  course,  provides  the  infection  in  more  concentrated  form. 
There  is  no  doubt  that  the  breath  of  a  patient  suffering  from  measles  carries 
the  infection,  and  so  does  the  nasal  and  pharyngeal  mucus,  so  that  the 
expulsion  of  these  secretions  by  coughing  or  sneezing  may  result  in  nurses 
or  visitors  becoming  a  means  of  transmitting  the  disease  by  their  garments 
being  contaminated  in  this  manner. 

Very  short  exposure  to  infected  air  is  sufficient  for  infection,  and  even 
when  careful  precautions  are  taken  to  prevent  the  spread  of  the  disease  it 
not  infrequently  happens  that  all  the  other  children  in  a  house  develop  the 
malady,  partly  because  it  is  infectious  from  the  earliest  period  of  invasion 
before  its  presence  is  recognized,  but  largely  because  of  the  ease  with  which 
it  is  conveyed  by  the  air.  This  great  diffusibility  of  the  virus  of  measles 
is  quite  in  contrast  with  the  limited  diffusibility  of  the  poison  of  scarlet 
fever. 

Although  it  is  true  that  the  diffusibility  and  activity  of  the  infection  of 
measles  is  exceedingly  active  while  the  disease  lasts,  it  is  also  a  fact  that  it 
speedily  disappears  after  convalescence  is  established.  Three  weeks  after 
the  attack  begins,  the  patient  rarely  transmits  the  disease,  and  by  this  time, 
with  ordinary  ventilation,  the  room  and  surroundings  of  the  patient  are 
usually  innocuous.  Any  condition  of  ill-health  which  diminishes  vital  resist- 
ance very  distinctly  increases  the  susceptibility  of  an  individual  to  infection, 
and  in  these  instances  the  disease  is  prone  to  be  severe. 

The  period  of  incubation  of  measles  is  usually  from  eleven  to  fifteen  days, 
but  cases  are  recorded  in  which  the  disease  began  one  week  afetr  exposure. 

Prevention. — Measles  is  to  be  prevented  by  complete  isolation  of  the 
patient,  by  the  disinfection  of  all  garments  of  the  patient  and  nurse  before 
they  leave  the  sick-room,  and  by  free  ventilation,  so  arranged  that  the  other 
rooms  in  the  house  are  not  exposed  to  a  draught  from  the  sick-room.  After 
the  attack  has  passed  the  patient  should  be  given  several  hot  baths  to  rid 
the  body  of  all  desquamating  skin,  and  the  scalp  should  be  cleansed  with 
special  care. 


no 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


Frequency. — Measles  is  one  of  the  most  common  of  the  acute  exanthemata 
and  affects  nearly  all  persons  living  in  cities  before  they  reach  adult  life. 
Indeed,  it  may  be  said  to  be  the  most  common  of  all  diseases  in  childhood. 

Pathology  and  Morbid  Anatomy. — There  are  no  noteworthy  changes  pro- 
duced in  the  various  viscera  by  measles,  if  we  exclude  those  ordinarily  con- 
sidered as  complications  and  the  changes  in  the  mucous  membranes  of  the 
respiratory  and  digestive  tract,  consisting  of  acute  irritation  and  catarrh. 
With  the  onset  of  the  disease  these  membranes  become  hypersemic,  and,  it 
may  be,  dotted  with  an  eruption  much  like  that  which  is  seen  on  the  skin. 

The  pathological  changes  due  to  complications  are  chiefly  those  of  bron- 
chitis and  bronchopneumonia,  conditions  which  are  exceedingly  common  in 
young  children,  and  in  patients  who  are  poorly  nursed  and  badly  nourished, 
when  suffering  from  acute  infectious  diseases. 


Fig.  27 


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Showing  initial  fever  with  the  subsequent  fall  and  then  a  rise  when  tlie  rash  is  well  developed 
in  a  case  of  measles.    Also  shows  an  ending  of  the  fever  by  crisis. 


Symptoms. — Measles  is  usually  ushered  in  by  the  symptoms  of  an  ordinary 
cold  or  attack  of  coryza.  There  may  be  an  initial  chill,  but  this  is  often 
absent,  the  fever  being  the  first  additional  symptom  which  becomes  mani- 
fest. The  patient's  face  looks  flushed  and,  it  may  be,  slightly  swollen  about 
the  eyes  and  nose,  and  the  conjunctivae  are  injected,  the  general  expression 
of  the  face  being  tearful.  At  this  time,  and  later,  in  the  disease  photophobia 
may  be  marked.  Sneezing  may  be  noticeably  constant,  and  an  examination 
of  the  pharynx  will  reveal  the  fact  that  its  mucous  membrane  is  reddened 
and  the  hard  palate  dotted  with  a  measles-like  rash,  which  often  appears 
here  before  it  develops  on  the  skin.  Some  cough  may  be  present  in  the  stage 
of  onset  as  the  result  of  the  pharyngeal  and  laryngeal  irritation,  and 
headache  may  be  complained  of. 

There  is  present  in  many  cases  upon  the  buccal  mucous  membrane  a 
number  of  small,  white-tipped,  reddish  spots  first  described  by  Filaton,  but 


PLATE  III. 


Fig.  1. 


Fig.   2. 


Fig.  8. 


Fig.  4. 


The  Pathognomonic  Sign  of  Measles  (Koplik's  Spots; 


Fig.  1. — The  discrete  measles  spots  on  the  buccal  or  labial  mucous  membrane,  showing  the  isolated 
rose-red  spot,  with  the  minute  bluish-white  centre,  on  the  normally  colored  mucous  membrane. 

Fig.  2. — Shows  the  partially  diffuse  eruption  on  the  mucous  membrane  of  the  cheeks  and  lips;  patches 
of  pale  pink  interspersed  among  rose-red  patches,  the  latter  showing  numerous  pale  bluish-white  spots. 

Fig.  3. — The  appearance  of  the  buccal  or  labial  mucous  membrane  when  the  measles  spots  completely 
coalesce  and  give  a  diffuse  redness,  with  the  myriads  of  bluish-white  specks.  The  exanthema  on  the  skin 
is  at  this  time  generally  fully  developed. 

Fig.  4. — Aphthous  stomatitis  apt  to  be  mistaken  for  measles  spots.  Mucous  membrane  normal  in  hue. 
Minute  yellow  points  are  surrounded  by  a  red  area.     Always  discrete. 


MEASLES  111 

more  commonly  called  "Koplik's  spots."  (See  Plate  III.)  When  present 
they  are  pathognomonic  of  measles,  but  their  absence  does  not  negative  the 
diagnosis  of  the  presence  of  this  disease. 

The  fever  usually  begins  to  rise  with  the  onset  of  the  catarrhal  symp- 
toms, increasing  day  by  day  till  it  reaches  its  acme  of  103°  to  105°  on 
the  fourth  or  fifth  day  from  invasion,  and  remains  fairly  constant  at  about 
this  level  until  the  rash  begins  to  fade,  on  the  fifth  to  the  seventh  day, 
when  the  fever  ceases  abruptly  or  by  lysis,  reaching  normal  in  a  few  hours 
or  by  the  end  of  two  or  three  days  (Fig.  27) . 

The  eruption  of  measles  develops  on  the  third  or  fourth  day  of  the 
disease,  and  at  first  is  most  marked  back  of  the  ears  and  about  the  roots  of 
the  hair  or  on  the  forehead.  The  individual  spots  look  like  a  flea-bite 
and  are  rather  dusky  red  in  appearance.  By  the  end  of  twenty-four  hours 
or  at  the  expiration  of  the  fifth  day  this  rash  is  usually  pretty  well  diffused 
all  over  the  body,  and  the  macular  appearance  of  the  eruption  begins  to 
become  papular,  so  that  it  can  be  distinctly  felt  by  the  finger-tip  of  the  physi- 
cian. This  rash  varies  greatly  in  its  degree.  Sometimes  it  is  so  profuse  that 
every  part  of  the  body  is  covered ;  in  other  instances  very  considerable  spaces 
of  unaffected  skin  can  be  found  between  the  groups  of  papules.  It  has  been 
generally  stated  that  the  crescentic  arrangement  or  grouping  of  the  rash  is 
diagnostic  of  measles.  That  this  is  erroneous  the  author  is  convinced,  as 
he  has  frequently  seen  it  occur  in  other  morbilliform  eruptions.  When  the 
disease  is  in  its  fully  developed  stage  the  skin  of  the  face  may  be  quite  swollen 
and  that  of  the  neck  and  chest  well  covered  by  the  eruption ;  but  as  the  lower 
part  of  the  trunk  and  the  lower  limbs  become  involved  the  rash  on  the  face 
usually  begins  to  diminish  and  slowly  fades,  leaving,  for  several  days  after  it 
has  entirely  disappeared ,  a  faint  mottling  of  the  skin  with  the  desquamation 
of  branny  scales,  which  is  scanty  in  some  cases,  but  profuse  in  those  who  have 
had  an  intense  eruption.  The  entire  duration  of  the  rash  is  from  five  days  to 
one  week,  and  the  period  of  desquamation  lasts  for  about  the  same  length  of 
time. 

During  the  well-developed  stage  of  the  disease  the  patient  nearly  always 
presents  some  symptoms  of  bronchitis.  This  may  be  so  mild  as  to  be  unde- 
monstrable,  or  so  severe  as  to  threaten  life.  The  thorax  should  be  frequently 
examined,  in  order  that  the  development  of  this  complication  may  be  recog- 
nized and  its  severe  effects,  as  far  as  possible,  avoided. 

Variations. — It  must  not  be  thought,  however,  that  measles  always  follows 
the  course  just  described.  All  the  acute  infections  present  widely  different 
symptoms  in  different  epidemics  and  in  different  persons,  and  measles  is  no 
exception  to  this  rule,  for  in  some  cases  the  systemic  or  constitutional  dis- 
turbance is  so  slight  as  to  be  of  no  importance,  whereas  in  others  it  is 
exceedingly  severe.  In  strong,  hearty  children  the  course  of  measles  is 
rarely  grave  if  they  are  protected  from  cold  and  exposure,  whereas  in  puny, 
badly  nourished  infants  it  is  one  of  the  most  fatal  maladies. 

The  following  variations  from  the  ordinary  course  of  measles  are  met  with : 

A  mild  type,  with  a  scanty  rash  and  almost  no  constitutional  disturbance, 
which  runs  its  course  without  complications  if  ordinary  care  is  exercised. 

A  severe  type,  in  which  nervous  and  constitutional  symptoms  predominate, 


112  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

in  which  the  eruption  may  be  exceedingly  profuse,  but  is  more  commonly 
indistinct  or  poorly  developed,  perhaps  because  of  poor  circulation  in  the 
skin  by  reason  of  toxaemia. 

Another  severe  type  is  known  as  hemorrhagic  or  "black"  measles, 
because  of  the  tendency  to  the  occurrence  of  hemorrhages  in  the  skin.  Still 
another  form  is  a  respiratory  type,  in  which  the  patient  may  suffer  from 
great  laryngeal  and  tracheal  distress  or  from  a  serious  bronchopneumonia. 
It  is  often  said  of  these  cases  by  the  laity  that  the  rash  has  been  driven  in  by 
exposure  to  cold  and  is  exerting  its  deleterious  influence  on  the  lungs.  This 
is  not  exactly  true,  but  it  is,  nevertheless,  a  fact  that  when  we  can,  by  means 
of  a  hot  pack,  restore  the  peripheral  circulation  and  so  indirectly  cause  the 
rash  to  be  manifest,  the  symptoms  of  toxaemia  and  respiratory  disorder  often 
become  decidedly  less. 

Rare  cases  are  met  with  in  which,  after  vomiting,  purging,  convulsions, 
and  coma,  death  speedily  occurs,  even  before  the  rash  has  had  time  to 
become  well  marked. 

Complications  and  Sequelae. — It  has  already  been  intimated  that  measles 
in  itself  is  a  disease  which,  in  most  individuals,  with  ordinary  care,  pursues 
a  safe  course  and  ends  in  recovery.  While  this  is  undoubtedly  true,  it  is 
also  a  fact  that  it  takes  high  rank  among  the  acute  infectious  diseases  which 
produce  death,  by  reason  of  the  complications  which  are  prone  to  occur. 

Of  all  these  by  far  the  most  frequent  and  deadly  is  bronchopneumonia,  a 
complication  which  is  often  severe  in  its  course  and  which  causes  a  great 
number  of  deaths  when  measles  attacks  young  infants.  The  physical  signs 
and  symptoms  are  described  in  full  in  the  article  on  that  disease,  but  it 
is  important  to  remember  that  in  measles  the  disease  is  insidious  and  speedy 
in  its  onset,  so  that  a  pneumonia  may  be  developed  before  the  physician  dis- 
covers it,  unless  he  be  on  his  guard  and  resorts  to  frequent  examinations 
of  the  chest.  Bronchopneumonia  during  an  attack  of  measles  in  a  child 
under  one  year  of  age  is  an  exceedingly  common  and  very  grave  complication 
of  the  disease.  In  children  of  five  years  or  more  this  complication  usually 
does  not  occur  if  the  primary  state  of  the  health  is  fairly  good  and  if  careful 
nursing  prevents  exposure  to  "catching  cold." 

A  second  complication  of  far  less  importance  than  bronchopneumonia, 
both  as  to  frequency  and  results,  is  diarrhoea  and  vomiting  due  to  a  catarrhal 
state  of  the  bowels  and  stomach.  It  also  is  a  complication  which  is  due 
in  a  considerable  proportion  of  cases  to  bad  nursing  and  can  generally  be 
avoided  by  proper  feeding  and  the  avoidance  of  draughts.  It  not  infre- 
quently happens  that  these  digestive  disturbances  are  mild  during  the  acute 
illness,  while  the  patient  is  required  to  be  prudent  and  quiet,  and  become 
pronounced  when  the  acute  illness  is  past  and  the  attendants  become  care- 
less as  to  exposure  and  feeding.  This  gastrointestinal  disorder  varies  from 
a  mild  catarrh  to  a  severe  enterocolitis. 

Another  complication  seen  in  many  cases  is  a  mild  degree  of  stomatitis, 
which  in  poorly  nourished  children  may  become  ulcerative.  Even  so  severe 
and  fatal  a  lesion  as  noma  may  develop  in  cases  with  very  low  vitality. 
Very  rarely  gangrenous  ulceration  of  the  ear,  the  labise,  or  the  prepuce  takes 
place. 


MEASLES  113 

So  far  as  the  nervous  system  is  concerned,  it  may  be  said  that  it  is  rarely 
affected.  In  the  stage  of  onset  in  very  young  children  with  poor  resistance 
and  an  unstable  nervous  system  there  may  be  convulsions,  but  they  are 
exceedingly  rare.  Meningitis  as  a  sequel  to  measles  is  also  very  rare.  Even 
meningitis  due  to  middle-ear  disease  is  rarely  met  with,  for  the  otitis  of 
measles,  while  not  uncommon,  is  usually  mild  and  rarely  causes  secondary 
lesions. 

The  eyes  are  usually  inflamed  and  there  may  be  a  mucopurulejit  con- 
junctivitis, or,  if  the  general  health  be  poor,  keratitis  may  prove  troublesome. 

So  rarely  are  the  heart  and  kidneys  affected  to  any  serious  degree  that 
these  organs  may  be  considered  almost  immune.  A  feebleness  of  the  heart 
due  to  the  infection  and  fever  may  be  present  for  a  time,  and  a  tran- 
sient albuminuria  is  often  manifested,  but  both  of  these  symptoms  usually 
rapidly  disappear  if  the  patient  is  kept  at  rest. 

Measles  is  an  infection  which  is  not  rarely  complicated  by  other  acute 
infections.  Diphtheria  may  develop  during  its  course,  and  whooping- 
cough  is  so  exceedingly  frequent  that  some  relation  between  the  two  dis- 
eases has  been  thought  to  exist.  When  whooping-cough  does  occur  as  a 
complication  the  danger  of  bronchopneumonia  is  greatly  increased.  Still 
another  sequel  of  measles  is  tuberculosis,  probably  because  the  catarrhal  state 
of  the  mucous  membranes  offers  a  path  for  infection  by  the  tubercle  bacillus 
or  because  the  devitalizing  influence  of  measles  permits  an  old  focus  of 
tuberculous  infection  to  become  active. 

The  persistence  of  a  febrile  movement  in  a  case  of  measles  after  seven 
days  should  always  arouse  the  suspicion  of  some  inflammatory  complication 
which  should  be  most  carefully  searched  for. 

Diagnosis. — Measles  must  be  carefully  separated  from  a  large  number  of 
conditions  which  somewhat  resemble  it.  Many  kinds  of  food,  particularly 
shell-fish,  produce  a  rash  which  looks  remarkably  like  measles,  but  which 
usually  lasts  only  a  few  hours.  Antipyretic  or  other  coal-tar  products  do  like- 
wise in  some  persons,  and  the  physician  should  always  enquire  as  to  the 
use  of  these  foods  or  drugs  before  stating  that  measles  is  present.  Some- 
times a  morbilliform  rash  follows  vaccination  or  precedes  smallpox.  The 
use  of  antidiphtheritic  serum  may  also  cause  such  an  eruption.  The  con- 
tact of  a  caterpillar  with  the  skin  in  some  persons  may  cause  a  measles-like 
eruption  which  lasts  only  a  few  hours.  None  of  these  states,  however,  are 
accompanied  by  the  appearance  of  Koplik's  spots,  by  marked  coryza,  nor 
by  the  appearance  of  the  rash  on  the  mucous  membrane  of  the  soft  palate. 
Fever,  too,  is  usually  absent.    (For  the  diagnosis  from  Rotheln,  see  Rubella.) 

Prognosis. — From  what  has  already  been  said  it  is  evident  that  the  prog- 
nosis in  a  case  of  measles  is  dependent  not  on  the  fact  that  measles  has 
developed,  but  rather  upon  the  age  of  the  patient,  the  vital  resistance  or 
the  general  condition  of  the  system,  and  the  surroundings  as  to  sanitation 
and  nursing.  Given  a  poorly  nourished  infant  in  bad  surroundings  and 
with  inefficient  care,  measles  becomes  one  of  the  most  fatal  diseases  to  be 
met  with,  whereas  in  a  case  where  these  conditions  are  good  the  prognosis 
is  fairly  favorable.  We  find,  too,  that  the  danger  of  the  disease  decreases 
greatly  with  each  year  of  life ;  so  that  children  near  puberty  rarely  die  from 


114 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


this  malady  unless  poorly  nourished  or  badly  neglected  (Fig.  28) .  If  broncho- 
pneumonia develops,  the  prognosis  must  be  guarded  in  direct  proportion  to  the 
youth  of  the  child.  Thus,  out  of  a  series  of  408  cases  of  measles  complicated 
in  this  manner,  290,  or  71  per  cent.,  died.    This,  however,  is  an  exceedingly 

high  figure  and  by  no  means  represents 
the  death  rate  in  a  general  run  of  cases 
in  which  all  ages  and  conditions  of 
patients  are  considered.  Under  these 
conditions  the  death  rate  for  all  cases 
is  probably  about  35  per  cent.  Thus, 
Holt  speaks  of  an  epidemic  in  the 
Nursery  and  Child's  Hospital  in  New 
York  in  1892,  in  which  the  mortality 
was  35  per  cent.,  and  in  9239  cases  of 
measles  occurring  in  France,  prin- 
cipally in  the  hospitals  of  Paris,  there 
were  3096  deaths,  or  a  mortality  of 
33.5  per  cent.  It  is,  moreover,  to  be 
carefully  borne  in  mind  that  hospital 
or  asylum  statistics  are  utterly  worth- 
less in  determining  the  death  rate 
for  ordinary  private  practice,  be- 
cause most  of  these  hospital  cases 
are  primarily  in  bad  health  or  are 
brought  to  the  hospital  desperately  ill 
from  neglect.  Including  all  cases  in 
private  practice,  the  mortality  should 
not  be  over  5  to  10  per  cent.,  and  in 
many  epidemics  it  is  much  lower,  even 
in  institutions  and  where  good  nursing 
is  not  to  be  had.  Thus,  in  an  epi- 
demic in  the  Faroe  Islands  only  8  cases 
out  of  1123  cases  died,  and  at  the 
Boston  City  Hospital  only  5  were  fatal 
out  of  366. 

Treatment. — When  measles  runs  a 
natural  course,  little  or  no  medication 
is  required;  for,  as  it  is  a  self-limited 


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Sl^owing  the  mortality  of  measles  according    ^-^^  J^    ^anUOt    bc     juguktcd.      The 

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to 


Courtenay  Fox. 


therapeutics  of  an  attack  of  measles, 
therefore,  consists  in  the  prevention  of 
complications  and  the  relief  of  symptoms  which  are  so  prominent  as  to  be 
distressing  or  perhaps  even  dangerous.  In  order  to  avoid  irritation  of  the 
eyes  and  to  lessen  the  suffering  due  to  photophobia  the  sick-room  should 
be  kept  dark.  Light  bed-covering  should  be  employed,  and  heavy  quilts 
which  cause  the  child  to  perspire  unnecessarily  are  to  be  tabooed.  As  a 
mild  gastrointestinal  catarrh  is  often  present  with  the  fever,  food  should 
be  light,  given  at  frequent  intervals,  and  should  consist  chiefly  in  nutritious 


RUBELLA  115 

fluids,  such  as  the  various  broths,  milk,  an  Q.gg  boiled  only  one  minute,  and 
similar  substances. 

If  the  irritation  of  the  conjunctivae  is  marked,  eye  drops,  composed  of  4 
grains  of  common  salt  and  4  grains  of  boric  acid  to  an  ounce  of  water,  may 
be  used  several  times  a  day ;  and  if  the  cough  is  sufficiently  constant  to  pre- 
vent sleep,  it  may  be  controlled  by  small  doses  of  codeine,  J^-  of  a  grain 
once,  twice,  or  thrice  in  twenty-four  hours,  to  a  child  of  two  years,  or 
heroin  may  be  used.  Should  the  fever  reach  105°  there  is  usually  no 
necessity  of  reducing  it  owing  to  its  short  duration,  but  the  child's  comfort 
can  be  much  increased  by  sponging  it  with  tepid  water  and  alcohol, 
or  even  with  water  at  70°,  using  active  friction  at  the  same  time.  These 
cases  do  not  need  an  immersion  bath  and  it  is  not  wise  to  give  it  to  them. 
If  the  circulation  has  a  tendency  to  fail,  carbonate  of  ammonium  in  the 
dose  of  2  grains  four  or  five  times  a  day  may  be  given  in  syrup  of  acacia. 
For  the  relief  of  headache  a  small  ice-bag  may  be  applied  to  the  head,  pro- 
vided that  a  nurse  is  at  hand  to  prevent  it  from  slipping  down  upon  the  neck, 
or  about  the  ears,  and  also  to  prevent  it  from  wetting  the  pillow.  It  should 
usually  be  wrapped  in  a  towel  to  prevent  the  accumulation  of  moisture, 
and  also  to  protect  the  head  from  too  great  cold. 

In  cases  in  which  the  rash  is  not  well  developed  and  the  skin  is  dusky  in 
hue,  the  brief  use  of  a  hot  pack  is  very  useful. 

Should  diphtheria  arise  as  a  complication  antitoxin  should  be  given. 

After  the  disease  has  run  its  course,  convalescence  should  be  aided  by 
the  use  of  simple  bitter  tonics,  the  hypophosphites,  iron,  and  arsenic,  and, 
if  malnutrition  is  present,  cod-liver  oil  proves  itself  an  exceedingly  valuable 
remedy,  since  it  improves  the  nutrition  of  the  patient  and  exercises  a  most 
beneficial  effect  upon  the  mucous  membranes.  If  the  bronchitis  is  per- 
sistent and  a  considerable  quantity  of  mucus  is  in  the  bronchial  tubes,  3 
grains  of  chloride  of  ammonium  may  be  given  in  a  teaspoonful  of  fluid 
extract  of  liquorice  and  a  teaspoonful  of  water  three  or  four  times  a  day, 
and  gentle  counterirritation  in  the  form  of  chloroform  liniment  or  ammonia 
liniment  may  be  applied  to  the  chest.  After  the  eruption  has  disappeared 
and  desquamation  has  begun,  the  child  should  be  bathed  daily  in  order 
that  its  skin  may  be  thoroughly  rid  of  dead  epithelium;  and  before  the 
patient  plays  with  other  children  the  scalp  should  be  shampooed  several 
times,  since  not  infrequently  desquamation  continues  upon  the  head  long 
after  it  has  ceased  upon  the  trunk. 

For  a  long  time  after  the  rash  of  measles  has  disappeared  the  greatest 
care  should  be  exercised  that  the  patient  is  protected  from  exposure,  as 
acute  and  chronic  catarrhs  of  any  or  all  the  mucous  membranes  are  very 
prone  to  develop  under  very  slight  provocation. 


RUBELLA. 

Definition. — Rubella  is  sometimes  called  "  rotheln  "  or  "  German  measles," 
"  rubeola  notha,"  "  epidemic  roseola,"  and  "  hybrid  scarlet  fever."  It  is 
a  disease  distinct  from  measles  and  scarlet  fever,  and  is  one  of  the  mild 


116  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

acute  infectious  eruptive  diseases  of  childhood.  It  rarely  affects  adults. 
Johann  Seitz  studied  an  epidemic  involving  21  families  and  comprising  111 
cases,  and  found  that  4  per  cent,  of  all  adults  were  attacked.  The  ratio 
for  children  was  much  higher,  being  64  per  cent.  Rubella  occurs  as  a  rule 
in  epidemics,  but  sporadic  cases  are  met  with. 

Etiology. — The  micro-organism  of  this  affection  has  not  been  isolated, 
but  the  disease  is  distinctly  infectious  and  is  contracted  by  one  patient 
from  another,  not  only  by  contact,  but  also  by  clothing  and  through  the  air. 

Symptoms. — After  a  period  of  incubation  lasting  from  ten  to  twelve 
days  the  stage  of  onset  manifests  itself  by  chilliness,  general  malaise,  some 
running  of  the  eyes  and  nose,  and  headache.  As  early  as  the  first  day  of 
the  illness  the  rash  appears  as  a  macular  eruption  which  is  red  in  hue,  but 
is  not  scarlet.  This  is  a  so-called  "rose  rash."  In  some  cases,  however, 
this  rash  does  not  develop  till  the  third  day.  The  rash  shows  itself  first  on 
the  face,  then  on  the  anterior  surface  of  the  thorax,  and  speedily  covers  the 
entire  body.  It  can  often  be  seen  on  the  soft  palate  before  it  appears  on 
the  skin,  in  the  form  of  bright  rosy-red  spots  (Forchheimer's  spots).  The 
individual  macules  may  remain  separate  or  coalesce.  In  some  instances, 
however,  the  skin  has  a  diffuse  redness  like  that  of  scarlet  fever,  but  it  is 
less  scarlet.  The  macules  last  about  three  days  and  then  fade  gradually, 
being  usually,  but  not  always,  followed  by  slight  scaly  desquamation.  The 
skin  is  rarely  as  much  stained  after  the  rash  disappears  as  it  is  after 
measles. 

A  noteworthy  sign  to  be  sought  for  is  the  enlargement  of  the  hjmph  glands 
below  the  ears,  in  the  lateral  cervical  region,  and  at  the  back  of  the  neck. 
Sometimes  the  inguinal  glands  are  also  affected. 

The  febrile  movement  is  usually  very  moderate,  the  temperature  often 
not  rising  above  100°.  The  general  symptoms  may  be  so  mild  that  the 
attention  of  the  nurse  is  first  called  to  the  illness  by  the  rash. 

If  the  child  is  carefully  nursed  and  clothed  and  properly  fed,  the  malady 
pursues  a  rapid  course  to  recovery.  If,  on  the  other  hand,  the  child  be  feeble 
and  exhausted,  this  disease  may  be  more  severe  in  its  manifestation  and  be 
accompanied  by  otitis  media,  catarrhal  pneumonia,  or  even  albuminuria 
and  jaundice. 

Diagnosis. — Rubella  is  to  be  separated  from  true  measles  by  the  moderate 
character  of  the  coryza,  by  the  absence  of  Koplik's  spots,  the  early  swelling 
of  the  glands  in  the  neck,  and  by  the  absence  of  bronchial  irritation.  From 
scarlet  fever  it  is  separated  by  the  absence  of  high  fever  and  of  the  well- 
diffused  scarlet  rash,  which  is  not  macular,  and  by  the  absence  of  the  sore 
throat  of  that  affection.  While  these  differential  points  are  of  value  in 
many  cases,  it  is  a  fact  that  in  some  instances  a  diagnosis  is  most  difficult 
until  the  case  has  been  studied  for  some  days,  when  the  mildness  of  the 
symptoms  and  the  brevity  of  the  attack  aid  in  deciding  that  neither  measles 
nor  scarlatina  are  present. 

Treatment. — ^The  treatment  of  rotheln  consists  in  rest  in  bed  and  the  use 
of  spirit  of  nitrous  ether  and  citrate  of  potash  as  diuretics  and  diaphor- 
etics, and  in  attention  to  the  bowels  and  kidneys.  Exposure  to  cold  should, 
of  course,  be  avoided. 


MUMPS  117 


MUMPS. 


Definition. — Mumps,  or  epidemic  parotitis,  is  an  acute  infectious  disease 
affecting  the  parotid  gland  and  accompanied  by  mild  systemic  symptoms 
which  may  not  be  severe  enough  to  demand  notice.  It  occurs  in  the  great 
majority  of  instances  during  childhood,  between  the  fourth  year  and  puberty, 
and  one  attack  protects  the  patient  from  a  second. 

Etiology. — Mumps  is  usually  conveyed  by  contact  from  one  patient  to 
another,  but  it  may  be  carried  by  a  third  person  or  by  garments  to  a  sus- 
ceptible individual.  It  is  contagious  from  the  beginning  to  the  end  of  the 
attack,  and  it  is  probable  that  persons  who  have  so  far  recovered  as  to 
have  no  visible  swelling  of  the  parotids  can  still  transmit  the  disease.  For 
this  reason  the  patient  should  be  kept  separate  from  other  children  .for  a 
period  of  ten  days  after  the  swelling  disappears.  It  is,  however,  a  note- 
worthy fact  that  mumps  is  by  no  means  so  infectious  as  are  the  eruptive 
fevers,  and  many  children  escape  the  disease  even  when  thoroughly  exposed 
to  it. 

The  period  of  incubation  is  uncertain.  Sometimes  it  is  brief,  in  other 
cases  surprisingly  prolonged.  Holt,  in  42  cases  collected  from  literature, 
found  it  varied  from  three  to  twenty-five  days.  In  all  probability  it  is  about 
fifteen  days  in  the  average  case. 

Pathology. — The  chief  change  in  mumps,  and,  indeed,  the  only  one  which 
is  characteristic,  is  the  swelling  of  one  or  both  parotid  glands.  The  swelling 
is  due  to  a  primary  parenchymatous  inflammation,  followed  by  involvement 
of  the  connective  tissue  of  the  gland  as  well.  Rarely  the  other  salivary 
glands  become  swollen,  and  still  more  rarely  the  parotids  suppurate.  This 
result  occurs  only  in  children  who  are  impoverished  by  other  diseases,  and 
is  due  to  an  invasion  of  the  gland,  through  the  duct  of  Steno,  by  pyogenic 
organisms. 

Symptoms. — The  chief  symptoms  of  mumps,  aside  from  the  swelling  of 
the  glands,  is  pain  in  the  parotid  region,  which  is  greatly  increased  by  moving 
the  jaw  or  by  taking  any  sour  material  into  the  mouth.  In  susceptible 
persons  there  may  be  some  feeling  of  malaise  or  wretchedness  and  the  fever 
may  reach  103°  or  104°  on  the  first  day,  although  a  temperature  of  102°  is 
more  commonly  met  with. 

The  swelling  of  the  gland  is  usually  at  its  height  by  the  third  day  and 
remains  at  this  stage  for  two  or  three  days  more,  when  it  begins  to  decrease 
and  then  gradually  disappears.  In  some  cases  the  degree  of  swelling  is  so 
marked  that  the  tissues  of  the  face  and  neck  share  in  it  to  such  an  extent 
that  the  patient  is  unrecognizable.  The  swelling  is  bilateral  in  the  vast 
majority  of  instances,  but  it  often  begins  in  a  single  gland. 

Complications  and  Sequelae. — While  mumps  is  a  very  mild  disease  in 
many  cases,  it  at  times  becomes  severe,  chiefly  because  of  the  complications 
which  arise.  These  are  more  frequently  met  with  in  adults  than  in  chil- 
dren. The  most  common  of  them  is  orchitis,  which  may  be  bilateral  and 
severe  enough  to  cause  the  patient  intense  suffering  and  force  him  to 
remain  in  bed. 


118  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Before  the  age  of  puberty  the  testicles  are  rarely  involved,  but  after 
puberty  orchitis  is  a  frequent  complication.  Bich  collected  statistics  on 
862  cases  of  mumps  occurring  in  young  men  between  the  ages  of  eighteen 
and  twenty-five  years,  and  found  that  29  per  cent,  of  the  number  were 
affected  with  orchitis.  Granvier's  record  of  cases  occurring  in  the  French 
army  gives  a  percentage  of  23.  Usually  only  one  testicle  is  involved.  Thus, 
of  159  cases  collected  from  various  sources  152  were  unilateral.  The  com- 
bined statistics  of  Grangier  and  Bich,  based  on  309  cases  of  orchitis,  showed 
that  atrophy  of  the  testicle  resulted  in  176  cases,  or  57  per  cent.  Active 
exercise  seems  to  predispose  to  this  complication,  and  it  seems  much  more 
frequent  in  some  epidemics  than  in  others.  Some  years  ago  mumps  appeared 
in  an  epidemic  among  the  students  of  the  Jefferson  Medical  College,  and 
a  very  large  proportion  of  those  attacked  developed  metastasis  to  a  testi- 
cle. The  development  of  the  orchitis  is  usually  associated  with  a  second 
rise  of  temperature  and  a  general  sense  of  illness  which  is  in  excess  of  that 
present  at  the  onset  of  the  primary  illness.  The  swelling  of  the  testicle 
lasts  about  a  week,  and  after  the  acute  inflammation  has  passed  the  gland 
may  be  enlarged  for  a  long  period  of  time. 

Cases  have  been  recorded  in  which  convulsions,  meningitis,  and  arthritis 
have  developed  as  complications  of  mumps. 

In  young  girls  who  have  mumps,  secondary  swelling  of  the  mammary 
glands,  of  the  ovaries,  or  of  the  labiae  may  develop,  but  secondary  changes 
are  far  more  rare  among  females  than  are  those  detailed  as  occurring  in 
males. 

Simonin,  a  French  surgeon,  has  reported  10  cases  of  pancreatitis  which 
occurred  among  652  cases  of  mumps.  The  symptoms  of  pancreatitis 
appeared  from  the  first  to  the  twelfth  day  of  the  disease,  but  usually  from 
the  third  to  the  sixth  day,  and  lasted  from  two  to  seven  days.  The  chief 
symptoms  were  epigastric  pain  and  vomiting,  but  no  glycosuria.  Cuche 
has  stated  that  he  found  epigastric  tenderness  present  in  20  out  of  26  cases 
of  mumps. 

Treatment. — The  treatment  of  mumps  consists  in  the  use  of  mild  alkaline 
diuretics  and  rest,  for  if  the  patient  can  be  persuaded  to  avoid  exercise  and 
to  use  a  light  diet  active  medication  is  never  needed.  Sour  foods  and  acid 
drinks  are  to  be  avoided,  for  when  they  are  taken  into  the  mouth  they  cause 
severe  pain.  If  the  febrile  movement  is  marked  and  the  pulse  is  quick  1 
minim  of  tincture  of  aconite  every  two  hours  is  useful  for  the  first  twenty- 
four  hours  of  the  malady.  By  decreasing  the  congestion  in  the  gland  the 
aconite  not  only  moderates  the  inflammation,  but  also  diminishes  the  pain. 
Local  applications  to  the  swollen  parotids  are  usually  not  needful,  but  if 
any  are  employed  they  should  be  hot  rather  than  cold.  Should  metastasis 
to  the  testicle  occur,  rest  in  bed  is  imperative,  since  taking  exercise  at  such 
a  time  causes  great  increase  in  the  swelling  and  pain.  The  scrotum  should 
be  supported  by  a  bandage.  Aconite  in  full  doses  and  citrate  of  potassium 
are  useful  remedies  when  the  swelling  of  the  scrotal  contents  is  severe. 


WHOOPING-CO  UGH  1 1 9 


WHOOPING-COUGH. 


Definition. — Whooping-cough  is  sometimes  called  Pertussis,  and  is  an 
infectious  disease  chiefly  met  with  in  childhood.  It  consists,  as  its  name 
implies,  in  a  respiratory  disorder  which  is  peculiar  in  two  particulars.  The 
patient  in  the  well-developed  stage  of  the  disease  is  seized  at  varying  inter- 
vals by  a  paroxysm  of  coughing  which  is  so  constant  and  violent  that  in  a 
few  seconds  the  quantity  of  residual  air  in  the  thorax  is  greatly  decreased 
below  the  normal  amount,  producing  in  this  way  a  sense  of  suffocation  and 
flushing  of  the  face  or  cyanosis.  Immediately  after  the  cough  ceases  the 
patient  endeavors  to  take  a  deep  inspiration  to  compensate  for  the  excessive 
expiratory  effort,  when  there  is  developed  a  narrowing  of  the  glottic  open- 
ing so  that  it  is  very  difficult  for  the  air  to  enter  the  larynx.  This  violent  effort 
to  draw  air  through  a  narrow  opening  produces  a  peculiar  "whoop,"  which 
gives  the  disease  its  name.  The  name  "whooping-cough"  does  not  signify 
that  the  cough  is  whooping  in  character,  but  that  there  is  a  cough  followed 
by  a  whooping  sound. 

Distribution  and  Frequency. — Whooping-cough  is  a  disease  which  is  found 
in  all  parts  of  the  world,  and  is  apt  to  occur  in  epidemic  form,  particularly 
during  the  months  of  March  and  April.  It  is  least  prevalent  in  September 
and  October.  As  already  stated,  it  is  particularly  prone  to  attack  children; 
so  that  few  persons  reach  adult  years  without  suffering  from  an  attack.  If 
they  do  escape  during  childhood,  they  may  suffer  from  it  even  in  advanced 
old  age.  Even  sucklings  are  attacked  by  it,  and  in  this  class  of  cases  it  is 
an  exceedingly  fatal  malady.     It  is  also  a  grave  disease  in  old  age. 

Whooping-cough  attacks  both  sexes  with  about  equal  frequency.  Rosen 
collected  43,393  cases,  of  which  21,850  occurred  in  boys  and  21,543  in 
girls.  If  the  statistics  of  Goodhart,  Comly,  and  Rilliet  and  Barthez  are 
combined,  it  is  found  that  in  4157  cases  1868  occurred  in  boys  and  2289  in 
girls. 

Etiology. — The  cause  of  whooping-cough  is  certainly  a  micro-organism, 
and  several  investigators  claim  to  have  isolated  it.  Unfortunately  no  uni- 
formity of  opinion  exists  as  to  the  specific  organism  of  this  disease.  In 
1887  Afanassjew,  of  St.  Petersburg,  isolated  from  the  sputum  of  children 
affected  with  whooping-cough  a  short,  slender,  motile,  anaerobic  bacillus, 
cultures  from  which,  when  injected  into  dogs  and  rabbits,  produced  a  dis- 
ease similar  to  pertussis.  This  organism  was  found  afterward  by  Szemte- 
schenko,  of  St.  Petersburg,  and  Koplik,  of  New  York.  In  1892  Ritter,  of 
Berlin,  described  a  diplococcus  which  he  thought  was  specific,  and  more 
recently  a  bipolar  bacillus  resembling  the  Bacillus  influenzm  has  been  con- 
sidered the  pathogenic  agent  by  Czaplewski  and  Hensel  (1897)  and  by 
Arnheim  (1900).  Jochmann,Krause,and  Moltrecht, of  Hamburg  (1903),  also 
have  isolated  an  organism  resembling  the  bacillus  of  influenza,  but  differing 
from  the  one  described  by  Czaplewski  and  Hensel,  which  they  have  named 
Bacillus  'pertussis  Eppendorf,  and  which  they  believe  plays  an  important 
role  in  the  production  of  whooping-cough,  and  also  the  bronchopneumonia 
which  complicates  it.     Davis  (1906),  found  this  organism  in  the  sputum 


120  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

of  almost  all  of  a  large  number  of  pertussis  patients.  Morphologically 
and  culturally  it  is  identical  with  t|ie  influenza  bacillus  which  he  believes 
it  should  be  called.  The  evidence  at  hand  does  not  prove  it  specific  for 
whooping-cough.  Leuriaux,  of  Brussels  (1902),  ascribes  the  disease  to  an 
aerobic  bacillus  ovoid  in  form  and  having  rounded  ends.  This  organism 
grows  on  all  ordinary  culture  media  and  stains  with  aniline  dyes  and  by 
Gram's  method. 

Whooping-cough  so  often  occurs  in  close  connection  with  an  attack  of 
measles  that  the  two  diseases  must  be  regarded  as  nearly  related.  _ 

The  exact  period  of  incubation  is  unknown.  It  probably  varies  greatly 
in  different  persons  and  in  different  epidemics.  Sometimes  it  seems  to  be 
as  short  as  two  days;  in  others  it  apparently  takes  ten  days,  or  even  longer 
than  this.  The  infection  is  perhaps  conveyed  by  the  air  and  certainly  is 
transmitted  by  the  sputum,  either  by  the  direct  expulsion  of  particles  of  it 
into  the  face  and  air-passages  of  the  child  not  as  yet  affected,  or  upon 
clothing  or  the  food,  so  that  it  gains  access  to  the  respiratory  tract. 
The  infection  is  most  marked  during  the  acme  of  the  malady,  but  is  active 
at  all  times  during  the  attack,  and  probably  for  a  week  or  more  after  the 
cough  has  lost  all  characteristics  of  the  disease.  Children  who  have  suf- 
fered from  this  disease  should  not  come  in  contact  with  those  who  have  not 
had  it  for  three  or  four  weeks  after  the  last  whoop  is  heard. 

Pathology  and  Morbid  Anatomy. — Primarily  the  only  noteworthy  change 
present  in  the  thoracic  organs  during  whooping-cough  is  a  mild  catarrhal 
state  of  the  mucous  membranes  of  the  whole  respiratory  tract.  Secondarily, 
the  pathological  results  are  far  more  serious  in  that  the  bronchitis  and  the 
great  strain  thrown  upon  the  heart  by  asphyxia  result  in  conditions  which 
may  destroy  the  patient,  death  usually  ensuing  in  fatal  cases  from  exhaustion 
due  to  excessive  cough,  lack  of  food,  and  lack  of  rest  combined  with  broncho- 
pneumonia, which  in  turn  is  also  due  to  several  causes  of  which  lowered 
vital  resistance  and  a  feeble  heart  are  important  factors.  Then,  too,  in  the 
violent  inspiratory  efforts  of  the  patient  small  particles  of  food  or  infected 
mucus  may  be  drawn  into  the  smaller  bronchi  and  so  produce  local  infec- 
tion. As  stated  in  the  article  on  Bronchiectasis,  this  condition  in  its  cylin- 
drical form  may  be  caused  by  pertussis.  (For  further  pathological  changes 
see  Complications.) 

Symptoms. — The  symptoms  of  whooping-cough  have  already  been 
described  to  some  extent.  Usually  the  patient  develops  what  is  apparently 
a  slight  cold  in  the  head  and  thorax,  followed  by  a  cough  which  may  be 
described  as  nervous  or  spasmodic.  Perhaps  the  word  "sudden "  can  best  be 
applied  to  it  in  the  sense  that  each  coughing  spell  is  sudden  in  onset.  At  first 
there  may  be  only  one  or  two  coughs,  but  soon  they  come  in  series,  which 
day  by  day  increase  in  frequency  and  violence.  Sometimes  the  whoop,  which 
occurs  at  the  end  of  the  series  of  short,  sharp  coughs,  does  not  appear  for 
several  days.  It  may  never  appear  in  the  mild  type  of  case,  the  patient  suf- 
fering only  from  the  paroxysms  of  cough  which  exhaust  the  chest  of  air  to 
a  considerable  degree.  When  the  whoop  does  come  on  it  appears  at  the  end 
of  the  repeated  coughs,  and  is  caused  by  the  attempt  to  inspire  air  suddenly 
and  forcibly  through  the  narrowed  glottis.     The  whole  paroxysm,  there- 


WHOOPING-COUGH  121 

fore,  consists,  first,  of  a  series  of  coughs  which  increase  in  rapidity  as  one 
would  count  1,  2,  3,  4,  5,  6,  7,  8,  9,  10,  11,  12  with  increasing  speed,  and, 
secondly,  in  the  long-drawn  inspiratory  whoop.  Owing  to  the  violence  of 
the  cough  the  face  becomes  suffused,  the  tears  run,  and  the  patient  may 
even  seem  more  or  less  convulsed.  The  frequency  of  the  paroxysms  varies 
very  greatly  in  different  cases  and  at  different  times  in  the  twenty-four 
hours.  Some  patients  cough  but  once  or  twice  a  day,  while  others  are 
seized  every  few  minutes.  Usually  the  child  is  greatly  frightened  if  the 
attack  is  severe,  and  often  it  soon  learns  to  recognize  the  early  signs  of  an 
approaching  seizure  and  runs  to  its  mother  or  nurse  for  help.  The  attacks 
are  provoked  by  crying,  laughing,  eating  or  drinking,  and  by  inhalation 
of  dust-laden  air.  Between  the  paroxysms  perfect  quiet  and  respiratory 
comfort  may  be  present  unless  complications  arise.  In  the  severe  cases 
nose-bleed  and  ecchymoses  of  the  conjunctiva  may  occur  and  blood  may 
come  from  the  ears  and  mouth.  The  convulsive  efforts  during  the  cough 
very  frequently  cause  vomiting,  and  at  times  the  urine  or  feces  may  be 
forcibly  expelled,  or  they  escape  after  an  attack  because  of  profound  exhaus- 
tion and  the  relaxation  produced  by  the  asphyxia.  A  nodular  infiltration, 
or  an  ulcer,  at  the  frsenum  of  the  tongue  is  often  produced  by  irritation  of  the 
projecting  organ  upon  the  lower  incisor  teeth.  The  circulation  is  usually 
not  much  affected  save  during  the  paroxysm,  when  it  is  labored,  owing  to 
the  asphyxia.  Between  the  paroxysms  it  may  be  rapid  and  feeble  if  the 
attacks  are  frequent  and  severe  enough  to  strain  and  dilate  the  heart.  Some 
clinicians  assert  that  permanent  cardiac  feebleness  and  dilatation  may 
result  from  this  disease. 

In  severe  cases  in  young  children  and  in  feeble  individuals  great  asthenia 
may  be  produced  by  the  violence  of  the  spasm,  the  loss  of  sleep,  and  the 
loss  of  food  from  vomiting,  which  may  occur  at  every  paroxysm. 

Inspection  of  the  bared  chest  during  the  inspiratory  part  of  each  attack 
reveals  in  the  stage  of  inspiration  deep  retraction  of  the  intercostal  spaces, 
of  the  episternal  notch,  and  of  the  epiclavicular  areas.  The  epigastrium  is 
also  retracted,  for  all  the  auxiliary  muscles  of  respiration  endeavor  to  aid 
in  the  drawing  in  of  air.  Auscultation  of  the  chest,  particularly  over  the 
posterior  surface,  almost  always  reveals  bronchial  rales,  due  to  the  bron- 
chitis which  is  present  in  all  cases,  even  if  they  be  mild.  Care  should  always 
be  exercised  that  this  bronchitis  is  not  increased  by  exposure  to  cold  and 
dampness,  since  it  is  exceedingly  prone  to  develop  into  bronchopneumonia, 
particularly  in  young  children  and  old  persons.  Indeed,  it  may  be  said  that 
the  high  mortality  of  the  disease  is  due  almost  entirely  to  this  complica- 
tion. 

A  number  of  clinicians,  particularly  Cima  and  Meunier,  have  shown  that 
even  in  the  very  early  stages  of  pertussis  there  is  present  a  very  extraordinary 
degree  of  leukocytosis.  This  leukocytosis  is  largely  composed  of  lympho- 
cytes, the  polymorphonuclear  cells  being  relatively  decreased.  As  in  most 
infectious  diseases,  a  small  amount  of  albumin  is  found  in  the  urine  in 
the  majority  of  cases. 

The  duration  of  whooping-cough  varies  from  six  to  eight  weeks,  more 
commonlv  the  latter  than  the  former. 


122  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Complications. — The  complications  of  whooping-cough  are  chiefly  con- 
nected with  the  respiratory  tract.  Bronchopneumojiia,  as  just  stated,  is 
very  common,  and  follows  the  bronchitis  which  usually  is  developed  in  the 
earher  stages  of  the  disease.  It  is  particularly  apt  to  attack  young  children 
and  to  occur  in  the  winter  months.  Sometimes  a  true  lobar  pneumonia 
develops. 

In  nearly  all  cases  of  whooping-cough  a  moderate  degree  of  compensatory 
emphysema  comes  on  because  of  the  violent  respiratory  efforts  of  the  patient, 
and  rarely  this  strain  on  the  tissues  of  the  lungs  results  in  the  rupture  of 
an  air  vesicle  and  the  development  of  interstitial  or  interlobular  emphy- 
sema. In  other  instances  the  quantity  of  air  which  escapes  in  this  way  is 
very  large  and  infiltrates  the  tissues  of  the  mediastinum,  the  subcutaneous 
tissues  of  the  chest,  and  in  extreme  cases  those  of  the  entire  body.  Instances 
of  this  condition  have  been  reported  by  Gelmo,  Ferrell,  and  Bierbaum, 
and  have  usually  proved  fatal.  Cases  are  also  recorded  in  which  pneumo- 
thorax has  been  produced.  It  is  by  no  means  uncommon,  particularly 
among  the  children  of  the  poorer  classes,  for  whooping-cough  to  be  followed 
by  pulmonary  tuberculosis,  probably  because  of  the  lowered  vital  resistance 
of  the  patient.  Another  complication  of  importance,  although  it  has  been  de- 
scribed as  a  symptom,  is  vomiting,  which  if  it  becomes  constant  is  a  serious 
condition,  particularly  in  infants,  since  it  may  cause  death  from  asthenia. 

The  bronchial  glands  are  nearly  always  enlarged  and  may  be  so  much 
increased  in  size  as  to  cause  dulness  on  percussion  over  the  sternum.  The 
area  of  cardiac  dulness  is  increased  by  reason  of  the  dilatation  of  the  heart 
due  to  the  strain  thrown  upon  it  in  the  attack  of  coughing. 

Measles  and  whooping-cough  are,  as  already  stated,  very  commonly 
associated,  but  the  whooping-cough  complicates  the  measles  more  fre- 
quently than  the  measles  complicates  the  pertussis.  Sometimes  in  very 
young  children  the  disease  becomes  so  severe  that  the  spasm  of  the  cough 
seems  to  spread  to  all  the  muscles  of  the  body  and  produce  general  convul- 
sions.   These  cases  are  nearly  always  fatal. 

Paralysis  complicating  whooping-cough  is  not  common.  It  is  usually 
in  the  form  of  a  hemiplegia,  and  occurs  either  during  the  acute  period  of 
the  disease  or  as  a  sequel.  When  it  takes  place  during  the  paroxysmal 
period  it  is  due  in  the  majority  of  instances  to  meningeal  or  cerebral  hemor- 
rhage in  all  probability,  although  statistics  as  to  this  question  are  scanty. 
Twelve  cases  of  cerebral  hemorrhage  due  to  whooping-cough  have  been 
collected  by  Townsend  of  which  seven  recovered,  and  Brown  has  reported 
a  case  in  which  he  operated  for  the  relief  of  cerebral  compression  due  to 
this  cause  with  excellent  results  to  the  patient.  The  literature  of  this  subject 
has  recently  been  analyzed  by  W.  G.  A.  Robertson.  Sometimes  paraplegia 
or  monoplegia  has  occurred  during  the  stage  of  convalescence.  The 
prognosis  seems  to  be  fairly  favorable,  indicating  that  the  lesion  producing 
these  conditions  cannot  be  permanent.  Small  conjunctival  hemorrhages 
are  not  infrequent,  and  more  rarely  large  extravasations  of  blood  into  the 
conjunctival  tissues  take  place,  amounting  to  ecchymoses.  Still  more  rarely 
temporary  amblyopia  develops  as  a  result  of  disordered  circulation  in  the 
retina  or  possibly  of  an  actual  retinal  hemorrhage. 


WHOOPING-COUGH  123 

Diagnosis. — The  important  points  in  the  diagnosis  of  whooping-cough 
are  the  repeated  and  rapid  coughs  in  series  until  the  chest  is  almost  emptied 
of  air,  followed  by  a  sudden  inspiration  through  the  narrowed  glottic  open- 
ing. Some  cases  develop  only  the  series  of  short  coughs,  and  present  no 
whoop  afterward. 

Prognosis  and  Mortality. — The  prognosis  in  whooping-cough  as  in  most 
infectious  diseases,  depends  upon  the  age  of  the  child,  its  general  nutrition 
and  vital  resistance,  and  upon  the  care  the  child  can  receive.  In  general 
terms  it  may  also  be  stated  that  the  prognosis  is  not  so  good  in  winter  as  in 
summer,  as  fresh  air  is  not  so  readily  obtained  and  there  is  greater  danger 
of  exposure  to  cold  in  the  winter  months.  In  itself  whooping-cough  is  not 
a  fatal  disease.  Death  is  due  to  the  complications  which  ensue,  and  if 
these  can  be  prevented  the  patient  alv/ays  gets  well.  In  very  young  children, 
however,  it  is  almost  impossible  to  prevent  the  development  of  broncho- 
pneumonia, and  this  is  a  dangerous  condition  in  proportion  to  the  youth 
of  the  child.  In  London  wdiooping-cough  stands  second  as  a  cause  of  death 
from  the  infectious  diseases  in  children  under  two  years  of  age. 

Hagenbach,  of  Basle,  gives  the  following  mortality  statistics,  which  are 
based  on  the  cases  that  came  under  his  observation  during  a  period  of 
eleven  years :  under  one  year,  26.8  per  cent. ;  between  one  and  two  years, 
13.8  per  cent.;  between  two  and  five  years,  3  per  cent.;  between  five  and 
fifteen  years,  1.8  per  cent. 

Holt  states  that  the  mortality  for  children  under  one  year  of  age  is  25 
per  cent. 

Treatment. — It  is  vitally  important  that  children  who  have  whooping- 
cough  should  be  put  under  the  most  favorable  hygienic  conditions  as  to 
sunlight,  fresh  air,  and  equable  temperature.  In  the  summer  they  do  best 
out-of-doors  when  the  w-eather  is  not  too  cool,  if  they  are  prevented  from 
acting  imprudently,  as,  for  example,  getting  the  feet  wet.  In  winter  they 
should  be  kept  in  a  warm  room,  the  temperature  of  which  should  be  70° 
night  and  day.  The  air  of  this  room  should  also  be  moistened  by  liberating 
in  it  small  quantities  of  steam  obtained  from  a  kettle  of  boiling  water, 
from  a  croup  kettle,  or  by  dropping  pieces  of  unslaked  lime  in  a  bucket 
of  water.  This  is  an  exceedingly  important  measure  if  the  room  is  heated 
by  a  furnace,  since  the  air  from  the  ordinary  furnace  is  exceptionally  dry 
and  often  laden  with  dust,  and  these  two  causes  act  as  an  irritant  to  the 
already  irritated  respiratory  tract.  When  it  is  not  possible  to  confine  the 
child  to  a  room  which  is  heated  evenly,  a  most  excellent  method  of  treat- 
ment, particularly  in  those  cases  where  the  paroxysms  are  frequent  at 
night,  is  to  place  the  child  in  a  bronchitis  tent.  A  bronchitis  tent  consists  in 
throwing  over  a  bed  a  large  sheet  which  is  supported  several  feet  above  the 
head  of  the  child  by  means  of  broomsticks  or  poles,  which  are  tied  at  each 
corner  of  the  bed.  This  tent  can  be  made  quite  attractive  for  children  by 
decorating  it.  Into  this  tent,  at  the  foot  of  the  bed,  may  be  discharged  a 
small  quantity  of  steam  such  as  is  given  off  from  an  ordinary  kettle  of  water 
when  it  is  kept  constantly  boiling.  In  this  way  the  child's  mucous  mem- 
branes are  not  irritated  by  dry  or  cold  air,  but  on  the  contrary  are  greatly 
soothed,  and  I  have  frequently  diminished  the  number  of   paroxysms  per 


124  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

clay  at  least  one-half  by  the  institution  of  this  plan  of  treatment,  which 
has  the  additional  advantage  that  it  is  prophylactic,  and  prevents  the 
development  of  those  serious  complications  like  vomiting  and  broncho- 
pneumonia, which  are  much  aided  in  their  development  by  repeated 
and  violent  paroxysms  of  cough.  With  a  little  attention  a  child  may 
be  kept  in  such  a  bronchitis  tent  night  and  day  through  the  entire 
attack. 

In  the  way  of  drugs  there  is  no  remedy  so  efficacious  in  diminishing  the 
severity  of  the  attack  as  small  doses  of  antipyrin;  that  is  to  say,  ^  to  1  grain 
of  antipyrin  every  three  or  four  hours  to  a  child  of  one  or  two  years,  or 
2  grains  every  three  or  four  hours  to  a  child  of  five  or  six  years,  care  being 
taken  that  the  drug  does  not  too  greatly  relax  the  skin  or  depress  the  cir- 
culation. There  is  a  widespread  belief  among  the  laity  that  quinine  in 
small  doses  is  not  only  a  prophylactic  against  whooping-cough  for  other 
children  in  the  family  who  have  not  as  yet  contracted  the  disease,  but  that 
it  is  also  of  curative  value.  Some  physicians  have  used  a  spray  of  a  weak 
solution  of  quinine  in  the  throat  with  asserted  advantageous  results,  but 
its  value  is  doubtful,  and  its  bitter  taste  makes  its  use  impossible  in  a  large 
proportion  of  cases. 

The  development  of  complications,  such  as  bronchopneumonia,  neces- 
sitates the  institution  of  those  lines  of  treatment  which  will  be  found 
suggested  for  that  disease.  For  the  relief  of  the  individual  paroxysms  of 
cough  several  remedies  may  be  employed,  of  which  the  best  is  probably 
chloroform.  It  is  needless  to  say  that  this  drug  should  be  used  with 
great  caution,  and  the  patient's  parents  and  the  nurse  should  be  instructed 
never  to  use  it  on  a  cloth,  but,  when  the  paroxysm  is  threatened,  to  pour 
the  remedy  over  the  back  of  the  hand  and  place  the  hand  under  the 
child's  nose.  Under  these  circumstances  a  sufficient  quantity  of  the  chloro- 
form is  often  inhaled  to  relax  the  spasm,  without  producing  any  of  the 
marked  physiological  effects  which  would  certainly  be  obtained  to  an  un- 
desirable degree  if  the  drug  were  poured  on  to  a  napkin.  This  method 
also  prevents  an  overdose  of  chloroform  being  given,  since  the  excess  of 
the  drug  rapidly  runs  off  the  hand  or  evaporates.  As  the  hurry  of  an 
approaching  paroxysm  often  makes  the  attendant  careless  as  to  the  quantity 
which  is  poured  out  of  the  bottle,  the  physician  should  insist  that  the  chloro- 
form be  used  in  no  other  way  than  that  which  has  just  been  described.  If 
the  paroxysms  are  too  severe  to  be  controlled  in  this  way,  nitrite  of  amyl 
may  be  occasionally  employed. 

An  innumerable  array  of  drugs  have  been  recommended  for  the  palliation 
and  cure  of  whooping-cough.  Suffice  it  to  say  that  most  of  them  are  entirely 
useless.  Even  such  powerful  nervous  sedatives  as  the  bromides  cannot  act  ad- 
vantageously in  many  of  these  cases,  and  the  use  of  more  powerful  ones  such 
as  chloral  and  opium  are  contraindicated  for  evident  reasons.  The  physician 
should  always  remember  that  whooping-cough  is  a  disease  which  is  bound 
to  run  its  course,  uninfluenced  in  its  duration  by  any  treatment  which  he 
can  employ.  The  most  that  the  physician  can  do  is  to  prevent  complica- 
tions, treat  them  if  they  arise,  and  endeavor  to  modify  the  frequency  and 
severity  of  the  individual  paroxysms,  being  careful  in  so  doing  that  the 


INFLUENZA  125 


remedy  is  not  worse  than  the  disease,  in  the  sense  that  it  produces  digestive 
or  circulatory  disorders  which  are  distinctly  disadvantageous. 


INFLUENZA. 

Definition. — Influenza  is  sometimes  called  la  Grippe.  It  is  a  pandemic 
disease;  that  is,  one  which  appears  in  widely  separated  parts  of  the  world 
simultaneously.  It  is  also  highly  infectious,  and  the  infection  is  produced 
by  the  bacillus  of  Pfeiffer.  Influenza  of  this  type  is  to  be  separated,  theo- 
retically at  least,  from  that  condition  sometimes  called  "common  cold"  or 
"coryza, "  which  often  causes  somewhat  similar  symptoms  in  a  milder  form, 
although  during  the  presence  of  an  epidemic  of  la  Grippe  the  differential 
diagnosis  may  be  impossible.  At  the  present  time  the  term  "influenza"  is 
often  employed  when  the  physician  is  unable  to  reach  a  diagnosis,  and  as  a 
consequence  is  greatly  abused,  particularly  in  the  early  stages  of  typhoid 
fever  and  tuberculosis. 

Leichtenstern  has  divided  the  disease  into  two  varieties,  namely,  true 
epidemic  influenza  (influenza  vera)  due  to  the  bacillus  of  Pfeiffer,  and 
endemic  influenza  due  to  the  same  cause  and  occurring  for  some 
years  after  an  epidemic  has  been  present.  Both  of  these  forms  are  to  be 
separated  from  ordinary  pseudo-epidemic  influenza  or  an  attack  of  ordinary 
cold  in  the  head.  A  peculiarity  of  true  influenza  in  its  epidemic  form  is 
the  large  percentage  of  persons  which  it  attacks  within  a  short  space  of 
time,  more  than  any  other  epidemic  disease  except  dengue. 

History. — At  various  times  in  the  past  great  epidemics  have  broken  out 
and  raged  over  the  entire  world,  and  have  been  followed  by  long  periods  of 
immunity.  Thus,  when  the  great  epidemic  of  1889  occurred,  only  a  few 
physicians,  and  they  of  advanced  years,  had  ever  seen  a  case,  for  the  previous 
epidemic  had  occurred  in  1847  and  1848. 

Pandemics  have  occurred  during  the  last  century  in  1830-33,  1836-37, 
1847-48,  and  1889-90.  In  1889  the  disease  began  in  remote  parts  of  Russia 
in  October,  reached  Moscow  in  November,  ten  weeks  later  it  got  to  Berlin, 
a  month  later  to  London,  and  soon  after  to  New  York  and  Philadelphia, 
and  thence  it  spread  all  over  the  continent  of  North  America.  Within  the  next 
few  months  nearly  the  whole  civilized  world  was  affected  by  it.  Since  the 
last  outbreak  the  disease  has  been  endemic,  but  it  is  an  attenuated  form  of 
the  infection.  An  individual  locality  is  rarely  subject  to  an  epidemic  for 
more  than  two  months,  but  sporadic  outbreaks  occur  for  a  long  period 
afterward. 

Etiology. — It  is  interesting  to  note  that  the  word  influenza  is  derived  from 
the  Latin  sentence  ab  coeli  occultes  quadam  influentia — from  some  hidden 
influence  in  the  sky.  Influenza,  if  entirely  dependent  upon  a  micro-organism 
for  its  infectious  character,  must  also  be  dependent  upon  certain  telluric 
influences,  at  present  unknown,  which  render  the  human  race  more  suscep- 
tible to  the  effects  of  the  germ  at  certain  times  or  which  render  the  germ 
more  capable  of  producing  infection  at  certain  periods. 

There  are  two  chief  factors  involved  in  the  production  of  an  attack  of 


126  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

influenza,  namely,  the  presence  of  the  bacillus,  usually  received  directly 
from  another  patient  by  contact,  or  through  the  air;  and,  second,  atmos- 
pheric states  which  are  favorable  to  the  growth  of  the  germ  or  to  the 
production  of  individual  susceptibility.  A  third  factor,  always  of  importance 
in  connection  with  infectious  diseases,  is  the  presence  of  pre-existing 
disease  which  decreases  the  general  vital  resistance  of  the  patient. 

The  bacillus  of  Pfeiffer  was  first  isolated  by  that  investigator  in  1S92. 
The  organism  is  small  and  non-motile,  and  can  be  well  stained  by  Loeffler's 
methylene  blue  or  by  well-diluted  watery  solutions  of  carbol-fuchsin.  It 
develops  in  myriads  on  the  nasal  and  bronchial  mucous  membranes  and  in 
the  secretions  of  those  parts.  A  number  of  observers,  and  more  particularly 
Ricciardi,  have  shown  that  the  bacillus  is  readily  distributed  and  spreads 
most  actively  by  droplets  of  mucus.  Even  after  the  patient  has  recovered 
from  an  attack  his  nasal  secretions  may  reinfect  himself  or  other  persons 
for  a  period  of  weeks,  and  therefore  all  handkerchiefs,  towels,  and  pillow- 
cases used  by  him  should  be  boiled  before  being  used  by  others.  The 
room  occupied  by  the  patient  should  be  fumigated  with  formaldehyde 
after  his  recovery  occurs  and  before  anyone  else  occupies  it. 

It  is  a  noteworthy  fact  that  during  an  epidemic  of  influenza  other  infec- 
tious diseases  seem  to  be  less  common.  This  is  particularly  true  of  malarial 
fevers,  if  the  statistics  collected  by  Anders,  of  Philadelphia,  are  correctly 
interpreted. 

Incubation. — The  period  of  incubation  is  probably  from  twenty-four  to 
seventy-two  hours,  but  in  some  cases  it  seems  to  be  longer  than  this. 

Symptoms. — The  onset  of  symptoms  of  epidemic  influenza  is  nearly 
always  sudden.  A  person  feeling  perfectly  well  may  suddenly  be  seized  by 
a  sense  of  chilliness  or  a  severe  rigor,  followed  by  severe  aching  pains  in  the 
back  and  in  the  legs.  There  is  usually  congestion  of  the  nasal  mucous 
membrane,  so  that  the  patient  seems  to  have  a  severe  cold  in  the  head. 
The  chill  is  quickly  followed  by  fever  which  may  rapidly  rise  to  a  point  as 
high  as  105°,  although  as  a  rule  103°  is  the  more  common  acme.  Associated 
with  these  early  symptoms  there  is  usually  a  sense  of  severe  illness  and  a 
feeling  of  great  wretchedness,  so  that  the  patient  not  only  expresses  himself 
as  feeling  very  ill,  but  seems  so  to  the  physician. 

About  this  time  the  symptoms  are  wont  to  be  associated  with  additional 
ones  indicating  involvement  of  certain  viscera.  Most  frequently  the  respi- 
ratory system  is  affected,  and,  in  addition  to  more  or  less  intense  conges- 
tion of  the  nasal  mucous  membrane,  an  acute  bronchitis  develops ;  the 
physical  signs  in  the  chest  being  typically  those  of  acute  bronchitis  with 
excessive,  unproductive  cough  and  a  sense  of  thoracic  soreness.  When  the 
nasal  mucus  is  examined  it  is  seen  to  be  unusually  thin,  and  if  any  bron- 
chial mucus  is  expelled  it  is  also  of  this  character.  As  the  disease  pro- 
gresses the  sputum  becomes  greenish-yellow  and  thick. 

The  general  state  of  the  patient  at  this  time  is  often  one  of  profowid 
depression,  far  in  excess  of  that  which  usually  accompanies  such  signs  of 
bronchitis.  The  action  of  the  heart  may  he  feeble  and  the  skin  is  relaxed 
and  clammy,  or  it  may  be  very  hot  and  dry. 

If  convalescence  is  not  soon  established  the  disease  often  develops  into  a 


INFLUENZA  127 

peculiar  form  of  'pulmonary  congestion  or  pneumonia,  in  which  the  sputum 
may  be  blood-tinged  and  frothy  or  in  which  no  sputum  may  appear.  A 
peculiarity  of  this  pulmonary  involvement,  in  one  of  its  forms,  is  the  fact 
that  it  moves  from  place  to  place  with  remarkable  rapidity.  An  area  of 
impaired  resonance  which  existed  yesterday  is  clear  to-day,  and  still  another 
area  of  congestion  develops  elsewhere — a  form  of  wandering  congestion. 
When  true  pneumonia  develops  it  may  be  croupous  in  type  and  be  due  to 
mixed  infection  by  the  bacillus  of  Pfeiffer  and  by  that  of  true  pneumonia,  or 
it  may  be  in  the  form  of  bronchopneumonia.  The  latter  type  is  the  more 
common,  but  both  forms  are  apt  to  be  serious  and  particularly  so  in  the 
feeble,  the  aged,  the  very  young,  and  in  alcoholic  or  renal  cases.  Pneu- 
monia and  heart-failure  due  to  an  action  of  the  toxin  of  the  disease  on  the 
heart  muscle  are  the  chief  causes  of  death  in  all  epidemics. 

Pleurisy  followed  by  empyema  is  not  very  rare. 

In  studying  a  case  of  influenza  accompanied  by  pulmonary  signs  the 
physician  must  always  bear  in  mind  the  possibility  of  the  presence  of  asso- 
ciated tuberculous  infection,  because  an  attack  of  influenza  not  only  often 
predisposes  to  this  disease,  but  in  addition  permits  unrecognized  foci  of  early 
tuberculous  infection  to  become  active. 

In  some  cases  of  influenza  the  heart  seems  to  bear  the  chief  brunt  of  the 
attack,  so  that  repeated  attacks  of  syncope  ensue.  These  instances  are  met 
with  chiefly  among  patients  who  have  persisted  in  remaining  at  work  during 
the  early  stages  of  the  disease,  or  who  have  had,  previous  to  the  attack,  an 
impaired  heart  muscle.  Thus,  a  heart  dilated  as  the  result  of  excessive 
exercise  may  succumb  readily,  or  one  in  which  early  but  hitherto  unrecog- 
nized degenerative  changes  were  developing  may  suddenly  fail.  Often 
the  symptoms  of  influenza  are  chiefly  gastrointestinal  or  nervous. 

The  gastrointestinal  form  of  the  disease  may  ha\e  its  onset  in  severe 
diarrhoea  and  vomiting,  with  collapse  and  violent  abdominal  pain.  In  some 
cases  the  pain  is  entirely  absent,  and  profuse  watery  stools  are  present. 
Jaundice  may  be  present,  due  to  an  extension  of  the  gastrointestinal  catarrh 
to  the  common  biliary  duct. 

In  the  nervous  form  the  symptoms  consist  of  profound  nervous  and 
mental  depression,  or  in  severe  neuralgic  pain  which  may  or  may  not  be  due 
to  neuritis.  Mental  disturbances  in  the  course  of  an  attack  of  influenza 
are  by  no  means  rare.  Indeed,  it  may  be  said  that  no  other  acute  infectious 
disease  is  commonly  so  complicated,  or  followed,  by  such  a  condition.  Leicli- 
tenstern  states  that  he  met  with  fewer  psychoses  among  2000  cases  of  typhoid 
fever  and  3000  cases  of  pneumonia  than  he  found  among  439  cases  of  influ- 
enza. These  psychoses  may  be  of  the  exhaustion  type,  but  usually  are  due 
to  a  toxic  state  induced  by  the  malady.  The  mental  disturbance  may 
develop  during  the  stage  of  onset,  the  febrile  stage,  or  the  stage  of  decline 
or  convalescence-  The  latter  cases  are  usually  of  the  exhaustion  type. 
The  prognosis  in  these  cases  as  to  the  state  of  the  mind  is  usually  good 
unless  there  is  a  bad  history  as  to  heredity. 

Very  rarely  meningitis  develops,  and  still  more  rarely  true  encephalitis. 
Cases  of  cerebral  abscess  have  also  been  ascribed  to  this  disease.  In 
rare  cases  a  toxic  neuritis  develops,  and  tliis  may  be  single  or  multiple. 


128  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Even  paraplegia  due  to  this  cause  may  arise.  Not  only  may  this  type  of 
influenza  affect  the  nerves  of  sensation  and  motion,  but  specialized  nerves 
such  as  the  vagus,  thereby  causing  disturbances  of  the  circulation  such  as 
paroxysms  of  tachycardia  and  bradycardia.  In  an  analysis  of  29,000  cases 
Lee  found  that  7000  were  of  the  nervous  type.  In  some  instances  the  dis- 
turbance of  circulation  is  due  more  to  an  influence  exercised  upon  the 
vasomotor  nervous  system  than  to  any  direct  effect  upon  the  nerve  supply 
of  the  heart,  so  that  attacks  of  syncope  come  on  from  acute  vascular  relaxa- 
tion. 

Complications  and  Sequelae. — It  is  difficult  to  separate  the  complications 
of  influenza  from  the  ordinary  symptoms  of  the  disease  because  the  natural 
course  of  the  disease  presents  such  diverse  manifestations  in  different 
organs.  Without  doubt  pulmonary,  cardiac,  and  renal  disorders  are  the 
most  common  complications.  In  many  cases  death  is  due  to  an  attack  of 
pneumonia,  which  rapidly  carries  off  the  patient  whose  vitality  is  already 
sapped  by  the  onset  of  la  Grippe.  In  other  instances  the  kidneys,  which 
have  been  impaired  before  the  attack,  suffer  from  an  acute  congestion  or 
true  nephritis  superimposed  upon  the  subacute  or  chronic  state,  and  so 
ursemia  speedily  comes  on,  with  its  helpmate,  pulmonary  oedema. 

Patients  with  influenza  develop  cardiac  complications  in  three  chief  classes : 
either  they  already  have  mild  cardiovascular  degeneration  which  enables  the 
influenzal  toxin  to  work  havoc  with  the  cardiac  muscle,  or  they  have  dilated 
feeble  hearts,  or,  again,  as  already  stated,  they  persist  in  remaining  at  work 
after  the  attack  begins  and  refuse  to  go  to  bed.  These  patients  not  only 
have  serious  cardiac  difficulty  during  the  attack,  but  very  frequently  suffer 
from  cardiac  weakness  and  distress  for  many  weeks  after  convalescence 
should  be  well  established.  The  man  who  persists  in  remaining  out  of  bed 
when  attacked  by  this  disease  literally  "takes  his  life  in  his  hand." 

The  German  collective  investigation  of  the  epidemic  of  1889-90,  based 
on  an  analysis  of  3185  cases,  gave  the  following  results  as  to  the  relative  fre- 
quency of  complications,  which  results,  however,  differ  materially  from 
clinical  experience  in  America  so  far  as  the  cardiac  complications  are  con- 
cerned : 

1.  Diseases  of  the  respiratory  organs,  exclusive  of  pneumonia,  48.76  per 
cent. 

Of  these  complications  pleurisy  was  the  most  frequent,  being  present  in 
27  per  cent,  of  the  entire  number  of  cases.  Pneumonia  was  present  in  from 
6  to  8  per  cent,  of  all  cases. 

2.  Diseases  of  the  nervous  system,  45.77  per  cent. 

3.  Diseases  of  the  ear,  37.95  per  cent. 

4.  Hemorrhages,  25.33  per  cent. 

5.  Diseases  of  the  heart  and  vascular  system,  14.09  per  cent. 

6.  Diseases  of  the  digestive  organs,  10.36  per  cent. 

7.  Polyarthritis,  7.28  per  cent. 

8.  Diseases  of  the  eye,  7.03  per  cent. 

9.  Albuminuria  and  nephritis,  4.52  per  cent. 

Diagnosis. — It  is  so  easy  to  make  a  diagnosis  of  influenza  during  the 
presence  of  an  epidemic  that  physicians  are  wont  to  be  careless  in  exam- 


INFLUENZA  129 

ining  the  patient  thoroughly,  and  so  may  overlook  complications  of 
importance  or  decide  that  the  case  is  one  of  influenza  when  in  reality  the 
chills,  the  fever,  the  aching,  and  the  prostration  are  due  to  an  oncoming 
typhoid  fever  or  an  acute  tuberculosis  or  malaria.  All  of  these  diseases, 
and  also  ulcerative  endocarditis  and  sepsis,  should  be  carefully  excluded 
before  a  diagnosis  of  influenza  is  made. 

Treatment. — Above  all  other  things  in  the  treatment  of  influenza  is  rest 
in  bed.  This  is  as  true  of  mild  as  of  severe  cases  and  of  the  patient  who 
is  stalwart  as  of  the  patient  who  is  feeble.  A  robust  man  who  fails  to  rest 
almost  always  sufi^ers  from  a  severe  attack  or  from  sequelse,  such  as  cardiac 
disorder  and  giddiness,  which  may  invalid  him  for  weeks.  Aside  from  rest 
in  bed  little  medicine  is  needed  except  for  the  purpose  of  relieving  symp- 
toms which  are  troublesome.  For  the  relief  of  the  excessive  pain  in  the  back 
and  limbs  the  coal-tar  products  have  been  employed  by  the  ton.  Although 
they  give  ease  they  are  harmful  if  the  doses  are  large,  and  often  fail  if  they 
are  used  in  moderate  amounts.  They  tend  to  increase  nervous  and  circula- 
tory depression,  and  to  decrease  the  ability  of  the  patient  to  resist  the  infec- 
tion from  which  he  is  suffering  and  the  possible  secondary  infections  which 
may  occur.  If  the  patient  will  rest  they  may  be  used  moderately;  if  he  will 
not  rest  they  should  not  be  used,  for  they  not  only  do  harm  directly,  but  by 
diminishing  discomfort  they  also  enable  and  encourage  him  to  remain  out 
of  bed. 

A  very  useful  drug  for  the  relief  of  the  aching  and  pains  in  the  back  and 
limbs  is  salicin  in  5  grain  doses  every  five  hours  in  capsules.  Many  prac- 
titioners believe  that  this  drug  alone,  or  when  combined  with  2  grains  of 
quinine,  acts  as  a  specific  in  the  cure  of  the  affection.  Should  the  pain  in 
the  back  be  intense  it  may  be  relieved  by  the  application  of  hot  stupes  or 
compresses  or  by  rubbing  with  soothing  liniments.  A  more  ancient  but 
nevertheless  very  useful  remedy  for  this  condition,  particularly  in  the  early 
stage  of  the  malady,  is  Dover's  powder  in  the  dose  of  from  2  to  10  grains 
once  or  twice  a  day.  At  one  time  used  as  a  matter  of  routine  in  all  infec- 
tions, it  has  fallen  into  an  undeserved  disuse. 

Headache,  if  it  be  due  to  congestion,  may  be  modified  by  the  use  of  an 
ice-bag,  or  by  the  administration  of  1  to  2  grains  of  caffeine  with  5  grains  of 
bromide  of  sodium  or  potassium  every  few  hours.  This  formula  can  be 
given  in  the  form  of  an  effervescent  granular  salt  without  the  use  of  the 
coal-tar  products  often  added  by  manufacturers  of  headache  cures.  Hot 
foot-baths  also  decrease  headache.  Menthol  pencils  may  be  used  locally 
for  neuralgia  or  a  spray  of  chloride  of  ethyl  may  be  used  locally  for  the  same 
purpose. 

As  in  all  infectious  maladies,  it  is  of  the  greatest  importance  that  the 
organs  of  elimination  be  kept  active.  The  bowels  may  be  first  moved  by  a 
grain  or  two  of  calomel,  followed  in  twelve  hours  by  a  Seidlitz  powder,  or, 
if  constipation  has  been  marked,  they  may  be  opened  at  once  by  citrate 
of  magnesium.  For  the  purpose  of  keeping  the  kidneys  active  5  grains  of 
citrate  of  potassium  or  of  bicarbonate  of  potassium  may  be  given  every  four 
hours  in  copious  draughts  of  water  if  the  urine  is  acid,  or  the  same  amount 
of  benzoate  of  ammonium  if  the  urine  is  alkaline.  The  latter  drug  is  best 
9 


130  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

given  in  capsules,  and  possesses  the  additional  advantage  of  acting  favorably 
upon  the  respiratory  mucous  membrane  and  upon  the  muscular  pains.  A 
hot  compress  or  poultice  applied  over  the  loins  will  often  establish  renal 
secretion  when  it  seems  scanty. 

Dryness  and  soreness  of  the  mucous  membrane  of  the  respiratory  tract, 
in  the  stage  of  onset,  may  be  much  relieved  by  telling  the  patient  to  inhale 
steam  which  may  be  medicated  by  the  addition  to  the  water  from  which  it 
arises  of  a  few  grains  of  menthol  or  of  equal  parts  of  menthol,  oil  of  eucalyp- 
tus, and  oil  of  pine.  In  other  instances  the  patient  may  add  to  the  boil- 
ing water  a  tablespoonful  of  compound  tincture  of  benzoin.  The  medi- 
cated steam  may  be  taken  directly  from  an  inhaler  or  the  vapor  may  be 
set  free  in  the  air  of  the  room  by  the  use  of  a  bronchitis  kettle.  When  the 
nasal  mucous  membrane  is  so  congested  and  occluded  that  breathing  is 
difficult  and  oppression  is  marked,  adrenalin  chloride,  1 :  5000,  with  chloretone 
may  be  sprayed  into  the  nostrils  or  applied  on  pledgets  of  cotton.  It  loses  its 
effect  if  applied  too  often,  but  it  does  not  do  so  as  rapidly  as  does  cocaine, 
nor  is  it  dangerous  in  its  systemic  effects. 

For  the  relief  of  the  congestion  of  the  respiratory  mucous  membrane, 
when  the  illness  has  lasted  for  several  days  and  the  secretion  is  thick  and 
tenacious,  chloride  of  ammonium  in  5  grain  doses  four  times  a  day  may  be 
administered  combined  with  codeine  or  heroin  to  relieve  cough,  or  terpin 
hydrate  may  be  used  with  the  same  sedatives  in  the  form  of  the  well-known 
elixir  of  terpin  hydrate  with  heroin.  For  the  persistent  cough  of  convales- 
cence, oil  of  sandal-wood  in  5  minim  doses  four  times  a  day  is  very  useful. 

Circulatory  and  nervous  stimulants  are  not  to  be  used  unless  there  is 
distinct  evidence  of  their  need.  Alcoholic  drinks  are  as  a  rule  to  be  ex- 
cluded, unless  the  patient  uses  them  habitually  when  well,  when  they  have 
to  be  given,  preferably  in  the  form  of  an  old  brandy  or  good  whiskey.  Great 
care  must  be  taken  that  the  patient  does  not  overuse  them  in  his  endeavor 
to  make  himself  feel  stronger.  For  acute  circulatory  failure  aromatic  spirit 
of  ammonia  or  Hoffmann's  anodyne  are  the  remedies  of  choice.  When  the 
failure  of  the  circulation  is  associated  with  nervous  depression  the  use  of 
strychnine  is  indicated,  but  it  is  greatly  abused  and  should  not  be  given 
day  after  day  except  as  a  tonic  in  convalescence,  as  it  loses  its  power,  is  not 
a  true  stimulant  but  a  nervous  irritant,  and  often  causes  great  irritability 
if  not  employed  skilfully. 

As  influenza  is  a  disease  which  produces  great  prostration,  a  diet  which 
is  easily  digested  and  nutritious  is  essential  for  the  maintenance  of  strength, 
particularly  in  the  very  young,  very  feeble,  and  very  old.  Animal  broths, 
oysters,  and  predigested  foods  are  useful,  and  they  may  be  fortified  with 
advantage  by  barley-gruel,  the  digestion  of  which  may  be  aided  by  the  use 
of  taka-diastase.  Indeed,  the  various  vegetable  gruels  with  taka-diastase 
are  in  many  cases  better  than  the  animal  broths.  Arrowroot  and  milk- 
toast  and  eggs  are  also  useful. 

Prophylaxis. — There  can  be  no  doubt  that  much  can  be  done  to  prevent 
the  spread  of  la  Grippe  from  one  person  to  another  by  isolating  the  ill  and 
by  forbidding  healthy  persons  to  occupy  the  sick-room  after  it  is  vacated, 
until  it  is  thoroughly  disinfected.    This  is  particularly  advisable  when  the 


DENGUE  131 

old  and  feeble  are  about  the  house  and  when  persons  who  are  still  weak 
from  one  attack  are  exposed.  Every  effort  should  be  made  to  keep  the 
malady  out  of  the  non-medical  wards  of  hospitals,  insane  asylums,  and 
almshouses.  Patients  in  these  institutions  when  taken  ill  should  be  iso- 
lated. 

All  rooms,  clothes,  and  books  used  by  patients  suffering  from  influenza 
should  be  disinfected  as  carefully  as  if  the  patient  had  suffered  from  some 
more  fatal  malady. 

DENGUE. 

Definition. — Dengue  is  an  acute  infectious,  but  non-contagious,  usually 
epidemic  fever,  which  is  probably  dependent  for  its  development  upon  the 
presence  of  some  specific  organism  the  exact  nature  of  which  is  still  obscure, 
although  McLaughlin  and  Graham  believe  that  they  have  succeeded  in 
isolating  it.  The  disease  is  characterized  by  two  febrile  attacks  with  severe 
pains  in  the  muscles  and  joints.  Because  of  these  latter  symptoms  it  is 
often  called  "breakbone  fever,"  and  from  the  peculiar  gait  caused  by  this 
condition  "dandy  fever."  A  large  number  of  other  popular  names  have 
been  given  it,  such  as  "three-day  fever,"  "bouquet  fever,"  or  sometimes,  as 
a  corruption  of  the  last  name,  "bucket  fever." 

History  and  Distribution.— The  earliest  accurate  description  of  dengue 
that  we  possess  is  that  of  Brylon,  who  described  the  outbreak  of  1779;  later 
the  celebrated  epidemic  in  Philadelphia,  in  1780,  was  described  by  Push. 
Since  then  it  has  occurred  in  a  considerable  number  of  epidemics  in  various 
parts  of  the  world,  such  as  Batavia,  Spain,  India,  Bermuda,  Brazil,  the 
West  Indies,  and  in  various  parts  of  the  Southern  United  States.  Within 
twenty  years  it  has  also  visited  Turkey,  Greece,  Fiji,  and  Tripoli.  It  is, 
however,  distinctly  a  disease  of  warm  climates,  and,  so  far  as  I  know,  has 
never  been  met  with  north  of  Philadelphia.  The  disease  spreads  from 
point  to  point  along  lines  of  travel,  being  carried  by  infected  individuals 
and  perhaps  by  clothing. 

A  peculiarity  of  dengue  is  the  rapidity  of  its  spread  and  the  few  people 
in  a  community  who  escape  its  attack.  In  this  respect  it  surpasses  epidemic 
influenza.  No  age  sex,  or  race  escapes,  and  in  an  incredibly  short  time 
after  the  first  case  is  seen  a  multitude  may  be  down  with  it.  As  Manson 
well  says,  it  "bursts"  upon  a  place.  The  spread  of  an  epidemic  is  always 
arrested  by  the  appearance  of  cold  weather.  High  altitudes  are  also  unfav- 
orable to  its  spread. 

Pathology  and  Mode  of  Propagation  of  Dengue. — H.  Graham,  of  Beyrouth, 
has  observed  in  the  blood  of  dengue  patients  an  unpigmented,  oval-shaped 
protozoon,  having  amoeboid  movements,  and  frequently  showing  a  sharply 
pointed  extremity  such  as  is  seen  in  the  parasite  of  the  so-called  Texas 
fever.  This  parasite  is  of  ligliter  color  than  the  red  blood  corpuscles  in 
which  it  constantly  changes  its  position.  Dr.  Graham  also  conducted 
experiments  for  the  purpose  of  determining  whether  the  disease  is  propa- 
gated by  mosquitoes,  as  a  result  of  which  he  came  to  the  conclusion  that 
the  Culex  fastigans  carries  the  parasite  from  the  sick  to  the  well, 


132  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

In  several  instances  Graham  placed  persons  suffering  from  dengue  in 
apartments  in  which  all  mosquitoes  had  been  destroyed  by  chlorine  gas,  and 
allowed  healthy  individuals  to  associate  with  the  sick.  In  no  case  of  this 
kind  was  the  disease  contracted.  In  addition  to  this  negative  evidence 
Graham  offers  positive  evidence  which  he  obtained  by  allowing  mosquitoes 
which  had  bitten  affected  persons  to  bite  two  healthy  individuals  who 
resided  in  a  district  where  no  cases  of  dengue  were  present.  Both  of  these 
men  developed  the  disease,  one  on  the  fourth  and  the  other  on  the  fifth  day 
after  they  were  bitten.  They  were  kept  under  mosquito  nettings  until  they 
had  completely  recovered  and  the  infected  mosquitoes  were  all  killed.  No 
other  cases  of  dengue  occurred  in  the  village  where  these  experiments  were 
made.  The  same  organism  which  was  found  in  the  blood  of  dengue  patients 
was  also  found  in  the  blood  and  the  stomach  of  Culex  fastigans,  even  up 
to  the  fifth  day  after  the  insect  had  bitten  an  infected  individual. 

The  organism  multiplies  by  sporulation  in  the  stomach  walls  and  veno- 
salivary  glands  of  the  mosquito.  Inoculation  of  a  human  subject  with  a 
solution  of  the  salivary  glands  of  an  infected  mosquito  produced,  on  the 
third  day,  a  chill  and  high  fever  followed  by  a  typical  attack  of  dengue. 
As  yet  Graham's  observations  have  not  been  confirmed. 

Symptoms. — Dengue  is  characterized  by  a  train  of  symptoms  which  is 
quite  remarkable.  In  the  first  place,  the  suddenness  of  its  onset  is  note- 
worthy. A  patient  may  be  in  perfect  health  at  one  hour  and  sick  in  bed 
with  well-developed  symptoms  the  next.  In  any  event  the  oiiset  is  sudden, 
and  sometimes  it  is  ushered  in  by  a  chill  or  by  pains  in  the  limbs.  Fever 
rapidly  develops  and  may  reach  as  high  as  106°  or  107°,  but  usually  the 
acme  is  103°  to  105°.  There  is  intense  headache  and  the  pains  in  the  limbs 
are  so  excruciating  that  the  term  "breakbon^  fever"  is  well  applied.  The 
discomfort  of  the  patient  is  increased  by  the  pain  caused  by  moving  the 
body.  The  tongue  is  usually  heavily  coated,  and  nausea  and  vomiting 
may  be  distressing  symptoms. 

With  the  onset  of  the  fever  there  develops  a  rash  which  is  of  the  nature 
of  erythema.  In  from  one  to  three  days,  usually  two  days,  the  fever 
suddenly  ends  by  crisis  and  simultaneously  the  patient  not  only  sweats 
freely,  but  also  has  free  diuresis,  diarrhoea,  and  nose-bleed.  This  nose- 
bleed, by  relieving  the  cerebral  congestion,  greatly  decreases  the  headache, 
and  the  rash  rapidly  fades. 

In  other  instances  the  fever  gradually  falls  by  lysis,  but  this  is  less 
common  than  crisis.  The  fever  having  fallen  to  normal  the  patient,  still 
feeling  weak,  is  able  to  be  about,  although  he  suffers  from  twinges  of  pain 
in  the  joints  and  muscles,  which  impress  upon  his  mind  the  fact  that  he  is 
as  yet  ill.  After  a  remission  of  several  days,  usually  from  two  to  four,  the 
fever  returns  with  some  violence,  but  it  is  rarely  as  severe  as  in  the  primary 
paroxysm,  and  it  usually  lasts  only  a  few  hours.  With  the  appearance  of 
this  secondary  fever  a  roseolous  rash  develops,  and  with  its  development 
the  patient  may  have  a  return  of  his  bone  and  joint  pains  to  a  very  severe 
degree.  Although  the  fever  soon  disappears  the  rash  lasts  for  several  days 
and  may  end  in  a  slight  desquamation.  Taking  it  all  in  all,  the  secondary 
attack  is  usually  much  milder  than  the  first. 


DENGUE  133 

The  rash  of  the  second  attack  is  roseolous,  and  is  peculiar  in  that  it  is 
usually  first  seen  on  the  hands,  both  the  palmar  and  extensor  surfaces, 
and  thence  rapidly  spreads  to  the  entire  body.  The  spots  are  as  large  as  a 
pea,  circular  in  appearance,  dusky  red,  and  perhaps  elevated.  As  the  dis- 
ease progresses  they  may  coalesce,  leaving  patches  of  healthy  skin  between. 
This  rash  is  more  apt  to  be  profuse  and  to  coalesce  around  the  joints  than 
elsewhere.  The  roseola  fades  as  it  begins,  first  on  the  hands,  then  on  the 
arms  and  body,  and  lastly  on  the  legs.  The  desquamation  may  last  for 
weeks,  but  it  is  so  fine  that  it  may  be  overlooked.  The  skin  never  peels 
as  after  scarlet  fever.  In  some  instances  the  patient  passes  on  to  rapid 
convalescence  after  the  terminal  or  roseolous  rash  fades,  but  in  others  he 
remains  miserable  for  a  long  time  from  wandering  pains  in  his  joints  or  in 
the  soles  of  his  feet.  The  muscles  are  sore  on  pressure  and  stiff  on  moving 
after  a  long  rest,  and  debility  may  be  persistent.  In  some  instances  insomnia 
or  furunculosis  delays  complete  recovery. 

In  certain  epidemics  there  is  sufficient  degree  of  swelling  and  redness 
about  the  joints  to  suggest  the  presence  of  acute  rheumatism. 

Relapses  of  dengue  occur  not  infrequently. 

Diagnosis. — Dengue  may  be  separated  from  rotheln,  which  it  resembles 
during  the  period  of  its  secondary  rash  by  the  lymphatic  swellings  of  the 
latter  disease.  The  differentiation  is  also  accomplished  by  the  sudden  severe 
onset  and  the  pain  in  the  joints.  It  is  distinguished  from  scarlet  fever  by 
the  lack  of  sore  throat  and  the  peculiar  scarlet  hue  of  that  disease,  and  from 
syphilitic  roseola  by  the  absence  of  a  history  of  venereal  infection,  and  the 
fact  that  associated  symptoms  of  the  early  secondary  stage  of  syphilis  are 
absent.  On  the  other  hand,  it  is  to  be  recalled  that  many  syphilitics,  with  the 
onset  of  the  roseola  of  that  disease,  suffer  from  a  chill  and  general  wretch- 
edness with  pains  in  the  bones.  Influenza  is  separated  by  the  absence  of 
catarrhal  symptoms  and  by  the  presence  of  the  rash  in  dengue.  Acute 
articular  rheumatism  and  malarial  infection  are  two  other  diseases  which 
must  be  borne  in  mind  when  the  diagnosis  of  an  individual  case  is  in 
question. 

Prognosis. — The  prognosis  in  a  case  of  dengue  is  always  favorable  if  the 
patient,  prior  to  the  attack,  is  in  good  health,  and  not  debilitated  by  some 
other  malady  or  old  age.  Death  may  be  said  not  to  be  known  as  a  result 
of  this  malady  in  ordinarily  healthy  persons.  Convalescence,  after  a  severe 
attack,  is,  however,  very  often  quite  slow,  and  if  the  patient  is  living  in  a 
hot  climate  recovery  may  not  be  complete  until  a  change  of  residence  is 
made. 

When  dengue  attacks  the  aged  and  feeble,  or  very  young  children,  it 
sometimes  indirectly  causes  severe  illness  and  death  by  predisposing  the 
patient  to  other  infections  so  that  there  develops  a  severe  bronchitis  or 
bronchopneumonia,  or  some  other  evidence  of  acute  infection.  In  such 
cases  the  prognosis  depends  chiefly  upon  the  character  of  the  secondary 
ailment. 

Treatment. — In  discussing  the  treatment  of  this  disease  it  is  to  be  recalled 
that  it  presents  very  different  degrees  of  severity  in  different  cases.  In 
many  persons  the  symptoms  are  so  mild  that  the  patient  seems  scarcely 


134  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

at  all  ill,  and  in  others  the  manifestations  are  so  severe  that  convulsions 
and  unconsciousness  may  be  present.  In  the  mild  cases  no  drugs  are  needed, 
but  in  the  severe  cases  active  treatment  may  be  essential.  In  general  terms 
it  may  be  stated  that  the  treatment  of  the  patient  suffering  from  dengue 
consists  in  absolute  rest  in  bed  from  the  earliest  stage  of  onset  till  the  con- 
clusion of  the  second  stage  of  fever.  Indeed,  the  longer  he  will  consent  to 
rest  in  bed  after  the  fever  develops,  the  more  rapidly  will  complete  convales- 
cence be  established. 

So  far  as  drugs  are  concerned,  there  are  no  specifics  for  this  disease, 
which,  if  permitted,  will  usually  run  its  own  self-limited  course  to  recovery. 
When  the  pains  are  intolerable  they  may  be  controlled  by  moderate  doses 
of  morphine  given  hypodermically  or  by  the  use  of  acetanilid  or  phenacetin. 
A  gentle  antipyretic  and  sedative  mixture,  containing  5  grains  of  potassium 
citrate  and  30  minims  of  sweet  spirit-  of  nitre  in  a  dessertspoonful  of  water, 
is  useful  to  keep  the  kidneys  active.  An  ice-bag  may  be  applied  to  the  head 
to  relieve  the  cephalalgia,  and  if  the  face  is  very  much  flushed  and  the  head 
throbs  a  hot  foot-bath  is  advisable.  Sometimes  a  hot  bath  is  useful  to 
develop  the  rash  and  relieve  the  pains  in  the  body  and  limbs.  In  these  cases 
the  salicylates  may  also  be  used  for  the  same  purposes,  20  grains  of  sodium 
or  strontium  salicylate,  or  of  aspirin,  being  given  every  three  or  four  hours. 

When  the  circulation  is  strong  and  full  McLaughlin  asserts  that  large 
doses  of  tincture  of  gelsemium  serve  to  quiet  the  excited  pulse  and  to 
relieve  the  neuromuscular  pains.  The  dose  he  recommends,  namely,  20 
to  30  minims  every  three  or  four  hours,  seems  to  the  writer  much  too  large 
and  capable  of  causing  serious  depressions;  but  as  McLaughlin  has  had 
large  experience  with  the  disease,  his  views  demand  respectful  attention. 
The  fever  is  rarely  sufficiently  high  or  prolonged  to  require  treatment. 
Should  it  require  attention  tepid  spongings  are  usually  sufficient  to  control  it 
within  safe  limits ;  but  should  it  reach  as  high  as  105°  or  more,  then  it  must 
be  reduced  by  cold  spongings,  or  even  by  the  use  of  the  cold  bath,  with  active 
frictions.  Should  nervous  symptoms  be  very  manifest  and  convulsions  be 
threatened,  chloral  should  be  given  in  the  dose  of  5  grains  by  the  mouth,  or 
10  grains  by  the  rectum,  if  the  patient  is  a  child,  and  bromide  of  sodium  used 
to  aid  it  in  its  sedative  action. 

The  patient  should  be  urged  to  drink  freely,  if  his  stomach  will  retain 
liquids,  in  order  to  keep  his  kidneys  active  in  eliminating  the  poisons  of  the 
disease.  When  the  stomach  is  not  retentive  a  pint  of  cold  water  may  be 
given  by  the  rectum  every  eight  hours.  Should  diarrhoea  be  troublesome 
it  can  be  best  controlled  by  giving  castor  oil  to  cleanse  the  bowels,  and 
following  it  by  opium. 

CEREBROSPINAL  FEVER. 

Definition. — Cerebrospinal  fever,  sometimes  called  "  cerebrospinal  menin- 
gitis," "  spotted  fever,"  or  "  petechial  fever,"  is  an  acute,  often  malignant, 
infectious,  but  rarely  contagious  disease,  due  to  the  diplococcus  of  Weich- 
selbaum,  which  is  sometimes  called  the  meningococcus  or  the  Diplococcus 
intracellular  is  meningitidis.     It  is  characterized  by  a  rapid  course,   rigidity 


CEREBROSPINAL  FEVER  I35 

of  the  neck,  retraction  of  the  head  and  the  formation  of  inflammatory  exu- 
dates under  the  membranes  which  cover  the  brain  and  spinal  cord. 
It  is  to  be  clearly  understood  that  a  number  of  pathogenic  micro-organisms 
are  capable  of  producing  inflammation  of  the  pia  arachnoid,  and  conse- 
quently all  the  symptoms  of  true  epidemic  cerebrospinal  meningitis.  Such 
cases  are  not  instances  of  this  disease,  but  rather  are  to  be  considered  as 
sporadic  cases  of  meningeal  infection.  Indeed,  it  is  a  noteworthy  fact 
that  the  sporadic  cases  of  cerebrospinal  meningitis  which  are  due  to  the 
pneumococcus,  are  prone  to  be  more  virulent  than  those  due  to  the  specific 
organism  just  named.  While  the  epidemic  form  has  been  proved  to  be 
always  due  to  the  Diplococcus  intracellular  is  meningitidis,  it  is  not  cor- 
rect to  call  all  cases  of  cerebrospinal  meningitis  instances  of  cerebro- 
spinal fever. 

History. — No  definite  description  of  this  disease  is  to  be  found  in  medical 
literature  prior  to  the  nineteenth  century.  In  1805  the  first  c^se  was  described 
by  Vieusseux,  in  Geneva,  Switzerland,  where  several  deaths  took  place 
from  the  disease.  In  America  it  first  appeared  in  Medfield,  Massachusetts, 
in  1806.  During  the  next  ten  years  the  malady  broke  out  in  different  parts  of 
Europe  and  America,  but  disappeared  after  1816  till  1822,  when  it  reap- 
peared in  France.  In  1828  it  broke  out  in  Ohio.  It  was  not,  how^ever,  till 
1839  that  it  became  sufficiently  prevalent  in  any  one  place  to  cause  a  very 
large  number  of  deaths.  In  that  year,  at  Versailles,  it  ravaged  the  town 
and  garrison  and  produced  a  mortality  of  nearly  75  per  cent.  Scattered 
epidemics  have  since  occurred  in  the  United  States  at  intervals  of  every 
few  years,  and  it  is  constantly  present  in  scattered  cases  in  the  central 
part  of  the  State  of  New  York.  (Eisner.)  A  noteworthy  point  in  con- 
nection with  the  disease  is  the  fact  that  it  suddenly  appears  simultaneously 
in  widely  separated  areas,  and  without  any  dependence  upon  lines  of 
travel.  Thus  during  a  recent  period  of  t\\elve  months  many  cases  occurred 
in  New  York,  but  none  in  Philadelphia,  which  is  only  ninety  miles  away. 
Certain  atmospheric  influences  may  make  this  possible,  but  its  cause  is 
not  definitely  understood. 

Etiology. — There  can  be  no  doubt  that  cerebrospinal  fever  is  due  to 
the  diplococcus  already  named,  but  the  same  anatomical  conditions  and 
a  similar  clinical  picture  may  be  produced  by  other  bacteria,  for  example, 
the  pneumococcus  and  other  pyogenic  cocci.  In  cases  of  cerebrospinal 
meningitis  which  have  appeared  sporadically  and  presented  all  the  signs 
of  the  epidemic  disease  the  streptococcus,  the  staphylococcus  pyogenes, 
the  pneumococcus,  the  gonococcus(?),  and  even  the  bacilli  of  influenza 
and  typhoid  fever  have  been  found  as  apparently  the  only  cause  of  the 
affection.  A  similar  acute  serofibrinous  meningitis  may  accompany  pyaemia 
or  septicaemia,  or  may  be  due  to  injury,  with  infection  or  extension  of  infec- 
tive processes  from  the  frontal,  ethmoidal,  sphenoidal,  or  mastoid  sinuses, 
middle  or  internal  ear,  or  other  parts  of  the  envelope  of  the  brain  and 
cord.  Such  forms  of  meningitis  are  often  called  consecutive,  incidental,  or 
secondary,  and  are  to  be  distinguished  from  the  epidemic  malady. 

Infection  probably  takes  place  through  the  respiratory  passages,  partic- 
ularly in  the  nose. 


136  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Climatic  conditions  undoubtedly  exercise  some  influences,  for  the  disease 
confines  itself  almost  entirely  to  the  colder  parts  of  the  temperate  zone,  but 
this  is  not  to  be  taken  as  indicating  that  it  is  a  disease  of  the  winter  months. 
On  the  contrary,  it  appears  about  equally  frequently  in  winter  and  summer. 
While  it  is  true  that  unhealthy  surroundings  favor  all  diseases,  it  is  also  true 
that  they  do  not  seem  to  greatly  influence  this  malady,  for  it  occurs  on  high 
and  on  low  land,  when  it  is  dry  and  when  it  is  wet,  on  hill  and  in  marsh, 
with  equal  frequency.  As  Stille  says,  "It  has  passed  by  large  cities  reeking 
with  all  the  corruptions  of  a  soil  saturated  with  ordure  and  populations 
begrimed  with  filth,  to  devastate  clean  and  salubrious  villages  and  the 
families  of  substantial  farmers  inhabiting  isolated  spots." 

The  disease  affects  children  and  young  adults  far  more  frequently  than 
persons  in  advanced  life.  It  is  slightly  contagious,  but  cases  of  undoubted 
transference  from  one  patient  to  another  occur.  The  occurrence  of  the 
malady  in  a  number  of  persons  hving  in  the  same  district  is  usually  due  to 
the  fact  that  they  have  all  been  exposed  to  the  same  cause. 

Prevention. — We  know  of  no  method  of  preventing  epidemic  cerebro- 
spinal meningitis,  but  physicians  and  others  who  are  attending  cases, 
should  wash  the  nasal  mucous  membrane  with  normal  salt  solution  to  aid 
in  preventing  infection.     Cases  should  be  isolated. 

Frequency. — From  what  has  already  been  said,  it  is  evident  that  this  dis- 
ease is  met  in  epidemic  form,  but  is  comparatively  rare.  Many  practitioners 
never  meet  with  a  single  or  sporadic  case  in  a  long  career;  whereas,  others 
may  be  so  unfortunate  as  to  meet  several  outbreaks. 

Pathology  and  Morbid  Anatomy. — In  fulminating  cases  death  may  occur 
before  the  meningeal  exudate  forms;  in  these  the  meninges  may  exhibit  no 
exudate,  showing  only  intense  hypersemia  and  cedema,  but  the  membranes 
and  cerebrospinal  fluid  are  usually  rich  in  the  specific  organism.  Death 
in  such  cases  seems  to  depend  on  the  toxic  action  of  the  serous  bacteria- 
laden  exudate. 

The  characteristic  lesion  of  this  disease  is  an  acute  inflammatory  exudate 
of  the  pia-arachnoid  enveloping  the  brain  and  spinal  cord.  These  mem- 
branes become  infiltrated,  and  the  surface  appears  to  be  covered  by  a  white 
or  creamy-white  exudate,  which  is  most  conspicuous  in  the  sulci.  The  ven- 
tricles may  contain  a  cloudy,  opaque,  or  even  distinctly  purulent  fluid.  The 
inflammatory  exudate  is  most  copious  at  the  base  of  the  brain  and  on  the 
dorsal  surface  of  the  spinal  cord,  particularly  in  the  lower  thoracic  and 
lumbar  regions.  When  the  disease  affects  children  the  lateral  ventricles  are 
often  found  at  autopsy  to  be  distended  with  purulent  fluid,  but  in  adults  this 
condition  is  not  likely  to  be  marked.  In  the  early  stages  of  the  disease  the 
diplococcus  is  found  in  large  numbers  in  the  leukocytes  contained  in  the 
exudates,  but  when  death  occurs  late  in  the  course  of  the  malady  the  germ 
may  be  demonstrated  with  difficulty,  if  at  all. 

In  addition  to  the  lesions  in  the  meninges  the  nerves  and  ganglia  exposed 
to  the  toxic  action  of  the  exudate  undergo  inflammatory  and  degenerative 
changes.  The  involvement  of  these  nerves  may  leave  irreparable  damage, 
manifested  by  blindness,  deafness,  or  other  phenomena  dependent  upon  the 
structures  involved.     Secondary  alterations  in  other  parts  of  the  body  may 


CEREBROSPINAL  FEVER  137 

be  present.  These  are  due  to  the  toxins  of  the  disease  or  to  the  presence 
of  the  micro-organisms  in  the  affected  areas.  Thus,  we  find  petechise  in 
the  skin  and  mucous  membranes  and  somewhat  similar  punctate  extrava- 
sations of  the  blood  in  the  endocardium.  Not  rarely  multiple  abscesses  are 
found  scattered  through  the  body  and  multiple  suppurative  arthritis  may  be 
present.  Hyaline  and  granular  degeneration  of  the  voluntary  muscles  is 
also  demonstrable,  and  the  heart  muscle,  kidneys,  and  liver  may  manifest 
necrotic,  degenerative,  or  inflammatory  changes.  Occasionally  there  is 
found,  associated  with  the  meningitis,  croupous  pneumonia,  ulcerative  endo- 
carditis, and  otitis  media.  These  pathological  conditions  are  characteristic 
of  the  severe  forms  of  the  disease. 

In  some  cases  the  lesions  are  much  more  moderate  in  that  hypersemia,  or 
intense  congestion,  of  the  pia  mater  only  is  seen,  although  the  sulci  between 
the  convolutions  of  the  brain  may  contain  fibrin  or  pus. 

Incubation. — The  period  of  incubation  is  from  one  to  four  days. 

Symptoms. — The  symptoms  of  epidemic  cerebrospinal  meningitis  may  be 
grouped  into  five  classes — viz.,  the  moderate,  the  malignant,  the  intermit- 
tent, the  typhoid,  and  the  chronic  form. 

In  the  moderate  form,  after  an  unknown  period  of  incubation,  the  patient 
suffers  from  a  sudden  chill,  which  may  be  preceded  by  headache  and  dizzi- 
ness. The  headache  rapidly  becomes  very  severe  and  is  accompanied  by 
severe  pain  in  the  back  and  down  the  back  of  the  thighs,  the  muscles  of 
which  are  often  tense  or  fixed.  The  fever  which  follows  the  chill  is  usually 
moderate,  rarely  exceeding  102°,  and  it  presents  no  characteristic  curves. 
On  the  contrary,  it  is  exceedingly  irregular  and  does  not  show  any  con- 
stant morning  and  evening  variations.  Very  rarely  hyperpyrexia  may 
develop. 

As  the  disease  develops  the  tenseness  of  the  muscles  of  the  legs  extends 
to  those  of  the  back,  neck,  and  arms,  and,  finally,  they  may  become  almost 
rigid,  and  contracted  to  such  a  degree  that  the  patient  develops  opisthotonos. 
The  abdomen  is  rigid  and  scaphoid.  Not  rarely  spasmodic  movements 
of  the  muscles  of  the  face  develop  as  the  result  of  irritation  of  the  roots 
of  the  cranial  nerves,  and  by  reason  of  this  same  cause  strabismus,  ptosis, 
amaurosis,  and  diplopia  may  be  present.  The  conjunctivae  are  usually 
reddened. 

Delirium  is  a  very  frequent  symptom,  and  is  sometimes  so  severe  as  to  be 
maniacal.    From  this  state  the  patient  may  pass  into  coma. 

The  pulse  and  respiration  are  not  greatly  affected,  except  that  as  the  disease 
progresses  they  may  become  feeble.  Toward  the  end  of  the  attack,  if  it  be 
fatal  in  its  nature,  Cheyne-Stokes  breathing  may  develop  and  the  pulse 
become  rapid  and  small. 

An  eruption  develops  on  the  skin  in  about  one-half  of  the  cases.  When 
it  appears  about  the  mouth  it  is  herpetic,  but  on  other  parts  of  the  body  it  is 
usually  petechial,  although  herpes  of  the  skin  of  the  trunk  and  about  the 
genitals  may  appear.  At  times  a  general  erythema  may  be  present  or  in  its 
place  an  urticaria  is  developed. 

The  presence  of  arthritis  has  already  been  referred  to.  It  appears  in 
about  20  per  cent,  of  the  cases,  and.  as  it  is  septic  in  nature,  it  may  cause 


138 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


serious  changes  in  the  joints  and  result  in  permanent  deformity  if  the 
patient  survives. 

The  hlood  shows  no  marked  changes,  save  that  the  inflammation  of  the 
meninges  results  in  a  leukocytosis  of  the  polymorphonuclear  cells. 

As  an  almost  constant  symptom,  mention  should  be  made  of  "  Kernig's 
sign,''  which  consists  in  the  fact  that  in  inflammatory  processes  in  the  mem- 
branes of  the  cord  it  is  not  possible  to  extend  the  leg  on  the  thigh  when  the 
thigh  is  at  right  angles  to  the  plane  of  the  body.  Rarely  this  sign  is 
unilateral  (Fig.  29). 

In  the  malignant  type  of  the  disease  the  onset  is  remarkably  sudden.  The 
patient  is  seized  by  a  chill,  followed  by  headache,  unconsciousness,  and 
death.  Convulsions  occur  more  commonly  in  children  than  in  adnlts. 
The  fever  may  be  absent,  the  pulse  slow,  the  breathing  labored,  the  urine 


Kernis 


sign,  showiiiLT  the  stroii 


jiitraetion  of  the  flexors  on  attempting  to  extend  the  leg. 
(After  Osier's  case.) 


greatly  decreased  in  amount  and  loaded  with  albumin,  and  the  stupor  pro- 
found. The  patient  in  such  an  instance  is  probably  overwhelmed  by 
toxaemia,  so  that  death  may  ensue  in  a  few  hours. 

In  the  intermittent  /orm,  which  is  probably  due  to  the  Streptococcus  pyogenes, 
or  Staphylococcus  pyogenes  alone,  or  to  association  of  those  organisms  with 
the  specific  coccus  of  Weichselbaum,  the  fever  intermits,  as  in  malarial  fever, 
but  the  intermittence  is  irregular,  as  in  sepsis,  and  is  not  distinctly  periodic, 
as  in  malaria.  The  typhoid  form  is  characterized  by  symptoms  of  apathy, 
feebleness,  and  abdominal  disorders. 

The  chronic  form  consists  in  the  prolongation  of  the  ordinary  type,  with 
special  symptoms,  such  as  headache,  pains  in  the  nerves,  vomiting,  and 
progressive  emaciation,  with  secondary  arthritic  changes  and  increasing 
inability  to  move  the  hmbs.     Here,  again,  it  is   probable  that  the   main- 


CEREBROSPINAL  FEVER  139 

tenance  of  the  illness  is  due  to  septic  organisms  rather  than  to  Weichsel- 
baum's  coccus. 

While  for  the  sake  of  description  these  several  types  of  the  disease  have 
been  named,  it  is,  of  course,  true  that  it  may  manifest  various  degrees  of 
severity  in  the  same  case  at  different  periods.  Some  cases  which  seem  quite 
severe  at  the  onset  gradually  ameliorate  and  pass  into  the  chronic  or  sub- 
acute form.  The  fact  that  the  malady  presents  widely  different  types  is  well 
illustrated  by  the  seemingly  exaggerated,  but  nevertheless  correct,  state- 
ment of  Hirsch  that  the  duration  of  epidemic  cerebrospinal  meningitis  may 
be  between  several  hours  and  several  months.  N.  S.  Davis  has  stated 
that  its  duration  in  his  experience  varied  from  twenty-four  hours  to  twenty- 
eight  days.     I  have  seen  death  occur  in  eighteen  hours. 

Complications  and  Sequelae. — The  complications  and  sequelae  of  epidemic 
cerebrospinal  meningitis  are  very  numerous.  During  the  attack  croupous 
pneumonia  not  only  often  develops  and  aids  materially  in  producing  a  fatal 
issue,  but  acute  pleurisy  also  is  not  uncommon.  So,  too,  inflammation  of  other 
serous  membranes,  such  as  the  pericardium  and  the  endocardium  and  the 
synovial  membranes,  is  often  met  with,  because  the  coccus  has  an  affinity 
for  these  membranes  in  all  parts  of  the  body.  In  the  nervous  sijstem  the 
most  common  sequelae  are  blindness  or  impaired  vision  due  to  optic  nerve 
atrophy,  ptosis  due  to  oculomotor  paralysis  following  neuritis  or  to  changes 
arising  from  the  inflammatory  exudate  at  the  point  where  the  nerves  leave 
the  membranes,  and  deafness  arising  from  the  effects  of  the  acute  inflam- 
mation or  infection  upon  the  auditory  nerves.  Sometimes  the  deafness  arises 
from  an  otitis  media  due  to  the  specific  coccus.  Aside  from  chronic  naso- 
pharyngeal disease  and  scarlet  fever,  this  disease  is  responsible  for  deafness 
in  larger  proportion  of  cases  than  any  other  malady. 

Diagnosis. — While  it  is  true  that  in  a  majority  of  cases  the  diagnosis  of 
this  disease  is  readily  made,  it  is  also  a  fact  that  many  other  diseases  may 
produce  symptoms  which  so  nearly  resemble  those  of  epidemic  cerebro- 
spinal meningitis  that  it  may  be  absolutely  impossible  to  make  a  differentia- 
tion. In  the  first  place,  it  must  not  be  forgotten  that  cerebrospinal  menin- 
gitis is,  as  its  name  implies,  an  inflammation  of  the  cerebrospinal  mem- 
branes, and  this  change  may  be  produced  by  a  host  of  causes,  none  of  which 
have  any  true  relationship  with  the  true  epidemic  form  of  the  disease.  As 
already  pointed  out  in  this  article,  and  in  that  on  typhoid  fever,  the  bacillus 
of  Eberth  may  cause  a  train  of  symptoms  and  morbid  changes  which  is 
identical  with  that  due  to  the  diplococcus  of  Weichselbaum,  yet  such  a  case 
would  not  be  one  of  epidemic  cerebrospinal  meningitis.  It  is  evident, 
therefore,  that  cases  of  retraction  of  the  head,  rigidity  of  the  limbs,  and 
twitchings  of  the  face  should  not  be  called  true  cerebrospinal  fever  unless 
the  specific  diplococcus  can  be  demonstrated,  or  unless  the  disease  can  be 
found  to  be  present  in  other  patients  in  the  vicinity.  In  the  midst  of  an  epi- 
demic of  typhoid  fever  the  development  of  cerebrospinal  symptoms  should 
be  credited  to  this  infection  rather  than  to  the  specific  fever  now  under  discus- 
sion. If  any  doubt  exists  as  to  the  true  nature  of  the  affection,  it  should  not 
be  forgotten  that  herpes  is  very  rare  in  typhoid  fever  and  in  typhus  fever, 
but  is  common  in  true  cerebrospinal  fever.      Both  these  fevers  run  a  course 


140 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


which  is  marked  by  a  natural  limit;  whereas,  epidemic  cerebrospinal  men- 
ingitis does  not  begin  to  decline  after  the  lapse  of  a  definite  course,  but  is 
exceedingly  irregular  in  its  duration. 

Croupous  pneumonia  is  the  infection,  above  all  others,  which  is  capable 
of  misleading  the  physician  in  his  diagnosis  of  cerebrospinal  fever.  It  has 
already  been  stated  that  pneumococcus  is  often  found  to  be  the  cause  of 
inflammation  of  the  meninges,  and  in  children  in  particular  the  cerebro- 
spinal symptoms  may  be  so  well  developed  that  unless  the  physician 
examines  the  lungs  very  carefully,  he  may  diagnosticate  cerebrospinal 
meningitis  when  in  reality  the  true  cause  lies  in  the  lung.  It  would  seem 
that  two  types  of  cerebrospinal  symptoms  develop  in  pneumonia,  namely, 
those  due  to  the  secondary  meningeal  infection  with  the  pneumococcus  and 
those  in  which  there  is  no  true  infection,  but  simply  irritation  produced  by 
the  toxaemia  of  the  pneumonia. 


Fig.  30 


A,  space  between  the  third  and  fourth  lumbar  vertebrae  which  can  be  used  for  puncture  ;  or  £,  the 
space  between  the  fourth  and  fifth  lumbar  vertebrae. 

Tuberculous  meningitis  is  practically  never  so  sudden  in  onset  as  is  the  true 
epidemic  form,  and  careful  physical  examination  of  the  patient  will  usually 
reveal  a  primary  tuberculous  focus  if  meningeal  tubercles  are  present. 
When  the  inflammation  is  tuberculous  the  leukocyte  count  is  not  materi- 
ally increased,  whereas,  in  the  specific  type  it  may  vary  from  9000  to 
26,000. 

When  cerebrospinal  symptoms  develop  in  the  presence  of  an  epidemic  of 
influenza,  the  differentiation  between  true  cerebrospinal  meningitis  and  that 
due  to  influenza  may  be  impossible,  although  the  fact  that  the  case  is  single 
points  to  the  influenza  bacillus  as  the  true  cause  rather  than  that  the 
attack  is  a  sporadic  case  of  the  disease  now  under  discussion.  The  cerebro- 
spinal symptoms  of  influenza  are  rarely  so  severe  or  so  persistent  as  those 
due  to  epidemic  cerebrospinal  fever. 

The  greatest  aid  that  we  have  in  differential  diagnosis  is  by  means  of 
lumbar  puncture.    This  operation  consists  in  inserting  a  large  hollow  needle 


CEREBROSPINAL   FEVER 


141 


between  the  third  and  fourth  or  fourth  and  fifth  lumbar  vertebrae,  a  little  to 
the  side  of  the  median  line  and  just  below  the  spinous  process.  The  needle 
as  it  enters  should  be  directed  upward  and  inward.  In  children  the  fluid  is 
reached  when  the  needle  is  inserted  about  2  cm.,  and  in  adults  when  it  has 
reached  the  depth  of  from  4  to  6  cm.  As  soon  as  the  membrane  containing 
the  fluid  is  punctured  it  flows  from  the  needle  in  drops,  which  should  be 


Fig. 31 


Introduction  of  needle  between  the  last  two  lumbar  vertebrae.     The  syringe  is  used  as  a  convenient 
handle  for  the  needle,  and  is  unscrewed  after  the  puncture  is  made. 

caught  in  a  sterile  test-tube  in  such  a  way  that  the  fluid  does  not  run  down 
its  side.  If  the  infection  is  due  to  the  specific  organism,  the  pressure  is  greatly 
increased,  so  that  the  fluid  may  escape  with  a  spurt.  This  fluid  is  clear  if 
tuberculous  meningitis  is  present,  but  cloudy  if  the  diplococcus  of  Weichsel- 
baum  is  the  cause  of  the  illness.  Under  these  circumstances,  too,  the  faint 
trace  of  albumin  found  in  the  normal  fluid  is  very  distinctly  increased. 
The  careful  staining  of  a  single  specimen  or  a  more  exhaustive  bacterio- 
logical examination  may  reveal  the  presence  of  the  diplococcus. 


142  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

Demonstration  of  the  meningococcus  in  the  nasal  mucus  is  an  important 
addition  to  other  signs,  but  a  number  of  observers,  and  more  recently  Lord, 
have  shown  that  meningitis  may  occur  without  the  specific  coccus  being 
present  in  the  nose,  and  also  that  a  meningococcus  rhinitis  neither  preceded 
nor  followed  by  meningitis  is  not  of  exceptional  occurrence. 

Prognosis. — ^The  prognosis  of  true  epidemic  cerebrospinal  meningitis  is 
always  grave,  but  its  rate  of  mortality  varies  in  wide  hmits,  namely,  from 
20  to  75  per  cent.  In  children  under  two  it  is  almost  always  fatal,  and  before 
puberty  its  mortality  is  very  high.  The  most  violent  cases  usually  meet 
death  by  the  fifth  day,  but  it  is  not  to  be  forgotten  that  many  others  reach  the 
fourteenth  day  before  death  occurs.  Then,  again,  it  sometimes  happens 
that  after  several  days  of  severe  symptoms  the  general  aspect  of  the  case 
improves,  but  the  favorable  signs  only  persist  for  a  few  hours  and  then 
the  symptoms  return  with  renewed  vigor.  Further  than  this,  patients  who 
seem  about  to  recover  not  rarely  suffer  from  a  relapse  which  may  prove 
fatal.  Koplik  asserts  that  the  character  of  the  spinal  fluid  is  of  great  prog- 
nostic value.  If  it  is  thick  and  purulent  the  outlook  is  bad;  but  if  it 
is  of  a  straw  color  and  clear  it  is  good. 

Treatment. — The  treatment  of  true  cerebrospinal  fever  is  not  very  satis- 
factory. We  know  of  no  remedies  which  exercise  any  true  curative  influence, 
and  all  the  physician  can  do  is  to  keep  the  patient  during  the  acute  stages  in 
a  quiet,  darkened  room,  and  give  bromides  in  suflSciently  large  doses  to  pre- 
vent convulsions  of  sufficient  violence  to  exhaust  the  patient.  Chloral  is  an 
even  more  powerful  and  useful  drug  for  this  purpose,  being  given  in  the  dose 
for  an  adult  of  20  grains  by  the  mouth,  or  60  grains  by  the  rectum,  in  starch- 
water.  Unless  the  nervous  symptoms  are  very  severe,  it  is  a  great  mistake  to 
attempt  to  overcome  moderate  rigidity  or  twitchings  by  full  doses  of  nervous 
sedatives,  because  they  in  no  way  influence  the  progress  of  the  disease,  and 
simply  give  the  stomach  the  task  of  absorption  and  the  kidneys  the  burden 
of  elimination.  The  idea  that  quinine  is  of  value  is  probably  erroneous. 
The  doses  usually  advised  are  too  small  to  act  in  any  way  as  specifics,  and 
if  large  doses  are  given  they  serve  to  distinctly  increase  congestion  of  the 
meninges  and  in  the  middle  ear.  Pain  is  to  be  relieved,  if  excessive,  by  the  use 
of  morphine  in  adequate  doses,  as  much  as  ^  a  grain  being  used  if  needed, 
particularly  at  night,  to  give  rest  and  sleep.  The  morphine,  or  deodorized 
opium,  had  better  be  given  by  the  mouth  when  this  mode  of  administration 
is  possible,  as  hypodermic  injections  may  cause  abscesses. 

Cold,  in  the  form  of  an  ice-bag,  may  be  applied  to  the  head  for  the  relief  of 
headache.  Blisters  have  been  applied  to  the  nape  of  the  neck  in  the  hope 
of  influencing  the  effusion  at  the  base  of  the  brain,  but  they  are  of  little 
value.  It  has  been  claimed  by  some  practitioners  that  a  very  liberal  use 
of  antidiphtheritic  serum  exercises  a  curative  influence. 

Mention  has  already  been  made  of  lumbar  puncture  for  diagnostic  pur- 
poses. When  headache,  high  temperature,  i-igors,  or  stupor  are  marked,  the 
relief  of  the  pressure  upon  the  brain  and  spinal  cord  by  this  means  may 
give  temporary  relief,  but  that  it  aids  the  patient  permanently  is  very 
doubtful.    The  amount  of  fluid  withdrawn  should  equal  40  to  50  c.c. 

Very  recently  several  clinicians  have  reported  good  results  from  the  injec- 


CROUPOUS  PNEUMONIA  143 

tion  into  the  cerebrospinal  fluid  of  an  antiseptic  substance.  The  method 
they  employ  is  as  follows:  after  withdrawing  about  50  c.c.  of  cerebrospinal 
fluid  by  lumbar  puncture  they  inject  an  equal  quantity  of  normal  salt  solu- 
tion (0.9  per  cent.)  through  the  same  needle  which  has  remained  in  situ 
after  the  withdrawal  of  the  fluid.  They  next  inject  into  the  spinal  cavity 
through  the  same  needle  about  10  c.c.  of  a  1  per  cent,  solution  of  lysol. 
After  this  is  done  the  needle  is  withdrawn.  It  is  claimed  for  this  plan 
that  it  causes  a  fall  of  the  fever,  which,  however,  returns  .after  one  or  two 
days.  The  same  procedure  should  be  repeated  at  intervals  of  two  days 
until  the  cerebrospinal  fluid  when  withdrawn  is  limpid  and  clear. 

Relief  from  the  severe  pains  in  the  limbs  and  back  may  be  obtained  in 
some  cases  by  immersing  the  patient  for  long  periods  of  time  in  a  hot  bath 
of  plain  or  salt  water  at  99°  or  100°. 

The  fever  is  rarely  high  enough  to  need  treatment.  If  it  is  above  105°,  the 
ice-bag  and  the  use  of  cool  spongings  with  frictions  may  be  resorted  to. 

In  all  cases  the  diet  should  be  one  which  is  easily  swallowed  and  easily 
digested,  and  everything  should  be  done  to  support  the  system.  This  is 
particularly  necessary  in  the  prolonged  types,  in  which  marked  emaciation 
is  often  present. 

CROUPOUS  PNEUMONIA. 

Definition. — ^There  is  no  condition  of  the  lungs  which  is  so  apt  to  be 
confused  in  the  mind  of  the  student  as  that  designated  pneumonia.  This  is 
because  the  word  "pneumonia"  is  used  by  some  medical  men  to  designate 
a  single  disease  affecting  the  lung  and  by  others  as  signifying  any  state  in 
which,  as  the  result  of  an  inflammatory  process,  a  part  of  the  lung  becomes 
congested  or  consolidated.  The  latter  is  the  better  use  of  the  word,  and 
when  the  physician  desires  to  state  that  a  lesion  representing  a  definite 
infection  is  present  he  should  specify  the  type  of  pneumonia  by  employ- 
ing an  adjective  to  qualify  the  noun — i.  e.,  he  should  speak  of  the  various 
forms  of  pneumonia  as  croupous  or  lobar  pneumonia,  catarrhal  or  lobular 
pneumonia,  and  of  tuberculous  pneumonia.  The  term  "pneumonia,"  while 
commonly  used  to  signify  croupous  pneumonia,  means  nothing  more  definite 
than  consolidation  of  the  lung. 

Croupous  Pneumonia  is  sometimes  called  Lobar  Pneumonia,  Pneu- 
monitis, Lung  Fever,  or  Fibrinous  Pneumonia. 

Croupous  pneumonia  is  an  acute  infectious  disease  depending  for  its  exist- 
ence, when  in  its  typical  form,  upon  the  activity  in  the  body  of  the  specific 
organism  known  as  the  Micrococcus  lanceolatus,  sometimes  called  the  pneumo- 
coccus  of  Fraenkel.  As  the  result  of  this  infection,  there  takes  place  in  the 
lung  an  acute  inflammation  accompanied  by  the  exudation  into  the  air 
vesicles  of  an  adhesive,  croupous,  or  fibrinous  exudate,  which  produces  con- 
solidation of  the  lobe  or  lobes  affected.  In  addition  to  these  changes  the 
patient  suffers  from  a  greater  or  less  degree  of  toxaemia,  due  to  the  poisons 
made  by  the  infecting  micro-organisms  and  from  the  changes  produced  in  the 
tissues  of  other  organs  than  the  lungs  by  the  growth  of  the  micrococcus  or  by 
its  toxins.    This  disease  is  also  characterized  by  the  fact  that  it  usually  lasts 


144  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

about  nine  days  and  ends  by  crisis,  although  this  crisis  may  occur  as  early  as 
the  third  day  or  even  earlier  in  very  rare  instances. 

Etiology. — The  development  of  croupous  pneumonia  is  dependent  upon 
many  causes,  some  of  which  v^e  do  not  know.  These  causes  are  those 
external  to  the  body  which  produce  conditions  in  the  individual  favorable  to 
the  growth  of  the  specific  germ,  and  internal  causes  which  exert  similar 
influences.  The  importance  of  these  conditions  is  shown  by  the  fact  that 
the  pneumococcus  is  periodically  or  continuously  present  in  the  oral  secre- 
tions of  a  large  percentage  of  healthy  human  beings.  Although  the  organ- 
ism is  capable  of  rapidly  increasing  in  virulence,  this  cannot  be  held  to 
account  for  all  cases  of  infection,  as  even  the  most  virulent  strains  are 
sometimes  found  in  normal  persons.  A  valuable  contribution  to  the 
various  phases  of  the  pneumococcus  question,  including  the  communica- 
bility  of  the  organism  from  person  to  person,  is  the  work  done  under  the 
auspices  of  the  Department  of  Health  of  New  York  City,  Journal  of  Ex- 
perimental Medicine,  August  25,  1905,  vol.  vii.,  No.  5,  pp.  401-632. 

So  far  as  season  is  concerned,  there  can  be  no  doubt  that  the  summer 
and  autumn  are  the  months  in  which  the  fewest  cases  occur.  Thus, 
the  combined  statistics  of  Seitz,  in  Munich,  and  Jiirgensen  for  six  large 
German  towns,  and  of  Sturgis  for  Westminster  Hospital,  London,  show 
that  in  winter  the  incidence  is  31.7  per  cent.;  in  the  spring,  34.6  per  cent.; 
in  the  summer,  15.1  per  cent.,  and  in  the  autumn,  18.5  per  cent.  The 
following  chart  is  based  upon  35,828  cases  occurring  in  hospitals  in  the 
United  States,  Germany,  and  x\ustria,  and  19,000  cases  occurring  in  the 
Confederate  army  during  the  year  1862,  collected  by  Joseph  Jones. 

Exposure  to  cold  was  thought  for  many  years  to  be  a  cause  of  croupous 
pneumonia,  but  we  now  know  that  this  only  acts  as  a  predisposing  cause 
which  decreases  the  general  systemic,  or  local,  powers  of  resistance  to  infec- 
tion; in  other  words,  it  is  prone  to  affect  all  persons  whose  vital  resistance 
is  diminished.  Living  in  poorly  ventilated  rooms  is  a  predisposing  cause, 
as  is  prolonged  physical  or  mental  strain,  or  any  condition  which  saps 
vitality.  A  very  interesting  illustration  of  the  effect  of  fatigue,  bad  air,  and 
exposure  in  the  production  of  croupous  pneumonia  has  been  recorded  by 
Connell,  of  Leadville,  Colorado,  who  reports  the  common  occurrence  of 
the  disease  in  miners  and  others  who  go  on  long  railway  journeys  for  a 
day's  outing  and  live  during  that  time  in  badly  ventilated  railway  cars. 

In  many  cases  of  acute  or  chronic  disease,  death  results  not  from  the 
primary  malady,  but  from  the  superimposed  croupous  pneumonia  which 
attacks  the  feeble  individual,  who  may  be  just  about  to  touch  the  shores 
of  convalescence.    In  these  cases  it  is  a  true  "terminal  infection." 

Croupous  pneumonia  is  also  a  disease  peculiarly  apt  to  attack  those  of 
advanced  years,  and  a  very  large  proportion  of  deaths  among  the  aged  is 
due  to  this  cause,  such  patients  seeming  to  possess  little  resistance  to  its 
attack.  This  inability  to  resist  the  infection  depends  upon  at  least  two 
causes — viz.,  a  feeble  heart  muscle  which  cannot  meet  the  circulatory 
demands  of  the  disease  nor  resist  the  depressant  effects  of  its  toxins; 
diseased  kidneys,  or  kidneys  impaired  in  function,  whereby  toxic  materials 
cannot  be  speedily  eliminated,  and  as  the  general  result  of  which  the  vital 


CROUPOUS  PNEUMONIA 


145 


Fig.  32 


S       SB 


resistance  of  all  the  tissues  is  diminished,  so  that  not  only  the  Micrococcus 
lanceolatus  is  permitted  full  sway,  but  the  patient  is  also  placed  in  a  favorable 
condition  for  the  growth  of  other  infecting  micro-organisms  which  aid 
in  producing  a  fatal  issue.  It  is  because  of  these  facts  that  pneu- 
monia so  frequently  attacks  those 
who  are  already  in  ill  health,  or 
who  are  suffering  primarily  from 
some  other  malady,  and  it  is  for 
these  reasons  that  it  so  often  ends 
in  death.  Acute  and  chronic  alco- 
holism greatly  predispose  to  croup- 
ous pneumonia,  and  it  is  a  sin- 
gularly fatal  disease  in  persons 
addicted  to  alcohol. 

Sometimes  an  injury  to  the  chest 
wall  will  be  followed  by  acute 
croupous  pneumonia,  probably  be- 
cause the  trauma  to  the  lung  ren- 
ders it  susceptible  to  infection. 
Numerous  experimental  observa- 
tions have  confirmed  this  clinical 
fact,  which  may  be  of  great  im- 
portance from  a  medicolegal  stand- 
point, as  well  as  from  the  purely 
clinical  aspect.  Without  doubt 
local  injury  renders  a  part  peculiarly 
susceptible  to  infection  by  any 
pathogenic  micro-organisms  which 
may  enter  it,  and  as  the  pneumo- 
coccus  is  a  constant  inhabitant  of 
the  mouth  in  healthy  persons,  a 
source  of  infection  is  ever  present. 

There  can  be  no  doubt  that  the 
disease  is  capable  of  being  spread 
from  one  patient  to  another.  On 
several  occasions  I  have  seen  pneu- 
monia contracted  by  the  wife,  or 
daughter,  of  a  patient  who  was  en- 
gaged in  nursing  him,  and  repeatedly  it  has  occurred  that  the  introduction 
of  a  case  of  pneumonia  into  a  ward  of  a  hospital  has  resulted  in  the  de- 
velopment of  the  disease  in  other  patients.  Thus,  out  of  eleven  women 
suffering  from  typhoid  fever  on  admission  to  my  wards  in  the  Jefferson 
Medical  College  Hospital,  no  less  than  eight  suffered  from  croupous  pneu- 
monia after  the  introduction  of  a  single  case  of  this  disease. 

Unlike  many  of  the  acute  infectious  diseases,  one  attack  does  not  protect 
against  another,  but  rather  predisposes  the  patient  to  subsequent  attacks. 

Distribution. — Croupous  pneumonia  is  met  with  in  all  parts  of  the  world, 
but  it  is  more  common  in  the  temperate  than  in  the  tropical  zones.    In  the 
10 


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Chart  showing  the  seasonal  incidence  of  croupous 
pneumonia. 


146  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

United  States  the  census  for  1900  shows  that  its  greatest  mortahty  occurs 
in  the  great  Northwestern  States  east  of  the  Rocky  Mountains,  in  which 
district  it  causes  120,  or  more,  deaths  per  1000  deaths  from  known 
causes.  Only  a  few  areas  in  the  States  east  of  this  area  have  so  heavy  a 
mortahty,  even  if  large  cities  like  New  York,  Philadelphia,  and  Chicago  are 
included. 

Frequency. — Statistics  as  to  its  frequency  are  to  some  extent  vitiated  by  the 
fact  that  in  many  health  reports  the  difference  between  the  various  forms  of 
pneumonia  is  not  specified.  There  can  be  no  doubt,  however,  that  it  is  one 
of  the  most  common  and  most  fatal  of  all  acute  infectious  diseases,  and 
that  its  frequency  and  mortality  are  increasing.  The  United  States  census 
for  1900  shows  that  during  that  year  the  total  mortality  from  pneumonia 
was  105,971,  of  whom  58,340  were  males  and  47,631  were  females.  The 
proportion  of  deaths  was  106.1  for  each  1000  deaths  from  all  known 
causes.    Its  average  mortality  is  about  1.5  to  2.3  per  1000  persons  living. 

At  times  croupous  pneumonia  may  occur  in  epidemic  form  and  cause 
an  extraordinary  increase  in  the  death  rate  of  a  given  district.  Thus,  the 
mortality  from  this  disease  in  Chicago,  as  shown  by  Reynolds  in  his  official 
report  covering  the  period  from  January  1  to  June  1, 1903,  became  remarkably 
high.  There  were  2891  deaths  from  pneumonia,  as  compared  with  1321  from 
consumption  and  1238  from  all  other  communicable,  contagious,  or  infectious 
diseases,  including  diphtheria,  erysipelas,  influenza,  measles,  puerperal  fever, 
scarlet  fever,  smallpox,  typhoid  fever,  and  whooping-cough.  This  is  an  excess 
of  382  pneumonia  deaths  over  the  deaths  from  all  the  other  preventable  dis- 
eases— 1570,  or  118.8  per  cent.,  more  than  the  deaths  from  consumption,  and 
1653,  or  133.5  per  cent.,  more  than  those  from  the  other  specified  diseases. 

Riviere  found  65  cases  of  croupous  pneumonia  in  260  cases  reported  as 
cases  of  "pneumonia"  occurring  in  infants  under  two  years.  He  believes 
that  the  disease  is  more  frequent  in  infancy  than  in  early  childhood. 

Croupous  pneumonia  occurs  with  the  greatest  frequency  between  the  ages 
of  forty  and  fifty  years,  but  it  is  also  very  common  between  fifty  and  sixty. 
The  mortality  is  in  direct  proportion  to  the  age  of  the  patient.  It  affects 
males  far  more  frequently  than  females,  the  proportion  being  as  high  as  88 
per  cent,  in  the  former  to  12  per  cent,  in  the  latter  (Kerr).  This  proportion  in 
favor  of  men  is  probably  too  high  for  the  average,  but  it  serves  to  emphasize 
the  fact  stated,  and  is  approximately  correct.  The  reason  probably  lies  in 
the  greater  exposure  of  men  to  cold  and  wet  and  to  their  abuse  of  alcohol. 

The  relative  frequency  with  which  croupous  pneumonia  affects  the  right 
and  left  lung,  as  based  on  many  thousand  cases  collected  by  Meltzer  in 
Russia;  Jiirgensen,  Moellmann,  and  Brach  in  Germany,  and  West  and  Pye- 
Smith  in  England,  is  for  the  right  lung,  51.4  per  cent.;  left,  39.4  per  cent, 
and  for  both  lungs,  9.2  per  cent. 

In  495  cases  examined  at  autopsy,  and  collected  by  Fowler,  Osier,  Kerr, 
and  Steven  in  this  coimtry  and  England,  the  disease  was  unilateral  in  83  per 
cent.  It  is  unilobar  in  the  proportion  of  about  50  per  cent.  The  disease 
affects  a  lower  lobe  in  nearly  75  per  cent,  of  the  cases. 

Prevention. — At  the  present  time  we  have  no  means  of  directly  preventing 
development  of  this  disease.    It  is  hardly  necessary  to  state  that  the  sputum 


CROUPOUS  PNEUMONIA  147 

of  the  patient  should  be  received  into  a  spit-cup  containing  some  suitable 
disinfectant,  or  into  a  cloth  which  should  be  speedily  burned.  A  patient 
suffering  from  croupous  pneumonia  should  not  sleep  in  the  same  bed  with  a 
person  who  is  in  health,  and  should  be  isolated  as  much  as  possible. 

Pathology  and  Morbid  Anatomy. — In  studying  croupous  pneumonia  it  must 
not  be  forgotten  that  the  disease  is,  at  least  in  some  cases,  a  general  infec- 
tion with  the  Micrococcus  lanceolatus,  the  morbid  changes  being  chiefly  man- 
ifested in  the  lungs,  just  as  in  typhoid  fever  they  are  chiefly  manifested  in 
Peyer's  patches.  The  pneumococcus  is  found  in  the  blood  during  the  prog- 
ress of  this  disease  with  great  frequency,  now  that  proper  methods  for  its 
discovery  are  employed.  Thus,  Prochaska  has  found  it  in  the  blood  in  38 
out  of  40  consecutive  cases,  and  Rosenow  has  isolated  it  in  77  out  of  83 
cases,  and  has  discovered  it  in  the  blood  as  early  as  twelve  hours  after  the 
initial  chill.  On  the  other  hand,  the  mere  presence  of  the  pneumococcus  in 
the  blood  of  a  patient  does  not  necessarily  mean  that  pneumonia  is  present, 
for  it  has  been  found  in  the  blood  in  cases  of  tonsillitis,  otitis,  arthritis,  and 
in  pulmonary  oedema.  Parker  and  many  others  have  even  described  cases 
of  purulent  peritonitis  due  to  this  organism. 

While  it  is  true,  as  already  stated,  that  croupous  pneumonia  is,  in  its 
typical  form,  due  to  the  Micrococcus  lanceolatus,  it  is  also  a  fact  that  lobar 
pneumonia  or  consolidation  of  the  vesicular  portions  of  a  lobe  or  lobes  may 
arise  from  infection  by  other  micro-organisms.  Such  an  occurrence  is,  how- 
ever, rare,  the  non-specific  infection  resulting  usually  in  abortive  changes  in 
the  pulmonary  parenchyma,  or  running  a  course  at  variance  with  that  com- 
monly pursued  by  the  true  infection. 

Engorgement  Stage. — The  first  change  taking  place  in  the  lung  in 
croupous  pneumonia  is  a  hypersemia  of  the  intervesicular  tissues  of  the  lobe 
or  lobes  about  to  be  consolidated.  This  engorgement  rapidly  becomes  more 
marked,  and  is  accompanied  by  the  exudation  into  the  air  vesicles  of  white 
cells  (apparently  transitional  leukocytes)  and  red  blood  cells  and  serum, 
with  fibrinous  material,  which  speedily  becomes  solidified,  so  that  all  that 
part  of  the  lung  which  is  affected  may,  in  the  course  of  a  few  hours,  be 
devoid  of  air  and  impervious  to  its  passage,  except  in  those  bronchial  tubes 
which  are  of  some  size. 

Stage  of  Red  Hepatization. — The  lung  is  now  said  to  be  in  the  stage 
of  red  hepatization  (Fig.  33) ,  since  the  exudate  is  red  from  blood-coloring 
matter,  and  the  consistency  of  the  organ  to  touch  and  on  section  resembles 
that  of  fresh  liver;  hence  it  is  said  to  be  hepatized  or  liver-like. 

When  a  cross-section  is  made  of  the  solidified  lung  the  surface  is  seen  to 
be  granular  because  of  the  protrusion  of  the  exudate  from  the  air  spaces.  In 
some  instances  the  cut  surface  is  found  not  to  be  uniformly  solid,  probably 
because  the  process  is  less  marked  in  some  places  than  in  others.  This 
appearance  of  the  lung  on  section  is  also  largely  modified  in  young  children 
and  in  greatly  enfeebled  individuals,  in  whom  the  degree  of  solidification 
may  be  much  less  marked.  If  the  exudate  is  examined  microscopically,  it 
will  be  found  to  contain  not  only  shreds  of  fibrin,  red  and  white  cells,  and 
desquamated  epithehal  cells  from  the  walls  of  the  vesicles,  but  large  numbers 
of  pneumococci  as  well.     That  the  amount  of  extravasation  is  in  many 


148 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


cases  extremely  large  is  shown  by  the  fact  that  a  lung  may  increase  in 
weight  by  six  or  seven  pounds. 

Stage  of  Gray  Hepatization. — Following  the  stage  of  red  hepatization 
there  ensues  the  stage  of  gray  hepatization.  At  this  time  the  acute  inflam- 
mation in  the  lung  has  passed  by  and  the  system  is  beginning  the  task  of 
clearing  away  the  results  of  the  disease,  which  is  accomplished  by  the 
cells  which  have  been  extravasated  undergoing  fatty  degeneration  and 
granular  change  while  the  fibrin  undergoes  softening.  During  this  stage 
of  resolution  the  exudate  is  gotten  rid  of  by  absorption  and  expectoration. 
Finally,  the  air  cells  are  freed  from  the  exudate  with  which  they  were 
filled,  the  epithelial  lining  is  reproduced,  and  recovery  results. 


Fig.  33 


Lung ;  croupous  pneumonia,  stage  of  red  hepatization.  The  centre  of  the  microscopic  field  is  occupied 
by  an  air  vesicle  containing  a  mass  of  exudate  composed  of  a  networli  of  fibrin,  red  blood  cells,  and  a 
few  leukocytes. 

Unusual  Changes. — In  rare  instances  the  normal  process  of  resolution 
is  not  followed,  and  in  its  place  organization  of  the  materials  which  have 
been  extravasated  takes  place  to  some  degree,  new  connective  tissue  is  pro- 
liferated into  the  air  vesicles  from  their  walls,  and  fibrous  bands  containing 
bloodvessels  extend  throughout  the  lungs.  Simultaneously  a  similar  growth 
takes  place  in  the  interstitial  tissues,  and  so  the  lung  gradually  becomes 
consolidated  by  overgrowth  of  fibrous  tissue. 

Flexner  and  others  have  urged  the  view  that  unresolved  lobar  pneumonia 
is  due  to  the  fact  that,  owing  to  some  disproportion  between  the  leukocytes 
and  other  constituents  of  the  exudate,  or  other  causes  as  yet  undiscovered, 
the  normal  process  of  autolysis  is  not  carried  out,  and  so  the  exudate  under- 
goes organization  instead  of  resolution. 

In  other  instances  which  are  far  more  rare  the  process  of  resolution  is  sup- 
planted by  the  development  of  abscess  or  gangrene  of  the  lung,  which  con- 


CROUPOUS  PNEUMONIA  I49 

ditions  are  probably  due  to  secondary  infection  of  the  lung  by  the  strepto- 
coccus pyogenes,  or  staphylococcus  pyogenes,  or  other  bacteria  capable  of 
producing  such  lesions.  Sometimes  the  process  of  fatty  change  and  death 
of  the  extravasated  cells  is  so  rapid  that  on  section  of  the  lung  the  vesicles 
exude  a  purulent  matter  looking  like  true  pus,  which  indeed  it  may  be,  but 
this  in  no  sense  is  an  abscess  of  the  lung. 

Associated  with  the  changes  in  the  lungs  we  find  adjacent  organs  involved 
by  direct  extension  of  the  inflammatory  process  or  by  the  infection  itself.  The 
most  common  of  these  is  inflammation  of  the  bronchi  (bronchitis),  which 
is  practically  always  present.  After  bronchitis  in  frequency  comes  inflam- 
mation of  the  pleura,  due  to  direct  extension  from  the  underlying  lung  and 
to  infection  of  the  pleura  by  the  specific  organism  of  the  disease.  Nearly 
always  this  is  manifested  by  the  formation  of  a  plastic  fibrinous  exudate  on 
the  serosa  and  an  abnormal  amount  of  fluid  in  some  part  of  the  pleural 
cavity,  which  fluid  is  often  serous  and  not  infrequently  purulent.  (See 
Pleuritis.) 

Sometimes  the  pericardium  is  similarly  affected,  and  even  the  endocardium 
may  be  infected  by  the  specific  germ.  (See  Pericarditis  and  Endocarditis, 
under  Complications.) 

Reference  is  made  elsewhere  to  the  meningitis  which  sometimes  develops. 

It  is  a  great  mistake  to  view  the  lesions  just  described  as  representing  all 
the  pathology  of  croupous  pneumonia.  It  is  true  that  these  changes  are  the 
most  evident,  but  it  is  not  to  be  forgotten  that  the  toxaemia  of  the  malady 
exerts  a  very  great  influence  in  producing  symptoms  and  lesions  during  life 
which  are  not  so  readily  seen,  but  are  equally  important  in  their  influence  on  the 
patient.  The  muscular  fibres  of  the  heart  and  the  epithelial  cells  of  the  kidneys 
undergo  albuminous  degeneration,  and  similar  changes  occur  in  the  liver. 
When  the  heart  is  opened  after  death  we  frequently  find  its  cavities,  partic- 
ularly those  of  the  right  side,  almost  filled  by  firm  clots,  part  of  which  may 
have  formed  so  long  before  death  as  to  be  of  the  "  chicken-fat"  type.  The  liver 
is  often  found  to  be  greatly  engorged  with  blood,  because  of  the  impeded  cir- 
culation in  the  vena  cava,  produced  by  the  difficulty  with  which  the  right  side 
of  the  heart  empties  itself.  The  bronchial  lymph  glands  also  show  by  the 
swelling  of  their  cells  and  by  their  distended  sinuses  that  they  have  en- 
deavored to  prevent  the  entrance  of  the  micrococcus  and  its  toxins  into  the 
general  system,  for  in  them  may  be  found  broken-down  cells,  red  cells, 
pneumococci,  and  phagocytes  containing  cells  or  organisms. 

My  colleague,  Coplin,  has  shown  that  definite  changes  take  place  in  the 
intercostal  muscles  in  the  course  of  pneumonia  and  pleurisy.  1.  Granular 
degeneration  or  cloudy  swelling  of  the  muscle  fibres,  which  is  probably  a  part 
of  the  general  action  of  the  toxic  bodies  circulating  in  the  blood.  2.  The 
muscle  fibres  are  dissociated,  oedema  is  present,  but  there  is  little  fibrin-con- 
taining substance.  Groups  of  muscle  fibres  and  bundles  show  changes  that 
cannot  be  differentiated  from  the  hyaline  degeneration  described  by  Zenker 
as  occurring  in  the  muscles  of  the  abdominal  wall  in  typhoid  fever.  3.  In 
addition  to  the  changes  already  described,  leukocytes  become  abundant, 
bacteria  are  often  present,  and,  finally,  if  the  inflammatory  process  is  chronic, 
there  is  an  overgrowth  of  fibrous  tissue  and  fatty  infiltration  of  the  muscle. 


150  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Incubation. — The  incubation  period  of  croupous  pneumonia  is  forty-eight 
hours. 

Symptoms. — Before  describing  the  symptoms  met  with  in  cases  of 
croupous  pneumonia,  it  is  essential  to  emphasize  the  fact  that  in  no  other 
infectious  disease  are  the  manifestations  of  illness  so  variable.  These 
variations  depend  not  only  upon  the  virulence  of  the  infecting  germ  and 
the  susceptibility  of  the  patient,  but  upon  his  habits,  age,  and  general  state 
of  health.  In  some  cases  the  malady  develops  as  a  frank,  open  inflamma- 
tion of  the  lung.  In  others  it  is  so  insidious  as  to  be  overlooked,  except 
by  the  most  careful  physician.  In  certain  cases  the  course  of  the  disease 
is  markedly  sthenic,  in  others  profoundly  adynamic.  In  still  others  the 
progress  is  so  mild  that  the  patient  is  never  seriously  ill,  and  in  some 
instances  it  springs  like  a  tiger  upon  a  seemingly  healthy  man  and 
destroys  him. 

The  symptoms  of  croupous  pneumonia  may  be  divided  into  three  stages 
for  readiness  of  description — namely,  those  of  onset,  those  of  the  well- 
developed  stage,  and  those  of  convalescence. 

Stage  of  Onset. — The  patient,  usually  an  adult,  is  seized  after,  or  without,  a 
brief  period  of  general  malaise,  with  a  chill,  followed  by  a  well-developed  fever, 
The  chills  may  be  repeated  and  may  vary  from  a  slight  feeling  of  creepiness 
to  a  severe  rigor  of  sufficient  force  to  shake  the  patient  severely,  and  to  last 
for  over  an  hour.  The  pulse  is  quickened,  but  not  as  much  so  as  we  would 
expect  from  the  sharpness  of  the  onset,  and  at  first  may  be  small,  but  soon 
becomes  full  and  bounding  if  the  patient  has  been  previously  in  good  health; 
the  respirations  are  also  markedly  increased  in  rate  per  minute.  More  or 
less  severe  pain  may  be  felt  in  the  chest  on  the  affected  side.  The  degree  of 
pain,  however,  varies  greatly,  some  patients  bitterly  complaining  of  it,  while 
others  seem  to  have  little  or  no  suffering,  probably  because  in  the  latter 
cases  the  inflammation  of  the  lung  is  so  deeply  situated  that  it  does  not 
extend  to  and  involve  the  visceral  layer  of  the  pleura.  It  is  important  to 
bear  in  mind  the  fact  that  this  pain  not  infrequently  is  referred  by  the 
patient  to  another  part  of  the  body.  I  had  a  case  admitted  not  long  since 
to  my  wards,  on  the  statement  of  a  well-known  physician  that  she  had  ap- 
pendicitis, when  she  was  really  suffering  from  a  pleuropneumonia  of  the 
right  lower  lobe.  Children  are  very  prone  to  refer  the  pain  to  the  epigas- 
trium. 

If  the  patient  is  very  feeble  it  sometimes  happens  that  the  onset  of  the 
malady  is  insidious  and  no  pain  is  felt.  This  is  especially  apt  to  be  true 
when  the  disease  complicates  chronic  alcoholism,  renal  disease,  or  other 
grave  malady. 

The  temperature  usually  makes  a  sharp  and  decided  rise,  immediately 
after  or  during  the  chill,  to  103°  or  105°,  and  in  some  cases  even  higher  than 
this,  and  remains  high  throughout  the  disease,  the  variation  in  the  morn- 
ing and  evening  temperature  not  being  more  than  a  degree  or  a  fraction 
thereof.     (See  Fig.  34.) 

The  face  is  usually  flushed,  particularly  over  the  cheek  bones,  and  it  is  a 
noteworthy  fact  that  this  flush  is  usually  most  marked  upon  the  cheek  of  the 
same  side  as  the  lung  involved.    The  expression  of  the  face  is  apt  to  be  some- 


CROUPOUS  PNEUMONIA  151 

what  anxious,  the  skin  dry  and  hot,  and  a  moderate  degree  of  cyanosis  may 
be  seen  in  the  capillaries  of  the  lips  and  finger-tips,  and  about  the  nose. 

Violent  headache  may  or  may  not  be  present.  A  more  or  less  active  delirium 
may  also  develop  at  this  time,  and  the  patient  may  be  quite  restless  unless  the 
pain  in  the  side  makes  it  more  comfortable  to  lie  quietly  in  bed.  An  incessant 
unproductive  cough  is  often  an  early  symptom  of  onset. 

The  physical  signs  of  the  disease  in  the  thorax  in  the  stage  of  onset  are  not, 
as  a  rule,  well  marked.  Inspection  may  reveal  some  impairment  of  expansion 
upon  the  affected  side;  palpation  may  evince  some  increase  in  vocal  fremitus; 
auscultation  will  show  in  many  cases  fine  crepitant  rales,  increased  bronchial 
breathing  or  tubular  sounds,  increased  loudness  of  vesicular  breathing  for  a 
few  hours,  and  often  some  exaggeration  of  the  normal  respiratory  sounds 
on  the  sound  side.  Indeed,  this  increase  in  the  harshness  of  the  breath 
sounds  over  the  normal  side,  due  to  the  increased  activity  on  the  part  of  the 
healthy  lung,  to  compensate  for  the  impairment  of  the  diseased  lung,  may 
mislead  the  beginner  in  physical  diagnosis  into  thinking  that  this  is  the 
lung  diseased.  Percussion  may  also  reveal  some  impairment  of  resonance 
over  the  affected  area. 

Developed  Stage. — The  developed  stage  of  the  disease  is  characterized 
by  certain  conditions  and  physical  signs,  some  of  which  are  almost  pathog- 
nomonic of  the  malady.  The  peculiarity  of  the  pulse  is  that  it  is  quite  slow 
as  compared  to  the  rapidity  of  the  respirations.  Usually  when  high  fever  is 
present  the  pulse  rate  is  as  high  as  110  or  120,  or  even  higher,  while  the 
respirations  are  about  24,  but  in  pneumonia  of  the  croupous  type  the  pulse 
rate  is  sometimes  only  90,  while  the  respirations  are  as  high  as  30  per  minute. 
More  commonly,  however,  the  respiratory  rate  mounts  to  as  high  a  point 
as  40  or  50  per  minute,  while  the  pulse  reaches  110  to  120,  the  relative  pro- 
portion being  1  to  3,  while  in  health  it  is  usually  about  1  to  4.5. 

A  second  peculiarity  of  this  stage  is  the  rusty  or  bloody  sputum,  which  is 
still  more  characteristic  in  that  it  is  sticky  and  tenacious,  and  therefore 
difficult  to  expectorate,  and  so  adherent  that  even  when  a  spit-cup  is  filled 
with  it  the  vessel  can  be  held  nearly  upsidedown  without  losing  its  contents. 

A  third  characteristic  of  croupous  pneumonia  at  this  stage  is  the  develop- 
ment of  single  or  multiple  fever  blisters,  or  spots  of  herpes,  upon  the  lips  or 
about  the  edges  of  the  nostrils. 

Dyspnoea  may  or  may  not  be  present.  If  present  it  depends  upon  the  fact 
that  so  much  of  the  lung  is  involved  that  respiration  is  difficult,  or  it  is  due 
to  feebleness  of  the  heart  from  engorgement  of  its  right  ventricle  by  the  blood 
which  cannot  pass  readily  through  the  diseased  lung;  or,  again,  it  may  be 
dependent  upon  actual  impairment  of  the  powder  of  the  heart  as  a  result  of 
the  action  of  the  toxin  of  the  disease  upon  its  muscular  tissues  and  nerve 
centres.  Dyspnoea  in  croupous  pneumonia  may,  therefore,  be  due  to  pul- 
monary, cardiac,  or  toxic  causes.  Cyanosis  may  be  very  marked,  and  not 
uncommonly  the  jugular  and  other  superficial  veins  can  be  seen  to  be  full 
and  distended. 

A  peculiarity  of  the  dyspnoea  of  pneumonia  is  the  fact  that  the  patient  does 
not  seem  capable  of  resting  quietly,  but  continually  moves  about,  making 
exertions  which  seem  scarcely  compatible  with  so  much  shortness  of  breath. 


152  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Delirium  of  an  active  type  is  common  in  this  stage,  and  it  may  be  difficult 
to  keep  the  patient  in  bed,  particularly  if  he  is  an  alcoholic. 

During  the  second  stage  of  croupous  pneumonia  the  pulse  may  become 
hobbling  or  dicrotic,  the  heart  sounds  tumultuous,  and  the  dyspnoea 
severe.  In  other  instances  the  pulse  seems  voluminous,  but  nevertheless 
is  very  easily  compressed  to  the  point  of  extinction,  while  the  sounds  of  the 
heart  reveal  the  fact  that  that  viscus  is  laboriously  endeavoring  to  fill  vessels 
which,  because  of  their  relaxation,  fail  to  offer  the  normal  resistance  to  its 
action.  In  still  other  instances,  if  the  heart  is  markedly  affected  by  the 
toxaemia  of  the  disease,  the  heart  sounds  will  be  feeble  and  difficult  to  differ- 
entiate, and  the  pulse  be  very  small  and  easily  extinguished  by  pressure.  In 
still  other  cases  auscultation  over  the  area  of  the  pulmonary  valves  at  the  third 
left  interspace  will  reveal  accentuation  of  the  pulmonary  second  sound  or  a 
murmur  due  to  incompetency  of  these  valves  under  pressure,  while  later  on 
the  labored  action  of  the  heart  is  shown  not  only  in  the  signs  named,  but  also 
in  the  pulsating  jugular  veins,  which  are  distended  and  full,  indicating  great 
venous  engorgement,  as  the  result  of  the  obstruction  of  the  flow  of  blood  out 
of  the  right  ventricle,  or  because  of  inco-ordination  of  the  auricular  and 
ventricular  contractions,  as  the  result  of  the  formation  of  a  heart  clot  or 
from  toxaemia. 

The  physical  signs  of  croupous  pneumonia  in  the  well-developed  stage  are 
quite  characteristic  in  typical  cases.  Inspection  shows  an  even  greater 
impairment  of  expansion  on  inspiration  on  the  affected  side  than  in  the  stage 
of  onset,  and  palpation  reveals,  when  the  patient  speaks,  a  distinct  increase  in 
vocal  fremitus  over  the  part  of  the  lung  which  is  diseased.  Auscultation  gives 
a  harsh  inspiratory  sound,  prolongation  of  expiration,  and  a  large  number  of 
fine  crackling  or  crepitant  rales  in  the  same  area,  so  fine  that  they  may  not  be 
heard  by  the  careless  examiner.  They  sound  very  much  as  does  that  noise 
which  is  produced  by  moistening  the  tip  of  the  forefinger  and  thumb  with 
saliva,  pressing  them  together,  and  separating  them,  or,  again,  as  does  the 
sound  made  by  the  hair  which  grows  over  the  examiner's  ear  when  it  is 
rubbed  between  the  finger  and  thumb.  Ordinary  vesicular  breathing  over 
the  area  diseased  is  absent,  and  in  its  place  is  heard  bronchial  breathing, 
which  is  caused  by  the  air  in  the  bronchial  tubes,  which  produces  a  sound 
which  is  transmitted  through  the  consolidated  lung  unmuffled  by  the  vesic- 
ular murmur  usually  present.  Auscultation  while  the  patient  speaks  will 
also  show  a  distinct  increase  in  vocal  resonance.  That  is  to  say,  the  sound 
of  the  voice  will  be  transmitted  through  the  chest-wall  with  a  greater  degree 
of  clearness  than  in  health.  While  auscultation  is  being  performed  in  cases 
which  have  a  delicately  developed  chest,  as  in  youths  and  children,  it  is 
often  noted  that  the  movement  of  the  anterior  chest-wall  under  the  ear  is 
not  uniform,  but  undulating,  one  part  expanding  at  an  appreciable  interval 
before  the  other. 

Percussion,  a  most  valuable  aid  in  the  diagnosis  of  this  disease,  reveals,  if 
the  lesion  in  the  lung  is  near  the  surface,  marked  impairment  of  resonance 
amounting  to  dulness,  but  it  is  a  fact  well  worth  remembering  that  if  the  lesion 
in  the  lung  is  deep  seated,  and  not  near  its  surface,  the  percussion  note  over 
the  area  diseased  may  not  be  impaired  or  dull,  but  hyperresonant,  or,  as 


CROUPOUS  PNEUMONIA  153 

Samuel  West  has  said,  "boxy"  in  character.  Usually  hyperresonance  is 
demonstrable  all  over  the  lung,  except  where  it  is  consolidated,  and  is  also 
to  be  found  upon  the  healthy  side  of  the  chest,  owing  to  the  increased 
amount  of  air  which  is  in  these  parts  to  compensate  for  the  area  of  consolida- 
tion; but  careful  examination  will  reveal  the  fact  that  the  hyperresonance 
over  the  consolidated  area,  or  in  its  immediate  neighborhood,  has  a  different 
tone  from  that  in  the  healthy  and  compensating  lung,  the  "boxy"  note  just 
named.  I  have  frequently  been  able  to  determine  the  presence  of  deep- 
stated  pneumonia  by  the  presence  of  this  sign.  By  the  aid  of  careful  auscul- 
tation and  percussion  it  is  usually,  but  not  always,  possible  to  definitely 
determine  the  exact  area  of  the  lung  which  is  involved. 

While  in  the  majority  of  cases  these  positive  signs  of  croupous  pneumonia 
may  be  found  in  a  more  or  less  well-developed  form,  it  is  not  to  be  forgotten 
that  negative  signs  may  be  as  valuable  in  making  a  diagnosis.  That  is  to  say, 
there  may  be  absence  of  any  one  or  all  of  the  signs  just  enumerated,  and  a 
total  absence  of  vesicular  breathing.  In  such  cases,  therefore,  the  physician 
must  exercise  care  lest  the  loud  and  exaggerated  breath  sounds  of  the 
healthy  part  of  the  chest  mislead  him  into  thinking  that  that  portion  is  the 
one  which  is  diseased. 

In  certain  instances,  in  which  the  action  of  the  heart  is  very  labored,  its 
sounds  distant,  and  the  pulse  is  small  and  insufficient,  careful  examination 
may  reveal  a  pericarditis  with  effusion,  which,  by  its  pressure,  interferes 
with  the  movement  of  the  cardiac  muscle.  This  question  as  to  whether  there 
is  pressure  by  pericardial  effusion  is  by  no  means  readily  determined,  because 
it  frequently  happens  that  there  is  a  marked  degree  of  cardiac  dilatation 
present  at  this  time,  which  naturally  increases  the  area  of  cardiac  dulness 
downward  and  to  the  right.  Further,  as  it  is  the  right  ventricle  which  is 
most  apt  to  be  engorged,  the  area  of  cardiac  dulness  may  be  abnormally 
great  in  this  direction.  Again,  it  not  infrequently  occurs  that  the  compen- 
satory fulness  of  the  healthy  lung,  if  the  disease  is  on  the  left  side,  pushes 
the  heart  downward  and  to  the  left,  or,  on  the  other  hand,  if  the  right 
lung  is  diseased,  the  unusual  expansion  of  the  left  lung  causes  an  extension 
of  pulmonary  resonance  to  the  right,  and  so  increased  area  of  cardiac 
dulness  is  very  effectually  masked. 

Patients  suffering  from  croupous  pneumonia  should  always  be  turned  on 
the  side  when  the  back  is  to  be  examined,  as  it  is  dangerous,  because  of  the 
state  of  the  heart,  for  them  to  sit  up  in  bed. 

The  urinary  flow  during  an  attack  of  croupous  pneumonia  is  usually  dimin- 
ished, so  that  the  passage  of  about  twenty  ounces  of  urine  in  twenty-four 
hours  may  be  taken  as  the  average.  This  urine  is  usually  highly  concen- 
trated, and  contains,  as  does  the  urine  in  most  febrile  diseases,  an  increased 
amount  of  urea  and  an  excess  of  amorphous  urates  which  are  deposited  on 
standing.  It  also  contains,  very  constantly,  a  moderate  amount  of  albumin, 
but  the  chief  peculiarity  is  its  scanty  content  of  chlorides,  which  may  be 
entirely  absent.  If  the  albumin  be  large  in  amount,  or  casts  are  present, 
the  probability  is  that  the  kidneys  were  diseased  before  the  onset  of  the 
pneumonia. 

During  the  course  of  croupous  pneumonia  the  function  of  the  alimentary 


154  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

canal  is  rarely  seriously  disturbed,  although  loss  of  appetite  because  of  the 
fever  may  be  a  marked  symptom.  The  most  important  change  in  any  part 
of  the  digestive  system,  if  it  may  be  so  called,  is  seen  in  the  tongue,  the  state 
of  which  is  noteworthy,  because  it  gives  some  idea  of  the  general  state  of  the 
patient.  It  is,  of  course,  prone  to  be  dry  and  somewhat  coated,  caused  by 
the  rapid  breathing  through  the  mouth,  and  because  of  the  fever;  but  if  it  be 
exceedingly  dry  and  red,  narrow  and  pointed  at  the  tip,  it  possesses  a  more 
positive  significance  as  to  the  general  state  of  the  patient  than  if  it  be  broad 
and  moist. 

Sometimes  when  pneumonia  is  very  severe  and  particularly  when  toxaemia 
is  marked,  an  excessive  degree  of  tympanites  develops,  which  is  of  evil 
significance,  in  that  it  shows  a  diminution  in  vitality  and  causes  interfer- 
ence with  the  action  of  the  lungs  and  heart  by  pressure.  I  have  seen  this  most 
commonly  when  the  disease  has  affected  those  addicted  to  the  excessive 
use  of  alcohol. 

The  nervous  symptoms  of  pneumonia  are  quite  various  and  depend  more 
upon  the  previous  habits  of  the  patient,  the  location  of  the  lesion,  and  the 
degree  of  toxaemia  than  upon  any  other  causes.  Delirium  varies  in  degree 
from  mind  wandering,  as  the  patient  is  about  dropping  off  to  sleep,  to 
active  mania,  during  which  it  may  be  very  difficult  to  keep  the  patient 
in  bed.  The  severity  of  the  delirium  depends  largely  upon  the  age  of 
the  patient  and  his  habits.  Alcoholic  patients  nearly  always  have  de- 
lirium in  a  well-marked  degree,  and  in  this  class  of  patients  it  is  grave 
from  a  prognostic  point  of  view  in  direct  proportion  to  its  constancy  and 
severity. 

The  type  of  the  delirium  also  varies  very  greatly  in  the  strong  and  in  the 
weak.  In  those  who  are  adynamic  from  some  previous  disease  or  from 
bad  habits,  it  is  often  of  a  low  muttering  type,  resembling  that  sometimes 
seen  in  toxic  cases  of  typhoid  fever,  while  in  other  instances  it  may  be  vio- 
lent, as  already  described. 

It  is  a  noteworthy  fact  that  delirium  is  particularly  prone  to  affect  those 
who  suffer  from  pneumonia  at  the  apex  of  the  lung,  and  I  have  frequently 
seen  in  children,  who  had  pneumonia  at  the  apex,  a  delirium  in  which 
there  seemed  to  be  a  constant  fear  of  falling,  so  that  the  child  clutched  its 
mother  every  time  it  was  moved.  Holt's  experience,  on  the  other  hand, 
leads  him  to  believe  that  the  portion  of  lung  involved  has  little  influence  upon 
the  production  of  nervous  symptoms,  and  without  doubt  the  recent  advances 
in  the  study  of  pneumococcus  infection  tend  to  show  that  the  toxaemia  and 
not  the  portion  of  lung  involved  is  responsible  not  only  for  the  marked 
nervous  manifestations,  but  also  for  the  dyspnoea  and  great  acceleration  of 
the  respiration.  A  peculiarity  of  the  delirium  in  many  alcoholic  cases  is 
that  they  labor  under  the  delusion  that  they  are  lying  in  a  coffin,  and  in 
their  constant  efforts  to  escape  greatly  exhaust  themselves.  This  form  of 
delirium  is  exceedingly  grave  from  a  prognostic  standpoint.  Delirium  is 
also  very  much  more  apt  to  be  marked  in  those  patients  who  suffer  from 
toxaemia  than  in  those  in  whom  a  very  considerable  area  of  the  lung  is 
involved,  but  who  have,  nevertheless,  comparatively  slight  signs  of  poisoning 
by  the  toxin  of  the  pneumococcus. 


CROUPOUS  PNEUMONIA 


155 


Very  rarely,  in  young  children,  the  onset  of  the  disease  is  characterized 
by  convulsions  instead  of  by  the  ordinary  chill. 

Insomnia  is  a  very  constant  symptom  of  croupous  pneumonia,  and  may 
become  so  persistent  as  to  require  medicinal  measures  for  its  relief,  par- 
ticularly if  it  be  accompanied  by  great  restlessness. 


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A  chart  of  croupous  pneumonia  In  a  girl  of  six  years,  sliowing  the  little  effect  produced  by  sponging 
upon  the  temperature  and  the  characteristic  crisis  on  the  sixth  day. 

The  skin  in  an  ordinary  case  of  croupous  pneumonia  is  usually  hot  and 
dry;  but  if  the  toxic  element  in  the  case  is  very  marked,  it  may,  as  death 
approaches,  become  cold  and  clammy  and  even  bedewed  with  sweat.  In 
toxic  cases,  too,  it  is  not  infrequently  somewhat  jaundiced.  If  this  jaundice 
is  associated  with  hcemoglobinuria  the  prognosis  is  almost  certainly  fatal. 
On  the  other  hand,  in  some  instances  jaundice  occurs  apparently  as  the 
result  of  the  action  of  the  toxin  upon  the  liver,  and  this  type  is  not  so 
grave. 

Profuse  sweating  nearly  always  occurs  at  the  time  of  crisis.  The  frequency 
with  which  herpes  appears  about  the  mucous  membranes  and  skin  of  the 
mouth  and  nose  has  already  been  mentioned. 

Stage  of  Resolution. — As  the  disease  approaches  the  period  of  crisis, 
and  sometimes  not  until  this  event  has  taken  place,  it  will  be  noted  that  the 
rapidity  of  respiration  as  compared  to  the  rapidity  of  the  pulse  more  nearly 
approaches  the  normal  ratio. 


156  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

The  first  change  which  can  be  noted  in  the  physical  signs  in  the  chest  is  the 
development  of  fine  moist  rales,  which  indicate  the  early  stages  of  resolution. 
These  rales,  when  they  are  first  heard,  are  fine  and  crepitant,  and  closely 
resemble  those  heard  in  the  stage  of  onset;  for  this  reason  they  are  called 
rales  redux. 

The  rales  in  the  chest  become  more  and  more  coarse  and  moist  in  char- 
acter as  convalescence  is  carried  on,  and  the  speed  with  which  nature  in 
an  otherwise  healthy  individual  clears  away  the  exudate  is  quite  extra- 
ordinary, although  usually  for  several  weeks  after  a  sharp  attack  of  croupous 
pneumonia,  involving  the  surface  of  the  lung,  impaired  resonance  on  percus- 
sion and  some  prolongation  of  expiration  with  harsh  inspiration  can  be 
demonstrated. 

The  critical  Jail  of  temperature  is  often  preceded  by  a  sharp  rise,  but 
when  the  fall  occurs  it  takes  place  with  extraordinary  speed,  the  patient 
being  afebrile  or  with  a  subnormal  temperature  within  a  few  hours,  or  even 
within  one  hour  (Fig.  34) .  Sometimes  this  critical  state  is  accompanied  by 
a  profuse  sweat,  and  even  collapse  may  develop,  with  urgent  dyspnoea, 
due  to  vasomotor  palsy  and  vascular  relaxation. 

When  the  fall  is  quite  gradual,  extending  over  a  day,  it  is  called  a  pro- 
tracted crisis  ;  this  very  commonly  occurs  in  children. 

Often  the  day  after  crisis  the  temperature  returns  to  slightly  above  nor- 
mal, and  sometimes  an  apparent  crisis  fails  to  reach  the  normal  and  the 
fever  rises  again.    Such  a  pseudocrisis  is  rarely  seen  after  the  fifth  day. 

The  critical  fall  of  temperature,  as  has  already  been  stated,  usually  occurs 
on  about  the  seventh  or  eighth  day  of  the  disease,  but  it  may  occur  as 
early  as  the  third  day  (Fig.  35).  In  feeble  persons  and  in  children  the 
disease  sometimes  ends  by  lysis. 

Complications. — The  complications  of  croupous  pneumonia  are  quite 
numerous.  Of  these  the  most  frequent  is  undoubtedly  pleurisy.  Indeed, 
it  may  be  said  that  in  almost  every  case  of  croupous  pneumonia  a  certain 
amount  of  inflammation  of  the  pleura  exists.  As  an  illustration  of  this  fact, 
the  statistics  of  Kerr  are  of  value.  Out  of  171  cases  which  came  to  autopsy 
from  croupous  pneumonia,  no  less  than  118  showed  acute  pleuritis.  Of 
these,  74  were  acute  fibrinous  pleuritis,  38  serofibrinous  pleuritis,  and  6  acute 
empyema.  In  Osier's  103  autopsies  pleuritis  was  present  in  all  but  2  cases. 
The  pleuritis  is  due  to  the  extension  of  the  inflammatory  process  to  the  vis- 
ceral layer  of  the  pleura  and  to  infection  of  the  pleural  membrane  by  the 
pneumococcus  or  by  some  other  organism  which  is  associated  with  it.  (See 
Pleurisy).  The  inflammation  of  the  pleura  manifests  itself  by  an  excess  of 
pain  in  the  area  involved,  by  a  friction  sound  on  auscultation,  and  later,  it 
may  be,  by  the  outpouring  of  a  considerable  amount  of  fluid  which  may 
be  serous  or  purulent.  When  the  fluid  is  serous  it  is  often  absorbed  with 
a  rapidity  only  equalled  by  the  absorption  of  the  croupous  exudate  in  the 
lungs.  In  other  instances  it  persists  and  actually  increases  in  quantity, 
relief  only  being  obtained  when  the  physician  performs  paracentesis.  In 
4523  cases  of  croupous  pneumonia,  occurring  in  twelve  large  hospitals  in 
the  United  States  and  England,  pleural  effusion  is  stated  to  have  occurred 
in  233  cases,  a  percentage  of  5.15. 


CROUPOUS  PNEUMONIA 


157 


In  still  other  cases  the  effusion  is  puru- 
lent from  the  beginning,  and  in  this  way 
an  empyema  is  formed.  Like  all  collec- 
tions of  pus,  recovery  can  only  be  reached 
in  the  majority  of  these  cases  by  giving 
vent  to  the  accumulation.  The  presence 
of  the  pus  is  usually  manifested  by  a  re- 
turn, or  maintenance,  of  the  febrile  move- 
ment seen  in  the  early  stages  of  the  dis- 
ease, accompanied,  it  may  be,  by  the  ordi- 
nary manifestations  of  septic  poisoning, 
such  as  chills,  sweats,  and  irregular  tem- 
perature. On  the  other  hand,  all  evi- 
dences of  the  presence  of  pus  may  be 
absent,  owing  to  the  non-absorption  of 
toxic  matters  through  the  pleural  mem- 
brane. In  10,076  cases  of  croupous 
pneumonia  collected  principally  from  the 
official  reports  of  hospitals  in  the  United 
States,  England,  and  Germany,  empyema 
is  stated  to  have  occurred  in  208  cases,  a 
percentage  of  2.06. 

In  all  cases  in  which  speedy  recovery 
from  croupous  pneumonia  does  not  take 
place  and  where  marked  impairment  of 
resonance  persists  upon  the  diseased  side, 
pleural  effusion  or  empyema  should  be 
strongly  suspected,  and  the  tests  for  the 
purpose  of  determining  these  complica- 
tions be  instituted.  Sometimes  the  pres- 
ence of  a  pleural  effusion  is  not  suspected 
because  it  produces  no  symptoms  until, 
by  the  increase  in  its  quantity  or  the 
taking  of  moderate  exercise  by  the 
patient,  it  produces  dyspnoea  by  inter- 
fering with  respiratory  movements.  (See 
articles  on  Pleural  Effusion  and  Em- 
pyema.) It  is  a  noteworthy  fact  that  if 
the  empyema  be  due  to  the  pneumococ- 
cus  the  prognosis  is  more  favorable,  both 
as  to  complete  recovery  and  to  speediness 
of  cure,  than  if  it  be  due  to  some  other 
infecting  micro-organism. 

Hydrojpneumothorax  has  occasionally 
been  recorded  as  a  complication,  but  it 
is  very  rare. 

Gangrene  and    abscess   formation   in   the  lungs  are   two  very  important 
and  serious  lesions  which,  fortunately,  are  not  of   common  occurrence  in 


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Chart  showing  day  of  crisis  in  acute 
croupous  pneumon  ia,  based  on  2166  cases  in 
hospitals  in  the  United  States,  England, 
and  Germany.  The  black  area  shows  the 
proportion  (percentage)  which  have  their 
crisis  on  any  given  day.  The  percentages 
for  third  and  fourth  days  are  taken  from 
Aufrecht's  statistics  alone,  as  they  could 
not  be  ascertained  in  all  the  other  cases. 


158  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

connection  with  cases  of  croupous  pneumonia.  Eisendrath  has  analyzed  96 
recorded  cases  of  pulmonary  abscess,  gangrene,  and  bronchiectasis  following 
croupous  pneumonia.  When  the  totals  are  computed  as  to  percentage  of 
recovery,  the  result  is  quite  striking,  especially  in  the  more  acute  cases.  Of 
25  cases  of  acute  single  abscess,  96  per  cent,  recovered  and  4  per  cent, 
improved;  of  28  cases  of  acute  gangrenous  abscess,  71.4  percent,  recovered, 
7.2  per  cent,  improved,  and  21.4  per  cent.  died.  Of  14  cases  of  chronic 
simple  abscess,  42.8  per  cent,  recovered,  21.4  per  cent,  improved,  and  35.8 
per  cent,  died;  while  in  26  cases  of  chronic  putrid  abscess  with  bronchiec- 
tasis 50  per  cent,  recovered,  15.3  per  cent,  improved,  and  34.7  per  cent.  died. 

Eisendrath  found,  from  his  review  of  the  subject,  that  the  symptoms 
usually  came  on  after  the  crisis  and  consisted  in  a  post-critical  rise  in  tem- 
perature, which  then  became  remittent  in  type.  The  sputum  became  puru- 
lent, and  there  was  a  distressing  cough,  accompanied  by  expectoration  of  pus 
in  large  quantities.  If  the  abscess  cavities  do  not  communicate  with  a  bron- 
chus there  is  but  little  expectoration.  There  is  in  all  cases  emaciation,  loss 
of  appetite,  and  a  rapid  decline  in  strength.  If  the  abscess  becomes  chronic 
there  may  be  recurrent  attacks  of  fever,  with  profuse  expectoration. 

Physical  examination  in  these  cases  is  rather  disappointing.  The  lesions 
are  most  frequently  in  the  lower  lobes,  and  this  is  of  some  aid  in  diag- 
nosis. There  are  no  typical  physical  signs,  owing  to  the  fact  that  the 
cavities,  be  they  due  to  abscess,  gangrene,  or  bronchiectasis,  may  be  near  the 
surface,  or  quite  deeply  situated,  and  may  or  may  not  communicate  with 
a  bronchus.  Dulness,  decreased  respiratory  murmur,  decreased  vocal 
resonance,  and  decreased  fremitus  are  present  in  the  majority  of  cases,  but 
bronchial  breathing  may  be  heard.  The  most  reliable  sign  is  the  presence 
of  large,  moist  rales,  not  infrequently  metallic  in  character.  Another  striking 
feature  is  the  variability  of  the  physical  signs,  so  that  dulness  and  then 
tympany  may  alternate  at  the  same  spot.  Clubbed  fingers  develop  quite 
early,  as  do  also  symptoms  produced  by  pressure  on  the  heart,  liver,  and 
spleen. 

Gangrene  must  be  suspected  when  there  occurs  a  rise  of  temperature,  a 
few  days  after  the  crisis,  and  the  breath  becomes  fetid.  The  sputum  is 
also  fetid  and  divides  itself  into  three  characteristic  layers.  (See  Gangrene 
of  the  Lung.) 

The  frequency  of  haemoptysis  in  cases  of  gangrene  is  due  to  the  fact  that 
the  vessels  are  more  apt  to  pass  freely  through  the  cavity,  owing  to  the 
more  rapid  destruction  of  tissue. 

In  bronchiectasis  following  pneumonia  the  sputum  may  be  fetid  at  times, 
but  the  odor  is  not  so  penetrating  as  in  gangrene  and  there  are  no  elastic 
fibres.  There  is  usually  a  history  of  long-continued  expectoration  of  large 
quantities  of  pus.  This,  however,  is  not  characteristic,  for  the  same  history 
may  be  true  of  chronic  simple  abscess. 

Pericarditis  is  not  a  very  infrequent  complication  of  pneumonia.  In  the 
majority  of  instances  it  is  of  such  mild  degree  that  it  does  not  jeopardize  the 
patient's  life;  but  in  other  instances,  when  the  effusion  which  follows  it  is 
profuse,  it  may,  by  mechanical  pressure,  produce  great  cardiac  disability. 
When  the  accumulation  is  extensive,  a  definite  increase  in  the  area  of  cardiac 


CROUPOUS  PNEUMONIA  159 

dulness  is  usually  demonstrable.  Not  rarely,  however,  the  presence  of  this 
compHcation  may  be  unsuspected  during  the  patient's  life.  Thus,  Thayer 
was  only  made  acquainted  with  the  presence  of  pericarditis  in  one  of  his 
cases  of  croupous  pneumonia  when  the  autopsy  disclosed  a  thick  layer  of 
pyogenic  membrane  over  the  visceral  pericardium,  with  a  large  quantity  of 
pus  in  the  pericardial  cavity.  Some  statistics  seem  to  show  that  pericarditis 
varies  in  frequency  in  from  5  to  16  per  cent,  of  all  cases,  but  in  21,383  cases 
of  croupous  pneumonia  collected  by  me  principally  from  the  official  reports 
of  hospitals  in  the  United  States,  England,  Germany,  and  Austria,  peri- 
carditis is  stated  to  have  occurred  in  only  266  cases  of  croupous  pneumonia, 
a  percentage  of  1.24.     (See  Pericarditis.) 

Endocarditis  is  a  rare  complication,  occurring  much  less  frequently  than 
pericarditis.  In  a  considerable  number  of  cases  the  pneumococcus  is  re- 
sponsible for  the  lesion.  It  often  affects  the  aortic  valves,  and  it  is  gener- 
ally of  the  ulcerative  type.  In  14,510  cases  of  croupous  pneumonia  col- 
lected from  several  series  of  cases  reported  by  German,  Enghsh,  and 
Swedish  physicians,  and  from  official  reports  of  hospitals  in  the  United 
States,  England,  Germany,  and  Austria,  endocarditis  is  stated  to  have 
occurred  in  106  cases,  a  percentage  of  0.73.  Norris  in  500  cases  found  it 
recorded  five  times,  while  Sears  and  Larrabee,  in  Boston,  found  it  9  times 
in  940  cases.  Aufrecht,  in  1500  cases,  met  with  endocarditis  only  once.  Out 
of  a  total  of  5738  cases  of  croupous  pneumonia  von  Brach  found  less  than 
0.2  per  cent,  complicated  by  endocarditis,  and  less  than  0.5  per  cent,  of  them 
complicated  by  pericarditis.  Preble,  from  an  exhaustive  study,  places  the 
average  at  1  per  cent,  in  all  cases  and  5  per  cent,  in  fatal  cases,  and 
these  figures  are  probably  correct.  Osier  found  16  instances  of  endocarditis 
in  100  fatal  cases.  Preble  believes  that  while  pneumonia  is  more  common  in 
males  than  in  females,  endocarditis  due  to  this  infection  is  most  common 
in  females.     (See  Endocarditis.) 

Two  apparently  distinct  types  of  meningitis  are  found  as  complications 
of  croupous  pneumonia;  one  appearing  at  the  onset  of  the  disease,  the  other 
during  the  active  or  post-critical  stage.  The  former  variety  is  seen  most 
frequently  in  children,  and  is  probably  symptomatic;  it  is  rarely  fatal,  and 
therefore  its  pathology  is  somewhat  uncertain.  On  the  contrary,  meningitis 
developing  during  the  course  of  the  well-developed  infection  is  generally  the 
result  of  meningeal  infection  and  is  very  frequently  associated  with  endo- 
carditis.    (See  Cerebrospinal  Meningitis.) 

Numerous  cases  are  on  record  of  croupous  pneumonia  in  children  which 
at  the  onset  simulated  meningitis,  cerebrospinal  meningitis,  and  even  hemi- 
plegia. But  the  subsequent  appearance  of  local  physical  signs,  the  pulse 
and  respiration  ratio,  and  the  crisis,  marked  by  a  sudden  fall  in  temperature 
about  the  eighth  day,  have  confirmed  the  diagnosis  of  croupous  pneumonia. 
The  favorable  termination  in  many  of  the  reported  cases  has  not  permitted 
an  adequate  pathological  investigation,  although  meningitis  due  to  the  pneu- 
mococcus is  well  recognized. 

Disturbance  of  the  nervous  system  over  and  above  the  signs  of  meningeal 
irritation  or  true  meningeal  inflammation  may  occur.  Hemiplegia  in  croup- 
ous pneumonia  was  recorded  by  Huxham;  later  it  was  described  by  Charcot, 


160  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Ldpine,  and  Vulpian  as  hemiplegie  pneumonique.  It  may  occur  early  in  the 
course  of  the  disease,  or  may  not  develop  until  the  period  of  convalescence. 
Such  a  paralysis  has  been  observed  in  cases  as  early  in  life  as  the  eighteenth 
month  and  as  late  as  the  seventy-sixth  year. 

Pierre  Boulloche  has  collected  56  cases  of  paralysis  resulting  from  croup- 
ous pneumonia.  In  this  analysis  the  type  of  paralysis  was  found  to  be  nearly 
always  hemiplegie.  In  advanced  years  death  nearly  always  ensued  upon  this 
complication,  while  in  the  young  the  mortality  was  very  much  lov/er,  recovery 
being  the  rule.  In  one  case  occurring  at  the  age  of  fifty-eight  years,  hemi- 
plegia, with  aphasia,  developed  during  the  course  of  the  disease,  but  ended 
in  recovery. 

In  some  instances  the  paralysis  is  monoplegic,  and  this  is  well  illustrated 
by  a  case  described  by  Boulloche  in  a  patient  thirty-two  years  of  age,  who, 
from  the  onset  of  the  disease,  was  delirious  and  who  presented  a  typical 
right-sided  croupous  pneumonia.  Paralysis  of  the  right  arm  and  right  side 
of  the  face  was  discovered  upon  the  sixth  day  of  the  disease.  Movements  of 
the  right  leg  were  entirely  retained.  There  was  aphasia,  but  no  loss  of  con- 
sciousness, neither  was  there  any  disturbance  of  sensibility;  twelve  days 
later  the  fever  had  subsided,  the  aphasia  had  diminished  considerably,  and 
the  muscles  of  the  face  were  less  drawn.  Sensation  in  the  pharynx  returned 
and  a  day  later  the  aphasia  disappeared.  The  facial  paralysis  passed  off; 
the  relative  strength  of  the  two  arms  showed  only  a  decrease  of  10  degrees 
in  the  affected  side,  and  at  the  expiration  of  twenty  days  the  monoplegia  had 
entirely  disappeared. 

Transitory  aphasia  is  a  complication  reported  by  Chantemesse.  This 
observer  has  found  that  aphasia  usually  occurs  about  the  second  or  third 
day  of  the  disease,  that  it  is  ordinarily  preceded  by  headache  and  giddiness, 
even  to  the  verge  of  syncope;  in  some  cases  numbness  or  a  sensation  of  pricking 
in  the  right  side  of  the  face  and  right  arm  is  experienced;  in  other  cases  it 
may  set  in  abruptly  without  loss  of  consciousness  or  become  manifest  after 
a  typical  apoplectiform  seizure.  The  characteristics  of  the  speech  impair- 
ment do  not  differ  from  those  dependent  upon  an  organic  lesion  of  the  third 
frontal  convolution  upon  the  left  side  of  the  brain.  The  paralysis  may 
involve  the  entire  right  side  of  the  body,  but  usually  only  the  inferior  portion 
of  the  right  side  of  the  face,  the  right  half  of  the  tongue,  and  the  right  superior 
extremity  are  affected;  as  a  rule,  sensation  and  the  reflexes  are  not  altered.  In 
pronounced  cases  the  paralyzed  parts  may  be  the  seat  of  increased  redness 
and  an  oedema,  which  is  more  or  less  circumscribed  and  increased  by  heat. 
The  phenomena  persist  commonly  for  from  a  few  hours  to  a  few  days,  and 
seem  in  no  way  to  influence  the  primary  disease. 

It  is  doubtful  whether  the  clinical  picture  and  pathology  of  these  cases  of 
transitory  aphasia  differ  in  any  particular  from  many  of  the  cases  already 
described  as  hemiplegie.  They  probably  represent  the  cases  in  which  no 
lesion  is  found  postmortem. 

Softening  of  the  brain  has  occurred  in  some  cases.  In  one  case,  reported  by 
Suckling,  it  was  due  to  thrombosis  of  the  basilar  artery,  and  thrombosis  of 
the  circle  of  Willis;  with  plugging  of  the  superficial  arteries  of  the  left  hemi- 
sphere.   While  these  lesions  have  been  found  as  the  causative  agents  in  pro- 


CROUPOUS  PNEUMONIA  161 

ducing  hemiplegia,  there  are  also  cases  on  record  in  which  the  autopsy  has 
been  negative.  In  other  words,  hemiplegia  with  lesions  and  hemiplegia 
without  lesions  occurs.  In  the  former  case  hemiplegia  results  from  either 
meningitis  or  softening,  or  is  due  to  thrombosis  or  embolism.  In  the  second 
class  the  paralysis  is  like  that  of  diphtheria — that  is,  of  the  toxic  type.  It  is 
important  to  remember  that  it  is  possible  for  hemiplegia  to  develop  in  pneu- 
monia without  there  being  any  relationship  between  the  two  conditions. 

The  fact  that  these  marked  nervous  manifestations  sometimes  come  on 
early  in  an  attack  of  croupous  pneumonia  emphasizes  the  importance  of 
examining  the  chest  in  all  cases  of  paralysis,  not  only  because  pneumonia  is 
competent  to  produce  hemiplegia  or  other  localized  palsy,  but  also  because 
these  conditions  are  quite  competent  to  produce  secondary  pulmonary 
lesions.  In  other  words,  pulmonary  lesions  may  be  the  cause  of  hemiplegia, 
and  hemiplegia  rnay  be  the  indirect  cause  of  croupous  pneumonia. 

Neuritis,  occurring  chiefly  as  a  sequel  to  croupous  pneumonia,  has  been 
described  by  several  observers.  These  cases  resemble  those  described  by 
Boulloche  as  paralysis  with  muscular  atrophy,  coming  on  during  the  period 
of  convalescence. 

Until  Weichselbaum  isolated  the  pneumococcusfrom  the  pus  aspirated  from 
the  synovial  sac  of  joints  involved  during  the  course  of  croupous  pneumonia, 
the  occurrence  of  arthritis  was  considered  a  coincidence,  but  since  1888 
arthritis  and  osteoarthritis  have  been  recognized  as  being  not  rarely  due  to  a 
pneumococcus  infection.  Herrick  has  collected  52  cases  from  the  literature 
of  the  subject,  including  some  of  his  own,  but  it  is  interesting  to  note  that 
in  2292  cases  of  pneumonia  collected  by  me,  treated  by  various  Swiss  and 
German  pliysicians,  only  2  cases  of  arthritis  occurred. 

In  regard  to  the  frequency  with  which  different  joints  are  involved  in  this 
complication,  the  following  quotation  from  Herrick's  paper  is  of  interest: 
"In  23  of  52  cases  the  upper  extremities  alone  were  involved;  in  18  cases 
the  joints  of  the  lower  extremities  alone;  in  11  tbere  was  involvement 
of  joints  of  both  the  upper  and  lower  extremities.  These  figures  show  a 
slight  preponderance  in  favor  of  limitation  to  the  upper  extremity,  but  so 
slight  that  little  or  no  significance  can  be  attached  to  it.  In  fact,  the  knee 
seems  to  be  the  joint  oftenest  affected,  being  involved  in  22  of  the  52  cases, 
in  3  of  which  both  knees  were  affected,  so  that  out  of  a  total  of  84  joints  the 
knee  makes  up  25,  or  about  30  per  cent.  The  involvement  of  other  joints 
was  as  follows:  the  sternoclavicular,  eight  times;  the  shoulder,  twelve  times; 
the  elbow,  nine  times;  the  wrist,  eight  times;  the  metacarpophalangeal,  twice; 
the  hip,  three  times;  the  knee,  twenty-five  times;  the  ankle,  three  times;  the 
metatarsophalangeal,  three  times.  The  arthritis  was  monarticular  in  thirty- 
two  instances,  or  in  61.5  per  cent,  of  the  cases.  The  joints  thus  solitarily 
involved  were:  shoulder,  ten  times:  knee,  nine  times;  wrist,  five  times;  elbow, 
twice;  sternoclavicular,  four  times;  and  the  hip,  ankle,  metacarpophalangeal, 
and  metatarsophalangeal,  each  once.  Of  the  remaining  cases  there  were  in- 
volved: two  joints,  nine  times;  three  joints,  four  times;  four  joints,  once; 
more  than  four,  three  times."  These  figures  bring  out  the  fact  that  the 
larger  joints  are  more  often  affected  than  the  smaller  ones. 

The  process  in  subacute  cases  is  sometimes  highly  destructive  to  the  joint, 
11 


162  DISEASES  DUE    TO   A    SPECIFIC  INFECTION 

It  is  a  noteworthy  fact  that  the  prognosis  as  to  hfe  is  grave,  the  mortahty 
amounting  to  65  per  cent.,  chiefly  because  this  lesion  is  associated,  as  a  rule, 
with  affections  of  the  serous  membranes  elsewhere,  and  particularly  in  the 
endocardium. 

Venous  thrombosis  is  an  exceedingly  rare  complication  of  pneumonia. 
Steiner  could  find  only  38  cases  recorded,  and  reports  3  of  his  own.  In  27 
of  these  the  thrombosis  occurred  during  convalescence.  In  1  case  it 
occurred  at  the  time  of  crisis  and  in  4  during  the  course  of  the  disease; 
and  in  the  cases  collected  by  him  the  lower  extremities  were  always  involved. 
The  left  lower  extremity  was  involved  in  16  cases;  the  right  in  10,  and  both 
legs  in  7.  The  more  frequent  involvement  of  the  left  extremity  is  attributa- 
ble in  this  disease,  as  in  typhoid  fever,  to  the  greater  length  and  obliquity 
of  the  left  common  iliac  vein  and  its  passage  beneath  the  right  common 
iliac  artery.  Adding  Steiner's  3  cases  to  the  38  which  he  found  in  the 
literature,  making  41,  we  find  that  recovery  occurred  in  25,  death  in  9, 
and  that  no  definite  information  is  given  of  7, 

Gangrene  of  a  limb  due  to  arterial  thrombosis  or  embolism  has  been 
recorded  by  Zuppin,  Benedict,  Grimm,  and  Nielsen. 

Parotitis,  while  a  rare  complication  of  croupous  pneumonia,  may  occur,  and 
not  infrequently  goes  on  to  suppuration.  Most  of  the  cases  so  far  reported 
have  not  been  due  to  the  pneumococcuS;  but  to  the  staphylococcus  or  strepto- 
coccus. 

Otitis  media  is  quite  a  common  complication  of  croupous  pneumonia  in 
children,  the  infection  taking  place  through  the  Eustachian  tube. 

A  relapse  in  croupous  pneumonia  is  practically  never  met  with,  but  recur- 
rence is  very  common. 

Duration  of  Croupous  Pneumonia. — It  is  important  to  remember  that  while 
croupous  pneumonia  often  runs  a  course  of  from  seven  to  ten  days,  it  not 
infrequently  reaches  its  crisis  at  a  much  earlier  period.  As  already  pointed 
out,  crisis  may  occasionally  occur  as  early  as  the  third  day,  and  by  no  means 
infrequently  takes  place  as  early  as  the  fifth.  AYhile  it  is  true  that  early 
crisis  usually  occurs  in  comparatively  mild  attacks  of  the  disease,  it  is  also  a 
fact  that  the  patient  may  seem  seriously  ill  throughout  the  whole  course 
of  these  cases  of  comparatively  short  illness. 

Varieties  of  Croupous  Pneumonia. — Croupous  pneumonia  varies  much  in 
its  character  with  the  condition  of  the  patient  that  is  attacked.  I  have 
already  mentioned  the  type  which  occurs  in  persons  who  are  addicted  to  the 
excessive  use  of  alcohol.  In  other  individuals  the  disease  is  accompanied  by 
such  marked  symptoms  of  adynamia  that  the  patient  seems  to  be  suffering  from 
typhoid  fever,  so  far  as  his  general  symptoms  are  concerned.  This  form  is 
known  as  typhoid  pneumonia,  in  that  it  is  typhoid  in  character;  but  this  term 
does  not  necessarily  imply  that  typhoid  infection  is  associated  with  that  by 
the  pneumococcus.  On  the  other  hand,  it  sometimes  happens  that  patients 
suffering  from  typhoid  fever  also  have  a  pneumococcic  infection  of  the  lung, 
and  this,  of  course,  is  another  form  of  so-called  typhoid  pneumonia.  True 
croupous  pneumonia  also  occasionally,  although  rarely,  complicates  malarial 
fever,  acute  articular  rheumatism,  and  pulmonary  tuberculosis.  Sometimes, 
too,  it  occurs  as  a  sequel  to  the  administration  of  ether  as  an  anaesthetic. 


CROUPOUS  PNEUMONIA  163 

This  is  probably  due  primarily  to  the  chilling  and  irritation  of  the  lung  by 
the  drug,  and  secondarily  to  the  inhalation  of  pneumococci  from  the  mouth, 
where,  as  already  stated,  they  are  almost  constantly  present  even  in  healthy 
persons. 

Diagnosis. — Croupous  pneumonia  is  to  be  carefully  differentiated  from 
acute  tuberculous  pulmonary  infection,  from  lobular  or  catarrhal  pneu- 
monia, from  infarction  of  the  lung,  accompanied  by  bloody  expectoration, 
due  to  cardiac  disease,  from  pleurisy  with  effusion,  and  from  chronic  inflam- 
mation of  the  pleura,  with  marked  thickening  of  that  serous  membrane. 
Finally,  it  is  to  be  separated  from  hypostatic  congestion  due  to  cardiac 
feebleness  arising  in  the  course  of  acute  diseases  or  chronic  ailments. 

The  differentiation  from  acute  pneumonic  phthisis  may  be  quite  impos- 
sible until  the  development  of  profuse  sweating,  a  feeble  and  rapidly  acting 
heart,  and  the  appearance  of  yellow  elastic  tissue  and  tubercle  bacilli  in  the 
sputum  takes  place.  From  pulmonary  infarction  it  is  to  be  separated  by 
careful  examination  of  the  heart,  which  may  reveal  valvular  lesions,  and  by 
the  fact  that  in  infarction  the  onset  of  pulmonary  disorder  is  instantaneous 
and  the  sputum  contains  bright  blood.  From  pleural  effusions  it  is  differ- 
entiated by  the  development  of  the  physical  signs  of  that  condition.  (See 
Pleurisy,  with  Effusion.)  Hypostatic  congestion  of  the  lungs  is  discovered 
by  the  character  of  the  sputum,  which  may  be  blood-stained,  although  it 
is  usually  serous,  by  the  fact  that  the  lesions  are  usually  bilateral,  and 
also  by  the  fact  that  the  heart  is  primarily  very  weak.  Catarrhal  or  lobular 
pneumonia  is  recognized  by  the  absence  of  the  typical  rusty  sputum,  by  the 
history  of  the  presence  of  some  primary  disease  prior  to  the  onset  of  the 
pneumonic  consolidation,  and  by  the  wide  distribution  of  the  lesions  and 
the  more  diffuse  physical  signs. 

An  important  aid  to  the  diagnosis  of  croupous  pneumonia  is  the  increase 
in  the  number  of  the  polymorphonuclear  white  cells,  the  so-called  leukocytosis 
of  croupous  pneumonia.  In  this  disease  in  most  instances  the  increase  in 
these  particular  white  cells  causes  a  leukocytosis  of  from  18,000  to  20,000- 

The  blood  serum  of  these  cases  is  capable  of  causing  agglutination  of  the 
pneumococcus  and  the  degree  of  agglutinative  power  seems  to  be  greatest 
about  the  time  of  crisis,  but  there  are  technical  difficulties  about  the  test 
which  render  it  of  little  value  in  diagnosis. 

It  is  of  the  greatest  importance  that  the  severe  pain  sometimes  described 
as  being  in  the  belly  at  the  onset  of  pneumonia  is  not  mistaken  for  that  due 
to  appendicitis.  Cases  frequently  occur  in  which  pain  due  to  thoracic  disease 
is  thought  to  be  abdominal,  particularly  if  the  base  of  the  lung  is  involved. 
The  presence  of  pain  on  pressure  over  McBurney's  point,  of  some  fixation 
of  the  abdominal  muscles,  and  of  a  high  leukocyte  count  may  be  so  misleading 
as  to  lead  the  physician  to  operate  for  disease  of  the  appendix. 

It  is  characteristic  of  croupous  pneumonia  that  the  chlorides  in  the 
urine  are  greatly  decreased. 

The  physician  should  always  be  on  his  guard  lest  he  overlook  a  "central" 
or  deep-seated  pneumonia,  which  presents  no  marked  physical  signs. 

Prognosis. — The  prognosis  in  croupous  pneumonia  is  always  to  be  governed 
by  the  recollection  of  the  fact  that  its  mortality  in  adults  is  usually  high,  and 


164 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


again  by  the  condition  and  habits  of  the  patient.  It  is  to  be  reniembered 
that  the  prognosis  in  a  case  of  croupous  pneumonia  is  grave  in  direct  pro- 
portion to  the  years  of  the  patient.  In  young  children,  unless  it  is  compli- 
cated by  some  grave  accident,  the  disease  has  a  very  low  mortality.     By 


Fig.  36 


Chart  showing  the  morbidity  and  mortality  of  croupous  pneumonia  at  different  ages,  based  on  868 
cases  in  the  Presbyterian  Hospital,  New  York,  and  Guy's  Hospital,  London.  Solid  line,  morbidity; 
dotted  line,  mortality. 

far  the  greater  number  of  children   recover,  whereas   in   advanced    years 
the  disease  is  exceedingly  fatal  (Fig.  36).    As  an  illustration  of  how  low  the 


CROUPOUS  PNEUMOMA  165 

mortality  may  be  when  young,  healthy  persons  are  affected  by  the  disease  and 
come  under  skilful  treatment  early  in  its  course,  Osier  states  that  in  40,000 
cases  occurring  in  the  German  army  the  mortality  was  only  3.6  per  cent. 

If  the  mortality  percentage  is  based  upon  the  total  number  of  deaths  from 
this  disease,  it  may  be  stated  to  be  as  high  as  from  25  to  40  per  cent. ;  but  if, 
on  the  other  hand,  those  cases  which  would  naturally  fall  victims  to  its 
ravages  are  excluded,  the  mortality  is  probably  only  about  10  per  cent.,  if 
we  accept  the  large  statistics  of  Townsend  and  Coolidge,  who  excluded 
patients  over  fifty  years  of  age  and  those  who  were  delicate  or  suffering 
from  some  other  disease  primarily  present.  In  private  practice  the  mortality 
varies  from  6  to  18  per  cent. 

Aside  from  advanced  years  the  other  causes  which  render  the  prognosis 
especially  grave  are  renal  disease,  with  secondary  cardiovascular  lesions,  alco- 
holism, and  diabetes.  Indeed,  these  three  states  contribute  a  very  large  pro- 
portion of  the  number  of  cases  which  suffer  from  this  malady,  and  also  the 
largest  proportion  of  deaths  in  the  statistics. 

It  is  stated  by  some  authors  that  any  history  of  previous  ill  health 
distinctly  increases  the  danger  from  croupous  pneumonia.  While  this 
may  be  true  in  certain  cases  in  which  vitality  is  greatly  depressed,  it  is 
also  a  fact  that  pneumonia  in  chronic  invalids  frequently  runs  a  com- 
paratively mild  course  unless  the  cause  of  their  ill  health  be  renal  or 
cardiac  disease,  whereas  it  may  speedily  produce  death  in  robust,  power- 
ful, muscular  men,  who  frequently  succumb  to  its  ravages  far  more  rap- 
idly than  more  lightly  built  and  apparently  delicate  individuals.  Indeed, 
the  physician  of  experience  dreads  the  onset  of  this  disease  in  powerful, 
well-developed  men  much  more  than  when  it  attacks  those  who  are  less 
given  to  active  exercise  and  feats  of  physical  strength.  Stout  persons 
also  seem  much  more  susceptible  to  the  lethal  influences  of  the  disease 
than  those  who  are  lean.  This  probably  depends  upon  two  causes:  first, 
the  heart  and  lungs  maybe  overweighted  by  fat,  and,  second,  such  persons 
usually  contain  in  their  tissues  a  large  amount  of  serum,  in  which,  perhaps, 
specific  micro-organisms  find  an  opportunity  to  grow  and  to  prepare  their 
toxic  product  in  large  quantity. 

Cases  of  croupous  pneumonia  characterized  by  moderately  high  fever  do 
not  possess  the  unfavorable  outlook  of  other  diseases  which  suffer  from  hyper- 
pyrexia; that  is,  a  temperature  in  the  neighborhood  of  106°.  On  the  other 
hand,  it  not  infrequently  happens  that  cases  running  a  temperature  course 
varying  from  101°  to  102°  are  more  severe  as  to  toxaemia  than  those  which 
range  in  the  neighborhood  of  103°  or  104°,  or  even  105°  for  a  short  time.  If, 
with  the  drop  in  temperature  which  occurs  at  crisis,  the  general  condition  of 
the  patient  does  not  markedly  improve,  the  prognosis  is  bad.  If  in  place  of 
the  ordinary  rusty  sputum  it  is  of  the  color  of  prune-juice,  it  is  usually  con- 
sidered that  the  disease  is  malignant. 

An  important  prognostic  point  in  any  given  case  is  the  degree  of  toxsemia 
which  is  present.  In  other  words,  the  prognosis  depends  not  so  much  upon 
the  area  of  lung  which  is  involved  as  it  does  upon  the  quantity  of  toxic 
material  which  the  infecting  micro-organisms  seem  to  be  producing. 
Again  and  again  death  occurs  in  apparently  otherwise  healthy  individuals 


166  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

who  present  a  small  area  of  consolidated  lung  and  almost  no  typical  signs  of 
pneumonia,  but  who  are  apparently  overwhelmed  by  great  toxaemia. 

An  absence  of  leukocytosis  in  a  case  of  croupous  pneumonia  usually  pos- 
sesses an  evil  import,  since  it  seems  to  indicate  a  degree  of  toxaemia  with 
which  the  system  of  the  patient  finds  it  difficult  to  deal.  Indeed,  in  some 
fatal  cases  the  leukocyte  count  may  not  only  not  be  increased,  but  very  much 
diminished. 

As  to  the  prognostic  value  of  finding  the  pneumococcus  in  the  blood, 
there  is  much  difference  of  opinion.  Some  observers  assert  that  its  pres- 
ence is  of  evil  import,  while  others  think  it  of  little  significance,  unless  the 
infection  is  manifestly  severe.    The  latter  view  is  probably  correct. 

Treatment. — The  treatment  of  a  case  of  croupous  pneumonia  varies  greatly 
with  the  condition  of  the  patient  who  is  sufi^ering  from  the  disease.  When 
it  attacks  the  stout  and  robust,  the  only  duty  of  the  physician,  in  a  large 
number  of  instances,  is  to  watch  the  patient's  symptoms;  to  insist  upon  rest  in 
bed  in  a  well-ventilated  and  quiet  room,  and  to  administer  a  sufficient  quan- 
tity of  bromide,  Dover's  powder,  or  morphine  to  relieve  pain,  if  that  symp- 
tom is  excessive.  If,  on  the  other  hand,  the  patient  is  one  who  has  been 
addicted  to  the  use  of  alcohol  in  excess,  whiskey  or  brandy  should  be  given 
him  in  amounts  varying  with  the  quantity  which  he  had  been  accustomed  to 
ingest  daily.  Not  only  does  his  system  require  the  effects  produced  by 
this  drug,  but  its  use  is  also  necessary  to  prevent  the  rapid  development  of 
delirium  tremens,  which  is  a  most  fatal  complication  in  these  cases.  An 
active  stimulation  is  also  usually  required  in  many  cases  of  croupous  pneu- 
monia in  which  the  patient  is  just  recovering  from  some  other  severe  infec- 
tion, such  as  typhoid  fever. 

It  is,  however,  a  fatal  mistake  to  think  that  every  patient  suffering  from  this 
disease  should  be  stimulated.  The  physician  should  always  bear  in  mind 
the  important  rule  not  to  meddle  with  the  course  of  the  disease  unless  symp- 
toms are  so  pressing  as  to  require  interference.  There  can  be  no  doubt  that 
one  of  the  best  stimulants  in  the  average  case  of  croupous  pneumonia  is 
alcohol,  in  some  form  which  will  agree  well  with  the  stomach.  The  dose  of 
this  drug  in  the  form  of  whiskey  or  brandy  must  depend  upon  the  needs  of  the 
individual.  Rarely  will  any  patient  require  more  than  8  to  12  ounces  in  the 
twenty-four  hours,  and  many  will  do  best  on  much  less  than  this.  Valuable 
adjuvants  to  alcohol  are  the  aromatic  spirit  of  ammonia,  given  in  the  dose  of 
30  minims,  well  diluted,  every  two  or  three  hours;  and  should  any  sign  of  acute 
cardiac  failure  develop,  Hoffmann's  anodyne,  in  the  dose  of  1  or  2  drachms, 
in  water,  every  hour  or  two,  is  an  invaluable  remedy. 

For  the  condition  of  acute  cardiac  weakness,  the  value  of  strychnine 
should  also  be  borne  in  mind.  Under  these  circumstances  it  is  often 
invaluable,  and  if  need  be  may  be  given  in  full  dose,  frequently  repeated, 
by  a  hypodermic  needle,  until  the  patient  rallies.  Usually  4^^^  to  ^^  grain, 
repeated  once  or  twice,  at  an  interval  of  two  or  three  hours,  approximates 
the  proper  dose.  At  the  present  time  it  has  become  fashionable  for 
physicians  to  administer  strychnine  as  a  cardiac  stimulant  throughout 
the  whole  course  of  pneumonia.  This  is  an  abuse  of  a  good  remedy. 
Strychnine  is  not  a  direct  cardiac  stimulant.    It  increases  the  activity  of 


CROUPOUS  PNEUMONIA  167 

the  heart  by  rallying  the  nervous  system  and  acting  as  an  indirect  whip  to 
the  circulation.  If  its  use  is  persisted  in  it  soon  loses  its  so-called  stimu- 
lant effects,  and  is  apt  to  produce  a  condition  of  nervous  irritation,  par- 
ticularly in  the  aged,  which  may  be  quite  distressing.  Its  constant  use 
deprives  the  physician  of  a  valuable  remedy  for  meeting  critical  moments 
in  the  course  of  the  disease. 

The  value  of  digitalis  for  the  purpose  of  combating  cardiac  failure  in  acute 
croupous  pneumonia  has  been  questioned.  It  is  a  well-known  fact  that 
digitalis  loses  a  large  amount  of  its  power  over  the  heart  in  the  presence  of 
high  fever;  and  fever  is  nearly  always  a  marked  symptom  in  this  disease. 
It  is  also  coming  to  be  a  well-recognized  fact  that  digitalis  is  of  little  value 
in  those  cases  in  which  the  heart  muscle  has  undergone  degenerative 
change,  and  the  toxsemia  of  pneumonia  often  produces  such  alterations  in 
the  muscle  fibre  of  this  viscus.  In  cases  in  which  there  is  marked  vascular 
relaxation  and  cardiac  dilatation,  I  have  known  it  to  do  good  when  given 
in  a  few  large  doses,  particularly  if  strychnine  and  atropine  were  simultan- 
eously administered.  Although  it  is  a  drug  which  contracts  the  bloodvessels, 
the  vasomotor  dilatation  or  relaxation  of  advanced  pneumonia  is  often  so 
marked  that  digitalis  seems  to  be  unable  to  raise  the  arterial  pressure,  and  I 
am  convinced  that  in  many  instances  death  occurs  more  largely  because  of 
the  relaxed  condition  of  the  bloodvessels  than  by  any  direct  effect  of  the  dis- 
ease upon  the  heart.  When  I  use  digitalis,  therefore,  I  am  in  the  habit  of 
prescribing  5  or  10  drops  of  a  physiologically  tested  tincture  every  eight  or  six 
hours,  and  the  same  quantity  of  tincture  of  belladonna  every  three  or  four 
hours,  in  order  that  the  belladonna  may  increase  the  tone  of  the  vessels. 
This  treatment,  however,  is  rarely  instituted  before  the  fifth  or  sixth  day,  or 
at  the  approach  of  crisis. 

If  cardiac  failure  is  the  result  of  cardiac  dilatation  due  to  the  obstruc- 
tion of  the  flow  of  blood  through  the  lung,  digitalis  may  be  advantageous, 
but  when  the  cardiac  weakness  is  due  to  toxsemia  it  is  probably  of  little 
value,  and  if  a  clot  has  formed  in  a  cardiac  cavity  it  is  manifestly  use- 
less. Sometimes  when  the  fever  is  high  and  digitalis  fails  to  act,  it  is 
well  to  aid  its  effect  by  quieting  the  heart  through  the  application  of 
an  ice-bag  placed  upon  the  prsecordium.  I  have  also  known  the  reduc- 
tion of  temperature  by  the  local  application  of  the  ice-bag  and  by  cool 
sponging  of  the  body,  with  friction,  to  be  followed  by  the  manifestation  of 
a  distinct  digitalis  influence.  If  moderate  doses  of  5  or  10  minims  of  a 
physiologically  tested  tincture,  three  or  four  times  a  day,  fail  to  produce 
good  effects  under  these  circumstances,  I  feel  quite  confident  that  larger  ones 
will  not  be  of  any  value. 

Should  sudden  coflapse  come  on,  a  hypodermic  injection  of  strychnine  and 
atropine  should  be  given,  and  it  may  be  wise  to  introduce  under  the  skin,  by 
hypodermoclysis,  a  pint  of  normal  saline  solution,  containing  1  drachm  of  a 
1:1000  solution  of  adrenalin  chloride.  The  normal  saline  solution,  under 
these  circumstances,  cannot  do  much  good  directly  because  the  relaxation 
of  the  bloodvessels  is  so  great  that  even  if  it  is  absorbed  its  influence  will  not 
be  felt,  but  it  forms  a  reservoir  from  which  the  adrenalin  chloride  will  be 
slowly  absorbed  and  so  raise  arterial  pressure  by  stimulating  the  walls  of  the 


168  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

bloodvessels  when  the  toxaemia  of  the  disease  has  perchance  paralyzed  the 
vasomotor  centre  When  the  skin  becomes  relaxed  and  bedewed  with  sweat, 
atropine  is  often  a  life-saving  drug. 

In  cases  in  which  the  heart  is  laboring,  where  there  is  evidence  of  dilata- 
tion of  its  right  cavity  with  pulsating  jugulars  and  other  evidences  of 
venous  stasis,  free  venesection  may  be  practised  with  advantage,  and 
sometimes  gives  wonderful  relief;  but  in  cardiac  failure  without  these 
signs  of  venous  obstruction,  venesection  is  practically  of  no  value  whatever. 

The  value  of  inhalations  of  oxygen  gas  is  problematical.  I  always  em- 
ploy them  because  they  seem  to  give  comfort  both  to  the  patient  and  his 
friends.  The  oxygen  should  not  be  given  through  an  inhaler,  but  be  allowed  to 
escape,  through  the  opening  of  the  rubber  tube  or  glass  nozzle,  about  the  hps 
or  nose  of  the  patient,  for  the  ordinary  individual  who  is  suffering  from 
dyspnoea  In  this  disease  will  not  permit  one  of  his  nostrils  to  be  blocked 
or  his  mouth  closed  by  such  an  inhaler,  as  his  desire  for  ordinary  air  is  too 
great.  If  the  dyspnoea  is  due  to  toxaemia,  the  oxygen  is  probably  useless. 
If  it  is  due  to  a  large  area  of  the  lung  being  incapacitated  by  consolidation,  it 
is  conceivable  that  oxygen  can  do  great  good. 

The  value  of  saline  infusion  also  depends  upon  the  degree  of  toxaemia 
which  is  present  and  upon  the  activity  of  the  kidneys.  If,  in  a  given  case, 
the  urinary  secretion  is  scanty  and  toxic  symptoms  develop,  a  pint  of  normal 
salt  solution  may  be  given  by  hypodermoclysis  every  six  or  eight  hours  for 
twenty-four  hours  with  advantage.  If,  on  the  other  hand,  the  pneumonia 
complicates  renal  disease,  and  there  is  any  tendency  to  oedema  of  the  sub- 
cutaneous tissues,  this  method  of  treatment  may  be  disadvantageous,  in  that 
it  tends  to  increase  the  dropsy,  and  perhaps  increases  the  tendency  to  pul- 
monary oedema.  As  marked  toxaemia  is  usually  associated  with  renal 
inactivity,  this  method  of  treatment  should  be  borne  in  mind.  Direct 
infusion  of  a  saline  solution  into  a  vein  is  probably  not  advisable  in  the 
majority  of  cases,  since  it  is  usually  absorbed  with  sufficient  rapidity  from 
the  subcutaneous  tissues. 

The  treatment  of  the  fever  during  the  course  of  croupous  pneumonia  is 
not  of  as  great  importance  as  it  is  during  the  course  of  a  more  prolonged 
malady,  like  typhoid  fever.  Indeed,  there  is  some  evidence  to  show  that 
fever  within  moderate  bounds  may  be  an  effort  on  the  part  of  the  organism 
to  protect  itself  from  the  infecting  germs.  If  the  temperature  does  not  exceed 
102.5°  to  103°,  antipyretic  measures  need  not  be  instituted,  although  spong- 
ing the  patient  with  tepid  or  cool  water  three  or  four  times  a  day  will  control 
the  temperature  somewhat,  allay  peripheral  nervous  irritation,  keep  the  skin 
clean,  and  often  produce  sleep.  These  spongings  are,  therefore,  useful  in  the 
ordinary  case  of  pneumonia  with  a  temperature  of  103°  or  more,  but  they 
are  not  to  be  carried  out  with  the  same  vigor,  either  as  to  the  activity  of  the 
rubbing  or  degree  of  cold,  as  is  employed  in  typhoid  fever,  for  the  temperature, 
as  a  rule,  does  not  resist  the  cold,  and  if  it  is  applied  too  freely  the  patient 
may  be  thrown  into  collapse  by  a  sudden  fall  of  fever.  Nearly  every  case 
of  acute  pneumonia  will  be  benefited  if  an  ice-bag  is  kept  applied  to  the  head, 
and  if  the  action  of  the  heart  is  very  rapid  when  the  fever  is  high  an  ice- 
bag  over  the  praecordium,  as  already  stated,  is  often  advantageous. 


CROUPOUS  PNEUMONIA  169 

The  administration  of  antipyretic  drugs  to  patients  suffering  from  pneu- 
monia is  absolutely  inexcusable.  In  the  first  place,  antipyresis  by  drugs  is 
rarely  if  ever  needed.  In  the  second  place,  there  is  overwhelming  clinical 
and  experimental  evidence  to  show  that  the  use  of  these  drugs  materially 
diminishes  the  vital  resistance  of  the  patient,  decreases  the  ability  of  his  blood 
to  convey  oxygen  to  his  tissues,  reduces  its  ability  to  destroy  infecting  micro- 
organisms, lowers  vascular  tone,  depresses  the  heart,  and  is  altogether  evil 
in  its  influence,  probably  also  diminishing  the  elimination  of  toxic  materials 
by  the  kidneys,  and  certainly  giving  these  organs  the  additional  labor  of 
eliminating  the  antipyretic  drug,  which,  perchance,  may  be  irritating  to  them. 

Quinine  is  employed  by  some  practitioners  with  the  idea  that  it  possesses 
antipyretic  power,  and  there  is  no  objection  to  its  use  in  small  doses;  large 
doses,  which  produce  cinchonism  or  irritation  of  the  stomach,  are  valueless, 
and  may  do  harm  by  irritating  the  stomach,  producing  cerebral  congestion 
and  meningeal  irritation,  or  irritating  the  kidneys. 

When  croupous  pneumonia  is  of  the  typhoid  type  and  asthenia  is  marked, 
valuable  results  can  be  obtained  very  frequently  by  the  hypodermic  injection 
of  ^  to  1  grain  of  camphor,  dissolved  in  sterilized  olive  oil.  This  injection 
may  be  given  once,  twice,  or  thrice  in  twenty-four  hours  for  one  or  two 
days,  but  ought  not  to  be  continued  too  long;  first,  because  it  rapidly  loses 
its  effects  if  used  too  frequently,  and,  second,  because  in  these  doses  there 
may  be  some  danger  of  camphor  poisoning.  Camphor  is  to  be  regarded  as 
a  remedy  for  an  emergency,  and  is  to  be  reserved  for  critical  periods. 

If  great  mental  and  nervous  excitement  is  present  and  persistent,  life  can 
often  be  saved  by  the  administration  hypodermically  of  i,  i »  or  |  grain  of 
morphine.  This  will  often  produce  several  hours  of  desired  sleep,  from  which 
the  patient  awakens  much  refreshed  and  perhaps  free  of  the  delirium  which 
before  the  administration  of  the  morphine  was  an  annoying  symptom,  in 
that  it  produced  physical  exhaustion  through  the  constant  activity  of  his 
body  and  mind. 

The  employment  of  nitroglycerin  in  the  treatment  of  pneumonia  is  limited 
to  those  cases  which  have  a  high  arterial  tension.  The  drug,  under  these 
circumstances,  is  of  great  value  in  that  it  diminishes  the  work  of  the  heart  by 
removing  the  vis  a  fronte.  If,  on  the  other  hand,  vascular  spasm  does  not 
exist,  the  drug  is  useless,  for  it  is  not,  as  some  have  thought,  in  any  sense  a 
direct  cardiac  stimulant. 

The  question  of  the  employment  of  circulatory  sedatives  in  the  early  stages 
of  acute  croupous  pneumonia  is  one  which  has  been  widely  debated,  particu- 
larly in  this  country.  There  are  many  excellent  practitioners  who  consider 
that  full  doses  of  veratrum  viride  or  aconite  in  the  earlier  stages  of  croupous 
pneumonia  are  advantageous.  Statistics,  or,  to  speak  more  correctly,  wide 
personal  experience  on  the  part  of  many  physicians,  seems  to  justify  the  use  of 
this  drug  in  some  cases,  namely,  in  those  instances  in  which  the  physician  sees 
the  patient  during  the  first  hours  of  the  attack,  and  if  the  patient  is  a  strong, 
sthenic  individual,  with  a  full,  bounding  pulse,  and  great  flushing  of  the  face. 
Under  these  circumstances  the  relaxation  of  the  general  vascular  system 
produced  by  the  veratrum  viride  and  the  quieting  of  the  excited  heart  seems 
distinctly  advantageous.     Whether  such  treatment  in  any  way  aborts,  or 


170  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

jugulates,  or  diminishes  the  violence  of  the  subsequent  attack  is  difficult  to 
de'termine.  In  a  few  instances  of  acute  croupous  pneumonia  and  acute 
pleurisy,  seen  in  the  very  early  stages,  I  have  noted  good  results  from  such 
treatment.  But  in  the  vast  majority  of  instances  the  physician  does  not  see 
the  patient  for  nearly  twenty-four  hours,  by  this  time  the  disease  is  well 
started  on  its  way,  and  the  symptoms  of  great  circulatory  excitement 
have  usually  passed  by,  so  that  circulatory  sedatives  are  distinctly  contra- 
indicated. 

As  the  rapid  development  of  the  signs  of  circulatory  depression  can 
be  aided  by  the  administration  of  sedative  remedies,  the  use  of  chloral 
and  the  bromides  as  nervous  sedatives  in  the  course  of  croupous  pneumonia 
is  usually  inadvisable.  Chloral  in  particular  is  contraindicated,  because  of 
its  well-known  depressant  effect  upon  the  heart  and  its  irritant  action  upon 
the  kidneys. 

The  diet  should  be  liquid  and  consist  of  milk,  with  a  little  pancreatin 
and  bicarbonate  of  soda,  to  aid  in  digestion,  and  of  animal  broths 
and  gruels  made  of  wheaten  grits,  oatmeal,  rice,  or  barley,  the  digestion  of 
these  starchy  foods  being  aided  by  the  administration  of  small  quantities  of 
taka-diastase  or  pancreatin.  I  am  quite  convinced  that  we  too  infrequently 
resort  to  these  cereal  fluids  in  the  treatment  of  diseases  of  this  nature,  since  they 
possess  much  nutritional  value  and,  if  their  digestion  is  aided,  agree  with  the 
vast  majority  of  patients,  and  enable  us  to  change  the  diet  so  that  the  patient 
does  not  become  tired  of  any  one  particular  kind  of  food,  which  is  a  great 
advantage. 

Care  should  be  taken  in  cases  of  croupous  pneumonia  that  the  patient 
receives  an  adequate  amount  of  water  to  drink,  so  that  the  kidneys  may 
be  well  flushed  with  fluid  in  each  twenty-four  hours;  but  it  is  important 
that  only  small  amounts  of  fluid  be  taken  at  a  time,  as  distention  of  the  stomach 
may  cause  fatal  cardiac  embarrassment.  The  bowels  should  also  be  moved 
each  day  in  the  early  stages  of  the  attack  by  full  doses  of  calomel,  and  in  the 
later  stages  by  salines,  or,  if  the  patient  is  too  weak  for  the  use  of  these  purga- 
tives, by  a  rectal  injection  of  water  or  of  glycerin  and  water. 

The  administration  of  expectorants  in  croupous  pneumonia  is  useless 
until  the  stage  of  resolution  is  reached.  Even  then  they  are  probably  of 
little  value  in  clearing  up  the  exudate  in  the  vesicular  portions  of  the  lung. 
But  the  chloride  of  ammonium,  the  oil  of  sandal-wood,  guaiacol,  and  terpin 
hydrate  often  prove  useful  at  this  time  in  aiding  in  removing  the  symptoms 
of  chronic  bronchitis  which  exist,  a  state  which  results  in  the  formation  of 
a  good  deal  of  thick,  tenacious  bronchial  mucus,  which  the  patient  may  have 
difficulty  in  expectorating. 

Excessive  cough  in  all  stages  of  croupous  pneumonia  is  best  controlled 
by  the  administration  of  Dover's  powder,  codeine,  paregoric,  or  the  newer 
drug,  heroin.  In  the  stage  of  resolution  cough  sedatives  should  not  be 
administered  unless  the  physician  is  certain  that  the  cough  is  in  excess  of 
the  needs  of  the  patient  in  getting  rid  of  the  materials  in  his  chest  which 
should  be  gotten  rid  of  in  this  way. 

Meningeal  symptoms  are  to  be  treated  by  the  application  of  cold  to  the 
head,  and  sometimes  it  is  wise  to  apply  a  blister  to  the  nape  of  the  neck. 


DIPHTHERIA  171 


DIPHTHERIA. 

Definition. — Diphtheria  is  an  acute  infectious  disease,  which  chiefly  affects 
children  under  puberty.  It  is  due  to  the  Klebs-Loeffler  bacillus,  and  is  char- 
acterized primarily  by  an  acute  local  inflammatory  process  which  affects,  as  a 
rule,  the  pharynx,  larynx,  or  nasal  mucous  membrane,  and  which  is  peculiar  in 
that  it  is  associated  with  the  development  of  a  false  membrane  due  to  a 
fibrinous  exudate.  From  the  spot  upon  which  this  condition  develops  the 
general  system  becomes  affected,  not  by  the  micro-organism  of  the  disease, 
but  by  the  poisons  or  toxins  produced  by  the  specific  organism  at  the  site  of 
primary  infection.  Other  infections  may  occasionally  cause  the  production 
of  a  false  membrane,  but  the  discovery  of  the  presence  of  the  Klebs-Loeffler 
bacillus  determines  that  the  affection  is  diphtheria.  All  cases  in  which  a 
false  membrane  develops  on  a  visible  mucous  membrane  should  be  considered 
to  be  cases  of  diphtheria  and  treated  as  such  until  proved  to  be  non-diph- 
theritic, because  in  this  way  the  spread  of  the  disease  is  prevented  and  the 
use  of  the  specific  remedy,  antitoxin,  will  save  life  if  the  disease  is  present 
and  do  no  harm  if  it  is  not. 

In  the  great  majority  of  cases  the  disease  primarily  affects  the  pharyngeal 
mucous  membrane,  or  the  mucous  membranes  immediately  adjacent  thereto, 
and  from  this  area  spreads  to  the  nose  or  larynx,  where  the  results  of  its 
development  are  very  fatal.  The  specific  inflammation  and  false  membrane 
may,  however,  develop  on  any  exposed  mucous  membrane,  and  even  upon 
the  true  skin  if  the  epiderm  be  removed  intentionally  or  by  accident. 

It  is  possible  for  bacteriologists  to  find  the  Klebs-Loeffler  bacillus  in  cases 
of  sore  throat  in  which  there  is  no  false  membrane  and  no  systemic  symptoms 
of  diphtheria,  and  in  some  of  these  instances  even  local  disturbances  may 
be  absent  because  of  the  resistance  offered  to  this  infection  by  some  persons. 
These  cases  are  not  to  be  considered  instances  of  diphtheria,  although  they 
are  entirely  capable  of  conveying  the  completely  developed  disease  to  others. 

On  the  other  hand,  cases  are  not  rarely  seen  in  which  the  physician  finds 
a  shaggy  false  membrane  on  the  throat  associated  with  signs  of  great  sys- 
temic toxaemia,  and  in  which  the  bacteriologist  fails  to  find  the  specific  micro- 
organism of  diphtheria.  This  condition  is  called  diphtheria  by  the  physician 
and  pseudodiphtheria  by  the  bacteriologist.  The  streptococcus  is  probably 
responsible  for  some  cases  of  the  latter  type,  while  in  other  patients  the 
pneumococcus  causes  a  similar  effect.  These  instances  are  met  with  most 
commonly  as  complications  of  scarlet  fever  or  more  rarely  of  measles,  and 
also  occur  as  manifestations  of  severe  tonsillitis  or  angina. 

History. — Diphtheria  has  been  recognized  for  many  centuries  as  a  disease, 
but  it  was  not  until  the  clinical  observations  of  Bretonneau,  of  Tours,  that 
its  separate  identity  was  established  under  the  name  of  "diphthdrite." 
He  classed  all  cases  of  "putrid  sore  throat,"  "cynanche  maligne,"  and 
"suffocative  angina"  under  this  one  heading,  and  much  more  recently  those 
cases  heretofore  called  "membranous  croup"  have  also  been  very  properly 
put  in  the  class  called  "diphtheritic."  This  sweeping  classification  is  not 
scientifically  justifiable,  as  has  just  been  pointed  out,  but  from  a  clinical 


172  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

standpoint  it  is  proper  because  in  the  majority  of  instances  the  false 
membrane  is  due  to  this  cause. 

Distribution. — Diphtheria  is  a  disease  which  occurs  in  nearly  all  parts 
of  the  world,  but  is  much  more  prevalent  in  the  temperate  zones  than 
elsewhere.  It  occurs  in  epidemics  and  in  sporadic  cases,  and  is  endemic 
in  nearly  every  large  city.  While  common  in  cities,  it  is  even  more  common 
in  country  districts.  No  special  influence  upon  its  development  is  known 
to  be  exercised  by  bad  drainage,  although  such  drainage  may,  by  diminish- 
ing vital  resistance,  very  greatly  increase  susceptibility  to  the  malady. 

It  is  a  disease  of  the  poor  rather  than  of  the  rich,  and  when  it  occurs 
in  the  well-to-do  it  is  usually  sporadic  and  its  source  can  often  be  traced  to 
some  single  exposure.  The  reason  for  this  does  not  lie  so  much  in  greater 
susceptibility  of  the  poor  as  in  greater  exposure  to  the  infection,  for  when 
the  children  of  the  well-to-do  are  attacked  they  succumb  as  readily  as 
their  otherwise  less  fortunate  fellows. 

Diphtheria  occurs  much  more  frequently  between  the  ages  of  two  and 
five  years  than  at  any  other  time  of  life  (Fig.  37). 

Etiology. — Diphtheria  is  due,  as  has  already  been  stated,  to  a  specific 
bacillus  first  described  by  Klebs  in  1883,  and  later  isolated  by  Loeffler. 
This  micro-organism  is  from  1.5  to  3.5  or  rarely  4.5  micromillimetres  in 
length,  and  from  0.3  to  0.8  in  breadth.  It  usually  appears  singly,  in  groups 
of  two  or  three,  but  true  chains  are  said  not  to  occur;  the  organisms  may 
lie  side  by  side  or  at  an  angle.  They  are  slightly  curved  with  straight, 
rounded  ends,  sometimes  branched,  and  commonly  beaded  or  barred. 
They  do  not  give  off  spores,  and  flagella  are  absent.  They  may  contain 
highly  refractive  bodies  which  cause  them  to  stain  irregularly.  The  best 
stain  is  that  of  Loeffler,  the  oval  bodies  in  the  organism  staining  more  highly 
than  the  rest  of  the  bacillus.  They  are  grown  best  in  Loeffler's  blood  serum, 
but  develop  in  all  the  laboratory  media.  The  organism  is  non-motile  and 
almost  purely  aerobic. 

All  cases  of  diphtheria  are  due  to  the  entrance  into  the  body  of  this  specific 
bacillus  originally  derived  from  some  patient  ill  with  the  disease.  The 
transfer  is  made  in  a  multitude  of  ways.  Sometimes  it  is  by  the  clothing, 
by  books,  by  foodstuffs,  or  drinks,  or  drinking-vessels,  by  pencils,  or  by  the 
coughing  of  an  individual,  who  may  have  the  bacilli  in  the  throat,  in  such 
a  way  that  the  infectious  agent  is  driven  into  the  respiratory  passages  or 
mouth  of  the  other  person.  Convalescent  patients  may  in  this  manner  act 
as  disseminators  of  the  disease  long  after  they  are  apparently  entirely  well,  and 
healthy  persons  with  the  bacilli  in  the  mouth  may  also  carry  the  in- 
fection. 

Thus  it  is  entirely  possible  for  a  nurse  who  has  been  in  charge  of  a  case  of 
diphtheria  to  carry  in  the  crypts  of  the  tonsils  the  specific  micro-organism, 
to  have  no  sign  of  the  disease,  and  yet  infect  a  child  or  adult  whom  she 
may  care  for  soon  after  leaving  the  first  case.  It  is  evident,  therefore,  that 
while  the  infection  is  not  carried  by  the  air,  as  in  smallpox,  it  is  very  easy  for 
a  patient  who  sneezes  or  coughs  to  distribute  the  infectious  agent  broadcast 
by  its  falling  on  neighboring  substances  which  act  as  agents  of  conveyance. 
These  are  some  of  the  causes  that  result  in  the  rapid  spread  of  the  disease 


DIPHTHERIA 


173 


in  tenement  houses,  schools,  and  other  pubHc  places  where  children  are 
congregated. 

As  the  specific  bacillus  possesses  great  vitality,  the  relationship  between 
cause  and  effect  may  not  be  readily  discovered.  Thus,  if  the  bacilli  fall  on 
a  garment  they  have  been  found  to  remain  capable  of  producing  the  disease 
six  months  later,  and  they  have  been  found  in  the  throat  many  months  after 
perfect  health  has  been  established.  So,  too,  the  dust  of  the  room  may  carry 
the  infection,  and  even  the  hair  or  beard  of  the  physician  may  do  likewise, 
if  the  patient  expels  any  secretion  upon  it.  Finally,  as  already  intimated, 
milk  may  act  in  this  manner,  and  cheese  made  from  contaminated  milk 


Fig.  37 


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Showing  the  age  incidence  of  diphtheria,  based  on  3360  cases  collected  from  various  sources. 


may  even  convey  the  bacillus.  Pet  animals,  such  as  cats  and  dogs, 
also  act  as  distributors,  and  rodents,  such  as  rats  and  mice,  may  do 
likewise. 

While  all  the  diseases  of  birds,  cats,  and  calves  characterized  by  the  for- 
mation of  a  false  membrane  are  not  communicable  to  man,  the  possibility 
of  a  true  diphtheritic  infection,  in  domestic  animals,  cannot  be  denied. 

There  are  a  number  of  causes  existing  in  the  patient  which  exercise  a 
predisposing  influence  in  connection  with  this  infection.  Some  of  these 
are  at  present  obscure  and  probably  depend  upon  a  lack  of  anti-bodies  in 
the  blood  and  tissues,  but  others  are  equally  active,  readily  recognizable 


174  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

and  in  many  cases  remediable.  There  can  be  no  doubt  whatever  that 
chronically  enlarged  tonsils,  overgrowth  of  the  so-called  pharyngeal  tonsil 
and  chronic  catarrh  of  the  nasopharynx  very  materially  increase  the  suscep- 
tibility of  a  child  to  diphtheria.  For  this  reason  these  conditions  should 
not  be  allowed  to  exist  in  otherwise  healthy  children.  Further  than  this 
the  crypts  of  the  tonsils  when  diseased  may  harbor  the  Klebs-Loeffler  bacillus, 
until  a  time  when  the  system  of  the  patient  is  favorable  for  its  growth  and 
then  develop  rapidly,  or  on  being  expelled  cause  the  malady  in  another 
individual. 

None  of  the  pathogenic  organisms  seems  to  possess  a  greater  degree  of 
variance  in  virulency  than  the  one  under  discussion.  In  some  instances 
it  fails  to  exert  any  malign  effect  beyond  a  local  influence,  and  even  this 
may  amount  to  nothing  more  than  a  sore  throat.  In  other  cases  it  attacks 
the  patient  with  a  virulence  which  is  perfectly  terrifying. 

It  is  not  probable  that  sex  has  any  influence  as  a  predisposing  cause. 
Statistics  vary,  however,  some  showing  that  a  greater  number  of  cases  occur 
among  boys  than  among  girls.  That  these  differences  are  merely  fortuitous 
is  exemplified  by  the  fact  that  of  22,005  cases  collected  from  various  sources 
11,006  occurred  among  boys  and  10,999  among  girls,  a  difference  of  only 
seven  cases. 

Pathology  and  Morbid  Anatomy.— In  studying  the  pathology  and  morbid 
anatomy  of  diphtheria  it  is  essential  to  remember  that  the  disease  is  primarily 
local  and  secondarily  systemic;  that  the  local  area  of  infection  is  the  site 
at  which  the  specific  organism  multiplies  and  produces  local  changes  by 
its  growth,  and  at  the  same  time  elaborates  a  toxin  which,  being  absorbed, 
acts  on  distant  parts  and  so  endangers  life.  The  bacillus  enters  the  blood 
stream  in  a  relatively  constant  percentage  of  cases. 

Local  Lesions. — The  local  change  produced  by  the  growth  of  the  bacillus 
is  now  well  understood,  for  a  large  number  of  researches  in  Europe  and 
America  have  given  us  clear  conceptions  of  it.  Of  these  researches  by  far  the 
most  noteworthy  is  that  carried  out  by  Councilman,  Mallory,  and  Pearce  in 
Boston. 

The  poison  produced  by  the  specific  bacillus  in  the  mucous  membrane 
of  the  throat  results  in  the  death  of  the  tissues  and  in  this  necrotic  mass 
the  bacilli  then  very  rapidly  develop.  The  epithelium  in  many  cases 
manifests  more  or  less  proliferation,  becomes  hyaline  and  necrotic,  eventu- 
ally fragmenting  and  disintegrating.  The  inflammatory  exudate  which  per- 
meates the  mucosa  and  even  the  submucous  stratum  is  very  rich  in  fibrin 
elements,  and  when  brought  in  contact  with  the  necrosing  structures  forms 
a  fibrous  reticulum  entangling  within  its  meshes  the  cells  and  bacteria. 
The  membrane  formed  by  the  coagulation  necrosis  and  hyaline  degeneration 
of  the  cells  may  be  so  transparent  as  almost  to  escape  detection  during  life 
(hyaline  type) ,  or  it  may  be  granular  or  fibrillar.  The  necrosis  may  extend 
into  the  superficial  epithelium  only  or  penetrate  the  submucosa,  in  some 
instances  involving  the  parenchyma  of  the  tonsil  or  even  the  submucous 
muscular  structures.  This  necrotic  membrane  is  subject  to  a  number  of 
important  changes.  It  may  disintegrate  and  form  a  mass  of  shreddy  detritus 
on  the  surface  or  it  may  be  thrown  off  by  being  elevated  by  the  exudate 


DIPHTHERIA 


175 


which  forms  beneath  it.  In  the  latter  process  a  very  thick,  false  membrane 
formed  of  consecutive  layers  may  be  produced.  The  membrane  always 
develops  on  a  necrotic  surface,  but  it  may  extend  a  short  distance  over  the 
surrounding  mucous  membrane. 

The  depth  of  the  destructive  process  is  not  very  great  in  the  majority 
of  cases,  but  in  rare  instances  it  has  become  deep  enough  to  erode  the 
carotid  artery.  In  many,  if  not  all,  such  instances  other  organisms  play 
an  important  part  in  the  spread  of  the  necrosis  and  add  to  the  intoxication 
their  own  poisonous  products.  It  is  important  to  bear  in  mind  in  diphtheria 
that  the  infection  is  "mixed"  in  the  vast  majority  of  cases;  that  is,  the  false 
membrane  not  only  holds  in  its  meshes  a  multitude  of  the  specific  bacilli 
but  many  other  micro-organisms  as  well,  many  of  which  possess  a  power 
for  evil,  as,  for  example,  the  streptococcus. 

The  membrane  is  closely  attached  to  the  tissues  beneath  and  is  stripped 
off  with  great  difficulty  except  when  it  develops  in  the  larynx  and  bronchi, 
when  it  is  dislodged  quite  readily. 

The  false  membrane  may  develop  on  any  mucous  membrane  or  upon 
any  wound  or  abrasion,  but  it  most  frequently  appears  on  the  tonsils. 
According  to  Lennox  Browne,  of  London,  the  relative  frequency  of  its 
appearance  is  as  follows: 


Above  the  larynx,  84.1  per  cent.: 

841  cases. 

Fauces  (including  tonsils)  alone 

.     672  cases 

Nose  alone 

2  cases 

Fauces  and  nose 

165  cases 

Mouth  or  lips  alone  ..... 

1  case. 

Hard  palate  alone     ..... 

1  case. 

Involving  larynx,  15.9  per  cent.: 

150  cases 

Larynx  alone    . 

4  cases 

Larynx  and  fauces    .         .         .         .         . 

100  cases 

Larynx,  fauces,  and  nose  .... 

46  cases 

The  growth  of  the  membrane,  whatever  its  site,  varies  greatly  in  rapidity, 
in  the  area  covered,  and  also  in  its  thickness,  but  the  virulence  of  the  systemic 
infection  is  not  always  in  direct  ratio  to  the  size  of  the  diphtheritic  patch. 
On  the  other  hand,  the  degree  of  secondary  infection  depends  largely  upon 
the  particular  surface  involved,  and  if  it  develops  in  the  nasopharynx  the 
toxaemia  is  apt  to  be  profound.  In  many  severe  cases  the  accessory  nasal 
cavities  are  infected,  particularly  the  antrum  of  Highmore. 

Visceral  and  Systemic  liESiONS. — The  action  of  the  toxin  of  diphtheria 
is  chiefly  expended  upon  the  heart,  the  nervous  system,  and  the  kidneys, 
The  heart  suffers  from  an  acute  myositis  or  inflammation  of  its  interstitial 
and  muscular  tissues,  and  this  may  be  followed  by  conversion  of  the  muscle 
fibres  into  hyaline  masses.  In  a  large  proportion  of  the  cases  in  which 
sudden  death  from  heart-failure  occurs  the  cause  lies  in  the  effect  of  the 
poison  upon  the  nervous  mechanism  of  the  heart,  possibly  to  a  greater 
degree  than  its  effect  upon  the  myocardium.  In  some  of  these  cases,  how- 
ever, death  is  due  to  thrombi  in  the  heart  cavities  (see  Sequelce),  or, 
again,  portions  of  these  thrombi  are  swept  out  of  the  heart  and  produce 


176  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

embolism  in  the  coronary  arteries,  in  the  pulmonary  vessels  or  in  the  gen- 
eral arterial  system.  As  would  be  expected  from  the  effects  upon  the 
heart,  just  described,  the  bloodvessels  are  also  affected.  An  acute  arteritis 
often  occurs  and  affects  particularly  the  intima. 

The  nervous  system  is  involved  chiefly  in  its  peripheral  portions.  The  nerve 
trunks  suffer  from  acute  toxic  neuritis  and  less  commonly  autopsy  reveals 
hemorrhage  into  the  spinal  cord  and  its  membranes  as  a  result  of  the  vascular 
action  of  the  poison.  A  much  more  common  spinal  lesion  is,  however,  an 
acute  anterior  poliomyelitis,  that  is,  involvement  of  the  cells  in  the  anterior 
horns  of  the  gray  matter.  Sometimes,  too,  the  posterior  nerve  roots  in  the 
cord  may  be  also  affected.  The  special  cranial  nerves  are  also  involved  in 
many  instances  and  loss  of  function  in  the  oculomotor,  vagus,  hypoglossal 
and  spinal  accessory  fibres  takes  place.  It  is,  however,  interesting  to  note 
that  while  paralysis,  due  to  peripheral  diphtheritic  neuritis,  may  be  absolute 
and  widespread,  it  usually  gets  well  unless  the  function  of  some  vital  part 
is  so  interfered  with  that  death  speedily  ensues.  The  brain  is  very  rarely 
affected. 

The  kidneys  are  more  or  less  affected  in  all  cases  of  diphtheria.  In  some 
there  is  only  a  mild  albuminuria  produced  by  the  irritative  effect  of  the 
toxin  upon  the  renal  epithelium.  In  more  severe  cases  an  acute  toxic 
nephritis  develops.  This  nephritis  primarily  is  parenchymatous,  involving 
the  Malpighian  tufts  and  the  tubules,  but  it  speedily  becomes  diffuse. 
Hyaline  degeneration  also  takes  place  in  the  renal  vessels,  as  elsewhere  in 
the  body. 

The  spleen  is  enlarged,  markedly  congested,  and  minute  hemorrhages 
are  to  be  seen  beneath  its  capsule.  The  liver  may  be  found,  on  cross-section, 
to  be  dotted  with  small  areas  of  coagulation  necrosis. 

As  the  infection  is  most  marked  in  the  throat  the  cervical  lymph  glands 
are  usually  infiltrated  and  the  poison  may  also  cause  enlargement  of  the 
lymphatics  in  the  mediastinum  and  in  the  retroperitoneum.  The  inflamma- 
tion of  the  lymph  nodes,  however,  rarely  ends  in  suppuration  or  extensive 
necrosis. 

The  lungs  are  often  the  site  of  bronchopneumonia  resulting  from  a  com- 
plicating pneumococcus  infection,  but  true  croupous  pneumonia  is  a  rare 
complication.  When  great  dyspnoea  is  present  because  of  laryngeal  stenosis 
compensatory  emphysema  may  develop.  In  the  laryngeal  form  the  mem- 
brane may  extend  to  the  smaller  bronchi. 

The  blood  is  affected  very  deleteriously  by  the  poison  of  diphtheria,  so 
that  a  great  diminution  in  the  number  of  the  red  cells  takes  place  with 
a  corresponding  fall  in  haemoglobin.  A  leukocytosis  occurs  except  in  the 
very  malignant  forms  of  the  disease.  Myelocytes  are  said  to  be  present  in 
severe  cases,  and  Engel  states  that  in  those  cases  in  which  they  appear  in 
as  high  a  percentage  as  2  per  cent,  death  occurs. 

Symptoms. — After  a  period  of  incubation  varying  from  two  to  seven  days 
the  disease  has  its  onset  in  the  form  assumed  by  most  acute  infections, 
namely,  with  general  malaise,  chilliness,  and  fever,  the  temperature  often 
reaching  102°  or  even  103°  in  the  first  twenty-four  hours.  The  severity  of 
these  symptoms  varies  greatly.    In  some  cases  they  are  so  mild  that  the  child 


DIPHTHERIA  177 

is  scarcely  thought  to  be  aiUng,  and  the  physician  at  his  second  visit  is 
shocked  on  examining  the  throat  to  find  distinct  local  lesions.  In  other  cases 
the  disease  is  fulminating  in  its  onset.  I  have  seen  a  small  patch  of  mem- 
brane on  a  tonsil  within  twelve  hours  involve  the  larynx  and  necessitate 
tracheotomy,  the  membrane  involving  the  external  edges  of  the  wound  in 
less  than  twelve  hours  more.  In  nearly  every  case  there  is  some  complaint 
of  sore  throat,  or  of  difficulty  in  swallowing  arising  from  this  cause.  The 
pharyngeal  mucous  membrane  is  reddened  and  upon  the  tonsil  or  tonsils 
is  seen  a  tiny  patch,  which  is  the  beginning  of  the  membrane,  but  which  may 
be  due  to  the  exudate  thrown  out  by  a  follicular  tonsillitis.  This  membrane 
rapidly  spreads  and  may  extend  to  the  pillars  of  the  fauces,  the  pharynx, 
nasopharynx,  and  the  uvula.  It  is  grayish  or  light  mouse  color  in  hue,  and 
in  many  cases  speedily  becomes  shaggy  and  dirty  looking.  If  the  physician 
attempts  to  remove  it  it  is  found  to  adhere  to  the  mucous  membrane,  and 
it  can  be  taken  off  by  only  tearing  it  loose,  so  that  a  raw,  bleeding  surface  is 
exposed  over  which  a  false  membrane  speedily  reforms  for  reasons  given 
when  discussing  the  pathology  and  morbid  anatomy  of  the  disease. 

There  is  nearly  always  some  enlargement  of  the  glands  at  the  angle  of  the 
jaw. 

The  degree  of  systemic  disturbance  depends  in  every  case  upon  the  virulence 
of  the  infecting  bacillus  and  the  rapidity  with  which  the  toxin  is  absorbed. 

Some  patients  who  present  on  examination  a  large  area  of  membrane 
suffer  shghtly  in  a  comparative  sense.  The  fever  does  not  rise  above 
102°  or  103°,  the  pulse  does  not  go  above  100  or  110,  and  the  general  state 
of  the  patient  is  favorable.  In  other  instances  from  the  very  onset  the  gen- 
eral systemic  state  is  bad,  even  when  the  local  changes  may  seemingly  be 
slight.  Even  in  severe  cases,  however,  the  fever  is  not  prone  to  be  high,  and 
often  it  never  rises  above  101°. 

The  nervous  symptoms  consist  in  restlessness,  sometimes  in  delirium,  and 
rarely  convulsions  come  on.  As  the  disease  approaches  a  fatal  issue,  the 
child  becomes  apathetic  and  it  may  be  difficult  to  rouse  it. 

The  circulation  is  feeble  and  irregularity  of  the  pulse  is  a  very  frequent 
symptom.  In  White's  recent  exhaustive  study  of  946  cases  this  irregularity 
was  present  in  60  per  cent.  The  younger  the  patient  the  greater  the 
frequency  of  irregularity  of  pulse.  Endocardial  murmurs,  systolic  in  point 
of  time,  occurred  in  94  per  cent. 

Albuminuria  is  a  very  constant  symptom  in  these  cases,  appearing  as 
early  as  the  third  day.  The  albumin  may  appear  in  considerable  quantities, 
but  the  urinary  flow  is  in  many  cases  not  greatly  increased,  although  the 
presence  of  granular  and  hyaline  casts  shows  that  a  true  nephritis  is  present. 
Dropsy  is  uncommon. 

In  cases  which  are  not  compKcated  or  treated  by  antitoxin,  and  which 
spontaneously  recover,  the  membrane  ceases  to  grow  by  the  fifth  or  sixth 
day,  and  gradually  separates  at  about  the  seventh  or  tenth  day,  leaving  at 
its  former  site  a  bright-red  surface  which  bleeds  easily.  The  nasal  false 
membrane  persists  longer  than  that  in  the  pharynx,  and  often  comes  away 
in  one  mass. 

After  this  period  convalescence  gradually  goes  on,  the  patient  being  pro- 
12 


178  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

foundly  weak  and  anaemic  and  in  great  danger  of  sudden  death  from  heart- 
failure  if  any  sudden  change  in  posture  is  made.  A  great  many  cases  thought 
to  be  on  the  high  road  to  recovery  meet  an  unexpected  fatal  ending  at  this 
time. 

Special  Forms. — There  still  remain  to  be  described  the  special  symptoms 
connected  with  those  cases  of  diphtheria  in  which  particular  portions  of 
the  respiratory  mucous  membrane  are  involved,  or  in  which  the  disease 
presents  conditions  which  may  be  considered  aberrant.  In  nasal  diphtheria 
the  false  membrane  may  be  so  hidden  by  the  swollen  turbinated  bodies 
that  it  is  overlooked  until  it  extends  well  forward  into  the  nostril,  when  it 
may  completely  occlude  the  nares.  Only  a  careful  rhinoscopic  examination 
will  reveal  this  form  in  its  early  stages.  Because  of  the  importance  of  insti- 
tuting treatment  in  all  cases  of  this  disease  at  the  earliest  possible  moment 
the  nasal  cavities  should  always  be  examined  at  the  same  time  the  throat 
is  investigated,  and  any  signs  of  nasal  obstruction  taken  as  of  importance. 
A  valuable  sign  of  nasal  diphtheria,  but  one  which  unfortunately  does  not 
manifest  itself  until  the  disease  is  well  advanced  is  a  nasal  discharge  which 
may  excoriate  the  upper  lip. 

It  is  never  to  be  forgotten  that  nasal  diphtheria  is  a  very  malignant 
type  of  the  disease  in  nearly  every  instance  in  which  it  occurs,  and  it  is 
particularly  prone  to  affect  infants  or  very  young  children. 

Laryngeal  diphtheria  manifests  itself  chiefly  by  the  marked  respiratory 
obstruction  which  it  produces  very  shortly  after  the  pathological  process 
begins  in  the  mucous  membrane  of  the  larynx.  Hoarseness  on  speaking, 
or  crying,  and  a  harsh  cough  of  a  metallic  sound,  sometimes  called  "  brassy," 
develops.  Following  these  symptoms  it  is  noted  that  there  is  slight  inspira- 
tory stridor  which  is  accentuated  at  intervals  by  what  seems  to  be  asso- 
ciated laryngeal  spasm.  This  is  followed  by  persistent  stridor,  harsh 
breathing,  and  manifest  unrest  and  respiratory  anxiety.  The  child  may 
grasp  its  throat  with  its  hands  as  if  endeavoring  to  remove  the  obstruction, 
and  as  it  becomes  livid,  partly  from  mechanical  failure  of  respiration  and 
partly  from  toxaemia,  it  often  grinds  its  teeth  and  looks  from  side  to  side  for 
relief,  presenting  at  the  same  time  signs  of  profound  toxaemia.  Its  pallid 
skin  may  be  bedewed  with  sweat.  As  the  disease  advances  the  child  becomes 
more  and  more  limp,  and  struggles  less  and  less  for  its  breath.  In  children 
old  enough  and  strong  enough  to  cough  violently  in  an  effort  to  dislodge 
the  membrane  it  often  happens  that  they  expel  pieces  of  false  membrane, 
and  in  some  instances  they  may  expel  complete  casts  of  the  larynx.  The 
fever  in  this  type  of  diphtheria  may  not  be  at  all  high  after  the  larynx  has 
become  infected,  but,  as  would  be  expected,  the  pulse  is  usually  exceedingly 
rapid  and  small. 

Laryngeal  diphtheria  rarely  occurs  without  extension  to  the  pharynx,  so 
that  at  the  time  of  death  the  membrane  usually  covers  a  wide  area.  When 
the  pharyngeal  and  laryngeal  symptoms  are  very  marked  there  is  usually 
great  enlargement  of  the  cervical  glands. 

Bronchopneumonia,  due  to  the  inspiration  of  septic  material,  is  a  frequent 
complication  of  this  type. 

Like  nasal  diphtheria,  laryngeal  diphtheria  has  a  very  high  mortality. 


DIPHTHERIA  179 

partly  because  it  causes  suffocation  and  partly  because  it  is  associated 
with  toxaemia  of  a  grave  type.  Sometimes  laryngeal  diphtheria  results  in 
diphtheria  of  the  bronchial  tubes. 

Diphtheria  of  the  conjunctiva  may  occur  as  a  complication  or  as  a  primary 
lesion. 

Complications  and  Sequelae. — The  complications,  involving  the  cervical 
glands,  the  lungs,  heart,  kidneys,  and  nervous  system,  have  already  been 
mentioned.    Nevertheless  it  is  proper  to  say  something  more  concerning  them. 

Sudden  heart-failure  toward  the  close  of  the  attack,  or  after  convalescence 
is  established,  sometimes  occurs  on  the  slightest  exertion.  The  child  sits 
up  to  take  a  drink,  or  to  grasp  a  toy,  or  becomes  angry,  and  drops  over 
dead. 

In  other  instances,  instead  of  almost  instantaneous  cardiac  failure  with 
sudden  death,  a  more  gradual  manifestation  of  grave  heart  disease  is  devel- 
oped. A  patient  apparently  on  the  high  road  to  convalescence,  except  for 
the  reddened  throat  and  profound  anaemia,  is  found  to  have  developed  a 
weak  pulse,  which  flags,  and  he  presents  unduly  feeble  heart  sounds. 
Endocardial  murmurs  may  be  present.  Sometimes  the  pulse  is  abnormally 
slow.  In  other  cases  it  is  too  fast,  and,  with  these  circulatory  symptoms, 
some  epigastric  distress  or  even  vomiting  occurs.  The  pulse  becomes 
weaker  and  weaker  and  arhythmia  increases,  the  face  is  more  and  more 
pallid,  and  cardiac  dyspnoea  with  lividity  comes  on.  Auscultation  reveals 
fetal  heart  sounds  or  there  may  be  a  ''delirium  cordis"  Death  finally 
closes  the  scene  at  the  end  of  twenty-four  or  forty-eight  hours  in  the  presence 
of  gradually  deepening  asthenia  and  a  mind  which  is  clear  almost  to  the 
very  last.     Acute  cardiac  dilatation  may  occur. 

There  are  three  causes  for  the  types  of  heart-failure  which  arise  as  a 
result  of  diphtheria.  When  the  heart  fails  in  the  course  of  an  attack  it  is 
usually  the  result  of  cardiac  thrombosis.  When  it  occurs  after  an  attack  it 
is  due  usually  to  a  toxic  myocarditis  or  to  the  failure  of  the  nervous  supply 
of  the  heart  through  bulbar  paralysis  or  paralysis  of  nerve  fibres.  Some 
statistics  indicate  that  thrombosis  is  the  most  common  cause  of  death  after 
disappearance  of  the  membrane.  Of  course  all  three  of  these  factors  may 
be  present  simultaneously.  It  is  probable,  however,  that  thrombosis  is 
more  frequently  the  cause  of  sudden  death  than  is  generally  thought.  Bar- 
bier  in  71  autopsies  on  cases  of  sudden  death  in  diphtheria  found  an  ante- 
mortem  cardiac  thrombus  in  no  less  than  52  per  cent.  These  thrombi  were 
commonly  found  on  the  right  side  of  the  heart,  usually  in  the  right  auricle. 

Sometimes  death  is  due  to  paralysis  of  the  'phrenic  nerve,  so  that  dia- 
phragmatic paralysis  ensues. 

The  septic  condition  of  the  throat,  the  labored  respiration,  the  decreased 
vital  resistance  of  the  patient,  and  the  feebleness  of  the  pulmonary  circula- 
tion in  severe  cases  very  greatly  predispose  the  patient  to  hronchoyneiimonia, 
and  this  complication  or  sequel  of  diphtheria  is  the  cause  of  death  in  a  very 
large  number  of  young  children. 

Local  or  widespread  paralysis  often  follows  an  attack  of  diphtheria,  and 
if  it  involves  vital  nerves  causes  death.  On  the  other  hand,  these  palsies 
are  noteworthy  because  of  the  fact  that  they  usually  recover.     It  is  by  no 


180  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

means  uncommon  to  see  a  child  so  paralyzed  that  it  can  neither  move 
hand  nor  foot  or  even  move  its  head,  that  lies  perfectly  limp  in  its 
mother's  arms,  entirely  recover  muscular  power.  These  palsies  are  not 
usually  immediate  sequences  of  an  attack  of  diphtheria,  but  are  all  the  more 
alarming  because  they  may  manifest  themselves  from  one  to  three  weeks 
after  an  attack.  Again,  it  often  happens  that  a  very  mild  attack  of  the  dis- 
ease is  followed  by  this  distressing  sequence,  although  as  a  rule  severe  cases 
usually  have  this  result.  The  palate  is  the  part  most  commonly  paralyzed, 
and  this  results  in  difficulty  in  swallowing,  regurgitation  of  liquids  through 
the  nose,  and  in  a  peculiar  tone  to  the  voice.  When  the  throat  is  examined 
the  palate  is  seen  to  hang  relaxed  and  motionless  when  the  patient  attempts 
to  phonate,  and  it  is  also  somewhat  anaesthetic,  so  that  the  contact  of  food 
is  not  well  recognized. 

The  time  of  onset  of  the  paralysis  varies  somewhat  with  the  parts  involved. 
The  form  that  occurs  most  frequently  and  which  affects  the  muscles  of  the 
pharynx  and  eyes  and  extremities,  or  even  that  of  the  heart  or  the  muscles 
of  respiration,  is  a  late  palsy  of  the  seventh  to  the  twenty-first  day  of  con- 
valescence, whereas  that  form  which  affects  the  palate  is  more  frequently 
met  with  at  the  end  of  the  first  week. 

True  facial  paralysis  very  rarely  occurs  except  as  a  result  of  otitis  media 
arising  secondarily  from  the  diseased  state  of  the  pharynx. 

Statistics  as  to  the  frequency  with  which  paralysis  accompanies  or  follows 
diphtheria  vary.  Hoppe-Seyler  states  it  to  be  27  per  cent.  Johannessen, 
for  all  Nor.way,  12.5  per  cent,;  the  report  of  the  Metropolitan  Asylums 
Board  of  London  for  1900,  18.5  per  cent. 

The  collective  investigation  of  the  American  Pediatric  Society  based  on 
3384  non-hospital  cases  treated  with  antitoxin  showed  that  328  cases  of 
paralysis  occurred,  which  gives  a  percentage  of  9.6. 

Hemorrhage  from  the  ulcerative  process  in  the  nose  may  be  sufficiently 
free  to  seriously  exhaust  the  patient.  When  subcutaneous  hemorrhages 
appear  they  are  always  a  sign  of  very  profound  toxaemia. 

When  that  practically  constant  sequel  of  diphtheria,  profound  ancemia, 
remains  persistently  present  and  is  but  little  improved  under  treatment,  the 
possibility  of  reyial  disease  being  a  serious  sequel  is  to  be  recalled. 

Diagnosis. — There  is  no  disease  in  which  it  is  more  important  for  the 
physician  to  make  a  correct  diagnosis  promptly  than  diphtheria,  because  if  it 
be  recognized  in  its  earliest  stage  it  can  be  cured  by  antitoxin  in  the  majority 
of  instances.  On  the  other  hand,  there  is  no  disease  which  is  more  diffi- 
cult of  prompt  diagnosis  in  some  cases.  As  diphtherial  infection  may  be 
present  without  marked  formation  of  membrane,  all  cases  which  manifest 
sore  throat  during  an  epidemic  or,  after  exposure,  should  receive  antitoxin 
as  a  preventive,  and  the  throat  should  be  swabbed  and  the  secretion  obtained 
examined  bacteriologically  for  the  bacillus. 

In  every  large  city  at  the  present  time  the  health  authorities  provide  tubes 
and  swabs  for  the  transmission  of  cultures  from  the  patient  to  a  laboratory. 
Usually  the  swab  is  delivered  in  a  sterile  tube  and  the  culture  medium  is 
placed  in  a  second  sterile  tube.  The  directions  issued  by  the  New  York 
Board  of  Health  are  as  follows :  "  The  patient  should  be  placed  in  a  good  light, 


DIPHTHERIA  181 

and,  if  a  child,  properly  held.  In  cases  where  it  is  possible  to  get  a  good 
view  of  the  throat,  depress  the  tongue  and  rub  the  cotton  swab  gently  but 
freely  against  any  visible  exudate.  In  other  cases,  including  those  in  which 
the  exudate  is  confined  to  the  larynx,  avoiding  the  tongue,  pass  the  swab  far 
back  and  rub  it  freely  against  the  mucous  membrane  of  the  pharynx  and 
tonsils.  Without  laying  the  swab  down,  withdraw  the  cotton  plug  from  the 
culture-tube,  insert  the  swab,  and  rub  that  portion  of  it  which  has  touched 
the  exudate  gently  but  thoroughly  all  over  the  surface  of  the  blood  serum. 
Do  not  push  the  swab  into  the  blood  serum  nor  break  the  surface  in  any 
way.  Then  replace  the  swab  in  its  own  tube,  plug  both  tubes,  put  them  in 
the  box,  and  return  the  culture  outfit  at  once  to  the  station  from  which  it 
was  obtained." 

A  loss  of  valuable  time  is  prevented  during  the  bacteriological  test  by 
using  antitoxin,  but  many  hours  need  not  be  lost  if  the  bacteriologist  is 
skilful.  Dr.  Park,  of  New  York,  who  has  done  such  excellent  work  along 
these  lines,  has  this  to  say  in  regard  to  this  matter:  "The  examination  by  a 
competent  bacteriologist  of  the  bacterial  growth  in  a  blood-serum  tube 
which  has  been  properly  inoculated  and  kept  for  fourteen  hours  at  the  body 
temperature  can  be  thoroughly  relied  upon  in  cases  where  there  is  visible 
membrane  in  the  throat,  if  the  culture  is  made  during  the  period  in  which 
the  membrane  is  forming,  and  no  antiseptic,  especially  no  mercurial  solu- 
tion, has  lately  been  applied.  In  cases  in  which  the  disease  is  confined  to 
the  larynx  or  bronchi,  surprisingly  accurate  results  can  be  obtained  from 
cultures,  but  in  a  certain  proportion  of  cases  no  diphtheria  bacilli  will  be  found 
in  the  first  culture,  and  yet  will  be  abundantly  present  in  later  cultures. 
We  believe,  therefore,  that  absolute  reliance  for  a  diagnosis  cannot  be 
placed  upon  a  single  culture  from  the  pharynx  in  purely  laryngeal  cases/' 

Diphtheria  is  to  be  separated  from  tonsillitis  with  exudation  from  the 
follicles  of  the  tonsils  and  from  the  diphtheroid  false  membrane  produced 
by  the  streptococcus  and  by  an  organism  closely  allied  but  not  identical 
with  the  Klebs-LoeflBer  organism,  which  is  found  in  scarlet  fever,  typhoid 
fever,  and  measles.  Sometimes  this  can  be  done  only  by  the  bacteriological 
test. 

In  follicular  tonsillitis  the  exudate  may  be  scattered  over  the  openings 
of  several  follicles,  it  is  rarely  as  dark  in  hue  as  the  true  membrane,  it  can  be 
wiped  off  with  an  applicator  more  readily  than  the  membrane  of  diphtheria, 
and  the  tonsillar  swelling  is  marked.  The  systemic  symptoms  are,  however, 
of  little  value  in  differentiation,  because  tonsillitis  is  a  disease  charac- 
terized by  very  severe  symptoms  as  compared  to  its  gravity,  for  aching  in 
the  back  and  limbs,  high  fever,  and  great  evidence  of  systemic  depression 
are  frequently  seen  during  its  course.  Holt  has  pointed  out  the  fact  that  the 
surfaces  of  the  wound  left  after  tonsillotomy  may  for  a  few  days  closely 
resemble  tonsillar  diphtheria,  and  I  have  seen  the  free  application  of  a 
strong  solution  of  silver  nitrate  to  the  pharynx  produce  an  appearance 
which  might  readily  be  mistaken,  if  examined  in  a  poor  light,  for  diphtheria. 

Reference  has  been  made  on  several  occasions  to  diphtheroid  conditions 
of  the  throat.  These  states  are  probably  in  a  large  number  of  instances 
due  to  the  streptococcus  pyogenes.     The  false  membrane,  if  none  of  the  true 


182  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

bacilli  of  Klebs  and  Loeffler  are  present,  is  usually  more  soft  and  creamy 
in  its  consistency,  it  is  not  so  tightly  adherent  to  the  underlying  mucous 
membrane,  and  is  often  very  foul.  Occurring  as  a  complication  of  grave 
infectious  diseases  such  as  scarlet  fever  and  typhoid  fever,  it  is  dangerous, 
but  otherwise  the  mortaUty  is  not  high,  being  about  2.5  per  cent.,  if  we 
can  take  the  New  York  city  statistics  as  representative  of  all  cases. 

Prognosis. — At  the  present  time  it  may  be  said  that  the  prognosis  of  diph- 
theria depends  entirely  upon  the  promptness  with  which  antitoxin  is  used. 
Without  antitoxin  the  death  rate  varies  greatly  in  different  epidemics.  In 
some  it  reaches  the  appalling  rate  of  50  per  cent.,  while  in  others  it  is  not 
more  than  30  per  cent.  It  is  very  much  more  fatal  in  babies  than  in  older 
children.  Symptoms  of  evil  prognostic  import  are  grinding  of  the  teeth, 
gallop  rhythm  of  the  heart  sounds,  epigastric  pain,  and  vomiting. 

The  cases  manifesting  laryngeal  and  nasal  involvement  are  always  grave 
as  to  prognosis.  The  physician  should  also  be  most  guarded  as  to  his  prog- 
nosis as  the  disease  passes  its  most  active  period,  because  everyone  of  experi- 
ence knows  that  an  attack  of  sudden  heart-failure  often  occurs  as  the  child, 
once  more  feeling  strong,  attempts  to  sit  up.  A  rapid  or  gradual  heart- 
failure  may  come  on  during  convalescence.     (See  Sequelae.) 

Prophylaxis. — As  the  intimate  association  of  a  person,  or  garments,  bear- 
ing the  specific  bacillus  with  another  individual  who  is  susceptible  to  the 
disease  is  essential  for  its  spread,  it  is  evident  that  by  proper  quarantine 
and  isolation  perfect  prophylaxis  is  possible.  All  patients  who  have  diph- 
theria should  be  isolated  at  once,  and  the  attendant  who  nurses  the  child 
or  adult  who  is  affected  should  not  associate  with  other  persons  until  after  a 
bath  has  been  taken,  the  face  and  head  well  shampooed  and  t^ie  pharynx 
and  nasal  cavities  well  douched.  After  the  patient  is  convalescent,  it  is 
to  be  recalled  that  the  specific  bacillus  may  remain  in  the  nasopharyngeal 
mucus  for  a  long  period  and  so  isolation  is  still  essential.  The  child  should 
not  play  with  other  children  for  at  least  two  weeks,  and  during  this  period 
should  have  its  nasopharynx  sprayed  daily  with  some  bland  antiseptic  wash 
such  as  Dobell's  solution,  alkathymol,  or  normal  saline  solution.  Whenever 
it  is  possible,  particularly  in  public  institutions,  the  nasopharyngeal  secre- 
tion should  be  examined  bacteriologically  during  convalescence  to  prove 
the  presence  or  absence  of  the  specific  infecting  germ  before  the  child  is 
discharged.  As  illustrative  of  this  fact  the  results  of  the  New  York  Board 
of  Health  investigation  are  of  interest.  Out  of  605  cases  examined  it  was 
found  that  the  bacilli  were  not  present  in  304  on  the  third  day  after  the 
membrane  disappeared,  in  176  they  were  present  for  seven  days,  in  64  for 
twelve  days,  and  in  36  cases  for  fifteen  days.  Twenty-one  days  after  the 
membrane  was  gone  12  showed  bacilli,  and  4  cases  showed  them  for  twenty- 
eight  days.  Another  set  of  4  cases  yielded  bacilli  for  thirty-five  days,  and 
2  for  sixty-three  days. 

It  seems  hardly  necessary  to  add  that  the  garments,  bedding,  and  toys  of 
all  diphtheritic  patients  should  be  destroyed  or  thoroughly  disinfected  by 
steam  or  formaldehyde.  The  floors  and  walls  of  the  room  and  the  furniture 
should  also  be  treated  with  formaldehyde,  and  it  should  be  done  as  thor- 
oughly as  if  the  case  had  been  one  of  smallpox.    All  discharges  from  the 


DIPHTHERIA  183 

patient  should  be  received  in  a  vessel  containing  bichloride  solution,  or,  if 
cloths  are  used,  these  should  be  burned. 

A  very  important  measure  in  all  cases  in  which  the  disease  arises  in  a 
family  of  children  is  the  use  of  immunizing  doses  of  antitoxic  serum  for  the 
protection  of  the  well  from  the  disease.  There  is  no  doubt  whatever  that 
this  is  a  most  efficient,  never-to-be-neglected  measure.  The  dose  is  not 
less  than  500  to  1000  units  and  the  protection  lasts  about  three  or  four 
weeks.     Nurses  as  well  as  children  should  be  protected  by  its  use. 

When  treating  or  examining  the  throat  the  physician  and  nurse  may 
protect  themselves  from  the  discharges  by  looking  through  a  pane  of  glass 
held  before  the  face  of  the  patient. 

Treatment. — The  treatment  of  diphtheria  at  the  present  time  is  more 
scientifically  accurate  in  its  basis  and  in  its  results  than  that  of  any  other 
malady  save  malarial  fever,  in  which  we  know  not  only  the  cause  but  the 
remedy  for  its  removal.  The  keystone  of  the  treatment  is  the  liberal  use  of 
antidiphtheritic  serum  derived  from  the  horse. 

It  is  not  necessary  in  a  work  of  this  character  to  give  massive  accumu- 
lations of  statistics  to  prove  that  this  plan  is  based  not  only  on  scientific 
laboratory  investigations,  but  upon  bedside  experience  as  well.  A  few 
instances  may,  however,  be  cited  as  illustrative  of  the  facts.  Thus  it  is 
interesting  to  note  that  a  decided  decrease  in  the  mortality  of  diphtheria 
occurred  immediately  after  the  introduction  of  antitoxin. 

The  first  statistics  furnished  by  Roux  are  interesting  because  they  permit 
a  comparison  to  be  made  between  the  death  rate  of  the  two  great  children's 
hospitals  of  Paris  for  a  certain  length  of  time  during  which  the  cases  in 
one  were  treated  by  antitoxin — while  those  in  the  other  did  not  receive  it. 
From  February  1  to  July  24,  1894,  the  mortality  at  the  Hopital  des  Enfants 
Malades,  where  antitoxin  was  used,  was  26  per  cent.,  while  the  mortality 
during  this  period  at  the  Hopital  Trousseau,  where  serum  was  not  employed, 
was  60  per  cent.  From  October  1,  1894,  serum  therapy  was  practised  at  the 
Hopital  Trousseau,  with  the  result  that  at  the  end  of  two  months  the  death 
rate  had  fallen  to  14.85  per  cent.  Similar  results  have  been  obtained 
wherever  antitoxin  has  been  used.  In  Geneva  the  death  rate  fell  from  35.7 
to  9  per  cent.,  and  the  report  of  the  American  Pediatric  Society,  based  on 
5794  cases,  gave  a  percentage  of  12.3.  The  largest  and  most  valuable 
statistics  are  those  of  Bayeux,  who  collected  more  than  200,000  cases  from 
all  parts  of  the  world  and  found  that  the  average  mortality  rate  was  16  per 
cent.  Making  a  most  conservative  estimate  of  a  general  mortality  of  35  per 
cent,  in  preantitoxin  days,  Bayeux's  figures  prove  a  reduction  in  mortality 
of  more  than  50  per  cent,  since  the  introduction  of  antitoxin.  In  the  first 
nine  years  during  which  antitoxin  was  used  in  the  treatment  of  diphtheria 
in  Chicago  the  mortality  was  6088,  while  during  the  nine  years  preceding 
the  use  of  antitoxin  the  mortality  was  11,488,  a  decrease  of  5400,  or  47  per 
cent.,  although  the  population  had  increased  nearly  600,000,  or  52  per 
cent.  If  this  increase  in  population  is  taken  into  consideration,  the  decrease 
in  the  mortality  of  the  disease  under  this  plan  of  treatment  is  63  per  cent. 
In  New  York  City,  out  of  1702  cases  injected  on  the  first  day,  including 
moribund   cases,  only  85  died — a   case   mortality  of  4.09  per  cent.     The 


184  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

following  figures,  which   are  Baginsky's,  show   the   decrease  in  mortality 
according  to  age: 

Before  the  introduction  of  antitoxin  the  mortality  of  diphtheria  accord- 
ing to  age  was — 


0  to  2  years     .         .     60,2 

6  to    8  years     . 

.     22.9. 

2  to  4  years     =          .     51  2. 

8  to  10  years     . 

.     28.8. 

4  to  6  years     .          .     38.0 

12  to  14  years     . 

.     18.5. 

3  the  introduction  of  antitoxin  the  death  rate  is — 

0  to  2  years     .          .     25.88. 

8  to  10  years     . 

.       5.17. 

2  to  4  years     .          .     17  12. 

10  to  12  years     . 

.     10. 

4  to  6  years     .          .     17.24. 

12  to  14  years     . 

.     13.3. 

6  to  8  years     .          .     11.39. 

The  physician  who  fails  to  use  antitoxin,  when  it  is  to  be  had,  is  guilty 
of  a  gross  lack  of  professional  knowledge  or  is  atrociously  careless  of  his 
patient's  welfare. 

There  are  several  points  to  be  borne  in  mind  in  regard  to  the  use  of 
antitoxin,  namely  (1)  it  must  be  employed  early  in  the  attack  to  get  the 
best  results,  for  it  is  manifest  that  after  the  disease  has  existed  long  enough 
to  do  permanent  damage  to  the  tissues  no  antidote  can  be  satisfactory.  No 
one  would  expect  to  give  the  antidote  for  arsenic  two  days  after  the  poison 
was  taken  and  get  good  results.  Nevertheless,  when  antitoxin  has  not  been 
used  early  it  must  be  given  freely  in  the  hope  of  its  aiding  the  patient 
sufficiently  to  help  him  withstand  the  infection.  (2)  The  antitoxin  should 
be  given  liberally.  A  few  large  doses  in  the  onset  of  the  attack  not  only 
are  of  great  value,  but  are  really  economical  so  far  as  cost  is  concerned. 
(3)  It  must  be  given  in  particularly  large  doses  in  cases  of  nasal  and  laryngeal 
diphtheria,  because  these  are  forms  in  which  rapid  absorption  of  the  toxin 
of  the  disease  and  respiratory  obstruction  takes  place  and  the  malady  must 
be  most  actively  opposed.  In  these  cases  it  may  be  useful  to  give  it  intra- 
venously, (4)  Whenever  a  person  is  exposed  to  diphtheria  he  should  receive  a 
moderate  dose  of  antitoxin  to  protect  him  from  infection.  The  dose  should 
be  about  500  units,  repeated  in  two  weeks,  if  exposure  continues.  (5)  When 
diphtheria  is  suspected  to  be  present  it  is  well  to  give  antitoxin  at  once 
rather  than  run  the  risk  of  waiting  for  a  sure  diagnosis.  In  administering 
antitoxin  the  following  rules  should  be  followed: 

1.  The  skin  over  the  outer  surface  of  the  thigh  or  over  the  flank  or 
lateral  abdominal  wall  should  be  cleansed  with  soap  and  water  and  alcohol. 

2.  The  serum  should  be  injected,  by  means  of  a  syringe  or  bulb,  through 
a  large  hypodermic  needle  which  is  inserted  through  the  skin  where  it  has 
been  cleansed. 

3.  The  injection  should  be  made  slowly  and  quietly  and  the  swelling 
which  results  should  not  be  rubbed. 

4.  At  least  1500  to  2000  units  of  antitoxic  serum  should  be  given  at  the 
first  dose  and  repeated  in  four  to  eight  hours,  according  to  the  severity  of 
the  case. 


DIPHTHERIA  185 

5.  In  nasal  and  laryngeal  cases  3000  or  more  units  for  the  first  dose  is 
usually  necessary. 

The  result  of  this  plan  of  treatment  is  often  magical.  The  symptoms  of 
general  systemic  disturbance,  such  as  a  rapid  pulse  and  fever,  become 
modified,  the  membrane  ceases  to  grow  and  loses  its  tenacious  hold  of  the 
subjacent  tissues,  becoming  not  only  loose  but  softened,  and  speedily 
disappears. 

The  only  disagreeable  effects  of  using  antitoxin  in  large  doses  is  the 
subsequent  development  of  some  pain  or  soreness  in  the  joints  or  the  appear- 
ance of  a  roseolous  rash;  but  even  if  these  symptoms  appear  they  are  not 
serious  and  need  give  no  alarm. 

The  local  treatment  of  diphtheria  consists  in  the  application  to  the  false 
membrane  of  peroxide  of  hydrogen  by  means  of  a  spray  or  swab.  This 
active  disinfectant  disintegrates  the  exudate  and  aids  in  its  removal.  The 
other  local  applications  which  have  been  used  in  the  past  are  painful, 
injurious,  or  ineffective  as  compared  to  this  agent. 

The  systemic  treatment,  aside  from  the  use  of  antitoxin,  consists  in  the 
employment  of  foods  which  are  easily  swallowed  and  which  will  maintain 
the  vitality  of  the  patient  to  the  highest  degree,  such  as  concentrated  broths 
fortified  by  barley-gruel  or  rice-gruel,  which  are  digested  in  great  degree 
by  the  administration  of  2  to  4  grains  of  taka-diastase. 

When  the  pulse  flags,  small  doses  of  aromatic  spirit  of  ammonia  or 
Hoffmann's  anodyne  (10  to  30  drops  in  water  may  be  used)  or  brandy 
which  is  old  enough  to  have  a  "bouquet"  may  be  given.  Full  doses  of 
strychnine  should  also  be  used  for  the  same  purpose.  Perfect  rest  of  mind 
and  body  should  be  obtained  if  possible  and  great  care  taken  during  the 
illness  and  during  convalescence  that  no  sudden  exertion,  which  may  cause 
cardiac  failure,  is  permitted. 

When  obstruction  of  the  larynx  takes  place  the  patient's  life  may  often 
be  saved  by  intubation  or  tracheotomy.  In  these  cases  the  patient  should 
be  kept  in  a  room  the  air  of  which  is  moistened  by  steam. 

The  complications  and  sequels  are  treated  in  the  following  manner: 
The  anemia  is  to  be  controlled  by  the  use  of  moderate  doses  of  reduced 
iron.  Large  doses  are  unnecessary  and  tend  to  cause  constipation  and 
disorder  digestion.  A  quarter  grain  three  times  a  day  is  quite  sufficient, 
given  in  a  small  chocolate-coated  tablet  or  placed  in  a  gum-drop.  In  some 
instances  3  to  5  minims  of  tincture  of  the  chloride  of  iron  is  equally  good; 
Y^  grain  of  arsenous  acid  in  a  sugar-coated  granule  may  be  given  simul- 
taneously or  in  alternate  weeks.  This  treatment  is  also  advisable  for  the 
relief  of  the  local  or  general  paralysis  which  is  usually  associated  with 
marked  anaemia.  In  other  instances  the  syrup  of  the  hypophosphites  may 
be  used,  and  phosphorus  is  often  of  value  in  the  dose  of  yfo  g^^V^  ^^^f^ 
times  a  day.  Another  remedy  of  great  value  as  a  roborant  is  cod-liver  oil. 
In  regard  to  the  use  of  strychnine,  which  is  so  largely  used  as  a  circu- 
latory and  nervous  stimulant  in  all  conditions  of  depression,  it  should  be 
remembered  that  it  is  never  a  stimulant  which  in  any  way  increases  the 
nutrition  of  the  part  involved.  It  simply  acts  as  an  irritant  stimulant. 
If  there  is  reason  to  believe  that  a  "whip"  is  needed  to  spur  atonic  nerves 


186  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

to  greater  effort,  it  may  be  used,  but  if  there  is  any  evidence  of  nervous 
irritation  it  is  better  not  to  employ  it.  Aside  from  the  treatment  already 
named  there  is  nothing  which  can  be  done  to  benefit  the  paralysis. 


GONORRHCEAL  INFECTION. 

There  are  still  some  roues,  and  ignorant  persons,  who  lie  under  the 
delusion,  at  one  time  prevalent,  that  an  attack  of  gonorrhoea  is  of  little 
more  gravity  "than  a  bad  cold."  A  considerable  number  of  both  classes 
learn  by  experience  sooner  or  later  that  this  is  a  most  mistaken  conception 
of  the  disease.  It  must  not  be  forgotten  that  within  the  last  few  years 
it  has  been  proved  again  and  again  that  the  gonococcus  may  find  entrance 
into  the  general  system  from  the  urethra  and  there  cause  the  most  disastrous 
consequences.  Further  than  this,  while  systemic  dissemination  of  the 
gonococcus  usually  is  secondary  to  venereal  infection,  it  is  to  be  remembered 
that  gonococcal  inflammation  of  any  susceptible  mucosa,  as  the  conjunctiva, 
may  afford  a  point  of  entrance.  Heimann  has  reported  a  case  of  gonococ- 
csemia  in  which  he  thinks  infection  occurred  through  a  wound,  and  Kimball 
believes  the  mouth  or  upper  air-passages  may  constitute  portals  of  entry.  He 
has  also  reported  a  series  of  cases  of  gonorrhoeal  pycemia  due  to  vulvo- 
vaginitis in  children,  some  cases  being  only  three  months  old.  If  it  gains 
access  to  the  joints,  it  may  not  only  produce  a  temporary  gonorrhoeal 
arthritis,  but  it  may  also  cause  a  chronic  arthritis  which  is  usually  mul- 
tiple, and  sometimes  is  so  widespread  that  the  patient  is  crippled  hand 
and  foot,  finger  and  toe,  for  the  balance  of  his  life,  the  incapacity  of  the 
patient  being  even  greater  and  more  rapid  in  its  onset  than  if  he  were 
suffering  from  rheumatoid  arthritis. 

Symptoms. — ^The  appearance  of  a  joint  suffering  from  gonorrhoeal  inflam- 
mation does  not  differ  materially  from  that  of  acute  rheumatic  fever.  It 
is  swollen  and  exquisitely  tender.  The  skin  about  the  joint  is  hot,  but 
often  it  is  not  much  reddened;  on  the  contrary,  in  some  cases  it  presents 
a  peculiar  leaden  hue.  The  temperature  of  the  body  in  general  is  usually 
normal,  but  there  is  often,  at  the  time  of  onset,  some  fever.  In  some  cases 
there  is  a  notable  serous  para-arthritis. 

Gonorrha;al  arthritis,  as  a  rule,  attacks  the  large  joints.  It  is  most 
commonly  multiple,  but  it  may  be  single.  I  have  seen  not  only  all  the 
large,  but  the  small  joints  infected  simultaneously.  Even  the  sacroiliac, 
maxillary,  and  sternoclavicular  joints  may  be  involved.  This  is  a  note- 
worthy point  when  we  remember  that  infection  of  the  maxillary  joint  almost 
never  occurs  in  ordinary  rheumatism. 

According  to  French  statistics  the  knees  are  attacked  more  frequently 
than  any  other  joint  in  the  body — 83  times  out  of  119  cases;  the  ankle 
32  times,  fingers  and  toes  23  times,  the  hips  16  times,  the  wrist  14,  the 
shoulder  12,  and  the  elbow  11. 

It  must  be  distinctly  understood  that  gonorrhoeal  arthritis  has  no  relation 
whatever  to  acute  articular  rheumatism.  The  tendency  on  the  part  of 
many  physicians  to  call  all  swellings  of  joints  rheumatism  is  to  be  deplored. 


GONORRH(EAL  INFECTION  187 

The  mere  presence  of  heat,  swelHng,  and  pain  in  a  joint,  with  or  without 
fever,  does  not  necessarily  indicate  that  rheumatism  is  the  cause. 

Suppuration  of  a  joint  as  a  result  of  gonorrhoeal  infection  very  rarely 
occurs,  but  ankylosis,  due  to  thickening  of  the  synovial  membranes,  liga- 
ments, and  periarticular  tissues,  and  atrophic  changes  in  the  cartilages  and 
in  the  ends  of  the  bone  are  met  with.  In  other  words,  gonorrhoeal  infection 
of  a  joint  may  result  in  fibrous  ankylosis  or  in  atrophy  or  in  overgrowth 
of  bony  tissue,  as  in  rheumatoid  arthritis. 

The  fascia  in  different  portions  of  the  body  may  also  be  infected.  This 
is  particularly  apt  to  occur  in  the  plantar  region  and  not  infrequently  stiffen- 
ing and  inflammation  of  the  tendo  Achillis  is  met  with.  - 

A  second  serious  consequence  of  gonorrhoeal  infection  is  the  development 
of  a  gonorrhoeal  endocarditis.  As  long  ago  as  1854  Brandes  recorded  two 
cases  of  gonorrhoea  with  arthritis  and  endocarditis,  and  in  1862  Traube 
reported  another  of  gonorrhoeal  endocarditis  without  joint  infection.  None 
of  these  cases  were  proved  to  be  due  to  the  gonococcus  because  this  organism 
was  not  known  at  that  time,  but  in  1893  Leyden  proved  the  presence  of 
the  gonococcus  in  the  heart.  Since  then  many  more  cases  have  been  reported 
in  which  the  gonococcus  has  been  isolated  from  the  endocardium  or  the 
circulating  blood.  Perhaps  the  most  noteworthy  paper  was  that  of  Thayer 
and  Lazear  in  1899. 

There  is  no  special  time  in  the  course  of  the  attack  of  gonorrhoea  at 
which  the  endocardial  involvement  takes  place.  Occasionally  it  has  come 
in  the  stage  of  onset,  but  in  most  cases  it  occurs  at  about  the  fifth  week. 
In  others  it  is  postponed  for  weeks,  or  even  for  months.  In  a  case  reported 
by  Finley  and  McCrae  a  fatal  endocarditis  developed  nine  months  after 
the  onset  of  the  urethral  discharge,  and  when  that  discharge  was  no  longer 
present,  although  a  microscopic  examination  of  the  urethral  mucosa  revealed 
gonococci. 

While  it  is  true  that  these  cases  are  comparatively  rare  when  we  consider 
the  frequency  of  gonorrhoea,  it  is  probable  that  they  occur  with  more  fre- 
quency than  has  been  generally  thought,  and  it  is  a  noteworthy  fact  that 
in  those  cases  in  which  the  physician  is  skilful  enough  to  examine  the  blood, 
or  the  endocardium,  for  the  gonococcus,  that  it  is  found  as  a  pathogenic 
micro-organism  much  more  frequently  than  in  those  cases  in  which  the 
physician  does  not  possess  such  pathological  training.  With  improvements 
in  technique,  general  gonorrhoeal  infection  will  probably  be  recognized  as 
being  by  no  means  as  infrequent  as  it  has  been  thought  in  the  past. 

Males  are  very  much  more  frequently  affected  by  systemic  infection  of 
this  character  than  are  women. 

Systemic  gonorrhoeal  infection  follows  not  only  the  primary  disease  in  the 
urethra  or  vagina,  but  has  been  met  with  in  infants  suffering  from 
ophthalmia  neonatorum  due  to  the  gonococcus.  In  some  cases  the  infec- 
tion is  pure;  in  others  it  is  mixed. 

Diagnosis. — The  statement  of  a  patient  suffering  from  an  acute  arthritis, 
acute  ophthalmia,  or,  indeed,  an  acute  endocarditis,  that  he,  or  she,  is 
also  suffering  from  gonorrhoea  will  do  much  toward  making  the  diagnosis 
of  the  condition  clear.    But  in  the  majority  of  instances  the  patient  neglects 


188  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

to  give  this  important  information,  and  in  a  considerable  number  of  cases 
denies  gonorrhoea!  infection  of  the  genitaha,  thinking  that  it  can  have  no 
bearing  upon  the  inflammations  elsewhere,  and  that  therefore  it  is  unneces- 
sary to  mention  the  fact  that  such  a  local  infection  exists.  Not  rarely  patients 
will  deny  the  existence  of  a  local  genital  lesion,  and  it  can  only  be  discovered 
upon  careful  examination.  It  may  be  necessary  in  some  cases  to  examine 
the  secretions  of  the  urethra  or  the  vagina  by  staining  and  by  the  microscope. 

It  may  be  said  that  in  every  male  suffering  from  acute  arthritis  between 
the  ages  of  fifteen  and  sixty  the  possibility  of  gonorrhoeal  infection  should 
be  considered  as  having  almost  equal  rank  with  the  possibility  of  acute 
articular  rheumatism,  and  the  development  of  endocarditis  should  not  be 
considered  as  indicative  of  one  condition  more  than  the  other,  although 
as  a  matter  of  fact  endocarditis  is,  of  course,  infinitely  more  common  in  true 
articular  rheumatism  than  it  is  in  gonorrhoeal  infection.  On  the  other 
hand  the  mere  discovery  by  the  physician  of  a  presence  of  a  purulent  dis- 
charge from  the  urethra  does  not  by  any  means  prove  that  the  patient  has 
gonorrhoeal  arthritis.  It  is  entirely  possible  for  him  to  have  acute  articular 
rheumatism  and  gonorrhoea,  and,  again,  it  sometimes  happens  that  gouty 
persons  have  a  purulent  discharge  from  the  urethra  which  does  not  depend 
upon  the  gonococcus.  Rarely,  too,  a  purulent  urethral  discharge  is  found, 
in  persons  who  are  not  gouty,  which  does  not  depend  upon  the  gonococcus, 
but  is  due  to  another  form  of  infection. 

A  therapeutic  test  of  some  value  lies  in  the  fact  that  full  doses  of  the 
salicylates  usually  cause  remarkable  improvement  in  the  arthritis  of  rheu- 
matism, and  affect  in  no  way  whatever  the  arthritis  of  gonorrhoea.  Again, 
it  is  characteristic  of  true  rheumatism  to  leave  one  joint  as  it  affects 
another;  whereas,  in  gonorrhoeal  rheumatism  it  is  rare  for  the  inflammation 
to  diminish  in  the  joint  primarily  affected  when  other  joints  become  involved. 

Prognosis. — The  prognosis  in  gonorrhoeal  rheumatism  is  favorable  in  the 
majority  of  instances,  provided  the  infection  is  not  very  severe,  and  is  not 
persistent.  The  physician,  however,  must  be  most  guarded  in  expressing 
an  opinion  as  to  ultimate  complete  recovery,  for,  as  already  stated,  some  of 
the  severest  cases  of  chronic  multiple  arthritis  are  met  with  as  the  result 
of  this  infection  of  the  joints.  The  prognosis  is  also  influenced  to  some 
extent  by  the  history  of  the  patient.  If  he  has  already  suffered  from  previous 
attacks  of  gonorrhoeal  arthritis,  the  probability  of  complete  recovery  is  not 
as  good  as  in  primary  attacks. 

Endocarditis  due  to  gonorrhoeal  rheumatism  is  a  very  serious  condition 
and  often  results  in  death. 

Treatment. — The  treatment  of  gonorrhoeal  arthritis  consists,  first,  in  the 
cure  of  the  local  area  of  primary  infection  as  rapidly  as  possible.  For  this 
purpose  the  ordinary  forms  of  treatment  for  gonorrhoea  are  to  be  followed. 
The  arthritis  is  to  be  relieved  by  the  use  of  a  splint  and  by  the  application 
of  a  50  per  cent,  ichthyol  ointment  to  the  joint.  If  the  inflammation  is 
exceedingly  acute  an  ice-bag  may  be  employed,  and  if  the  effusion  is  con- 
siderable aspiration  may  be  needed  to  relieve  pressure.  In  some  instances 
the  best  results  are  obtained  by  opening  the  joint  and  permitting  free 
drainage.     Should  the  physician  place  the  limb  of  the  patient  suffering 


ERYSIPELAS  189 

from  gonorrhoeal  arthritis  upon  a  splint,  it  should  not  remain  so  fixed 
for  any  length  of  time,  as  ankylosis  is  particularly  prone  to  ensue.  The 
splint  is  used  only  for  the  relief  of  pain  in  the  acute  inflammatory 
stages. 

As  already  stated,  the  salicylates  are  useless  in  gonorrhoeal  arthritis. 
Indeed,  they  are  worse  than  useless  in  that  they  in  no  way  influence  the 
infection  and  they  are  apt  to  disorder  the  stomach.  Rest  in  the  acute 
stages  and  the  treatment  of  the  local  infection  is  the  most  that  can  be 
done  for  the  patient  aside  from  local  applications.  Later,  passive  move- 
ments of  the  joints  and  the  use  of  the  iodides  or  of  the  syrup  of  the 
iodide  of  iron,  if  anaemia  is  also  present,  must  be  resorted  to.  Endocar- 
ditis is  to  be  treated  as  is  ordinary  ulcerative  endocarditis. 


ERYSIPELAS. 

Definition. — Erysipelas  is  an  acute  infectious  disease  due  to  the  entrance 
into  the  skin  in  its  deeper  layers  of  the  Streptococcus  pyogenes,  sometimes 
called  the  Streptococcus  erysipelatis .  The  skin  of  the  part  afi^ected  becomes 
dusky,  red,  and  swollen.  A  peculiarity  of  the  area  of  redness  is  that  it  has 
a  sharp  line  of  demarcation  separating  it  from  the  surrounding  healthy 
tissue,  which  is  usually  of  its  natural  color  and  appearance.  The  line  of 
demarcation  cannot  only  be  seen  but  can  be  felt  by  the  finger-tip,  and  if  the 
affected  area  be  punctured  and  the  serum  which  then  exudes  stained  with 
methylene  blue  the  chains  of  streptococci  can  readily  be  found  under  the 
microscope.    Erysipelas  is  sometimes  called  "St.  Anthony's  Fire." 

Frequency. — Erysipelas  is  found  in  nearly  all  parts  of  the  world  and  is 
not  infrequently  present  in  epidemic  form  in  hospitals  and  other  institutions 
in  which  large  numbers  of  persons,  with  impaired  health,  are  together  in 
wards  and  dormitories.  Under  these  conditions  it  spreads  rapidly  from 
patient  to  patient,  particularly  if  wounds  afford  an  entrance  into  the  body. 
For  this  reason  the  outbreak  of  the  disease  in  an  institution  shoukl  be  fol- 
lowed by  the  immediate  isolation  of  the  patient  and  a  thorough  disinfection 
of  the  entire  ward  in  which  he  has  been  lying.  The  disease  occurs  most 
frequently  in  the  spring  months,  particularly  in  April,  but  is  met  with  at  all 
seasons  of  the  year. 

Etiology. — As  already  stated  the  cause  of  erysipelas  is  the  entrance  into 
the  deeper  layers  of  the  skin  of  the  streptococcus  in  a  form  which  cannot 
be  separated  from  that  which  sometimes  produces  purulent  infection  in 
other  parts  of  the  body.  The  anatomical  and  many  of  the  clinical  features 
of  this  disease  may  be  produced  by  several  closely  allied  bacteria,  but 
the  clinical  manifestations  of  erysipelas  are  so  constantly  associated  with 
the  Streptococcus  erysipelatis  that  the  different  infections  may  be  ignored 
or  grouped  with  this  one.  Two  additional  factors  are  nearly  always 
active  in  the  production  of  the  disease,  namely,  a  break  in  the  skin  or  in  a 
neighboring  mucous  membrane,  so  that  the  streptococcus  gains  access  to 
the  tissues,  and,  secondly,  some  cause,  local  or  general,  which  diminishes 
vital  resistance  to  such  a  degree  that  the  tissues  afford  a  favorable  site  for 


190  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

the  growth  of  the  micro-organism.  Thus  erysipelas  may  be  due  to  the 
infection  of  a  small  pimple,  by  scratching  it  with  the  finger-nail,  and  it  is 
not  uncommonly  met  with  in  those  who  are  suffering  from  renal  disease, 
from  diabetes,  from  alcoholism,  or  from  some  condition  which  distinctly 
decreases  the  ability  of  the  body  to  protect  itself  from  infection. 

Sometimes  the  resisting  power  is  decreased  by  local  causes,  as  by  exposure 
to  great  cold,  but  it  is  very  doubtful  if  this  cause  alone,  with  the  presence 
of  the  streptococcus,  is  capable  of  causing  the  disease  unless  the  general 
systemic  vital  resistance  is  impaired. 

The  course  to  be  followed  in  cases  of  early  erysipelas  is  to  examine 
into  the  state  of  the  urine  at  once,  and,  even  if  this  be  found  normal,  to 
examine  it  repeatedly  for  evidences  of  renal  disease  or  diabetes,  since  such 
causes  render  the  patient  very  susceptible.  Search  for  other  causes  of 
impaired  health  should  also  be  made,  because  erysipelas  is  a  malady 
which  is  particularly  prone  to  attack  those  who  are  already  ill,  even  if  the 
primary  illness  is  not  apparent.  Occasionally  the  physician  meets  with  a 
case  in  which  there  is  no  underlying  dyscrasia  which  predisposes  to  the 
disease.  In  these  instances  the  patient  may  have  repeated  attacks,  due 
apparently  to  general  susceptibility  to  this  infection,  the  streptococci 
remaining  inactive  in  the  tissues  in  certain  cases  for  weeks  at  a  time. 
Women  during  the  puerperal  period  are  especially  susceptible  to  the  infection. 

Pathology  and  Morbid  Anatomy. — Primarily  the  lesion  of  erysipelas  con- 
sists of  a  hyperemia ;  later,  an  exudate  composed  of  cells  and  fluid  appears 
in  the  layers  of  the  true  skin,  associated  with  a  rapid  growth  of  the  strep- 
tococcus in  the  lymph  spaces  in  the  margin  of  and  often  beyond  the  inflam- 
matory zone.  In  severe  cases  the  lesion  spreads  with  great  rapidity  and  may 
affect  not  only  the  deeper  layers  of  the  skin,  but  the  underlying  connective 
tissue  as  well.  The  destructive  action  of  the  bacterial  toxin  may  lead  to  the 
formation  of  sloughs,  gangrenous  erysipelas,  or  the  polymorphonuclear 
leukocytes  may  accumulate  in  such  numbers  as  to  constitute  pus,  forming  the 
so-called  phlegmonous  erysipelas.  In  rare  instances  the  streptococcus,  after 
entering  the  body  through  some  solution  of  continuity  in  the  skin  or  mucous 
membrane,  is  carried  by  the  blood  or  lymphatic  system  to  distant  parts, 
causing  a  development  of  the  disease  far  from  the  site  of  the  primary  lesion. 

The  accompanying  visceral  lesions  may  be  due  to  the  absorbed  toxin  or 
to  streptococcsemia.  The  former  may  cause  degenerative  changes,  such  as 
focal,  or  even  diffuse,  necrosis  in  the  liver,  spleen,  kidneys,  or  myocardium. 
The  entrance  of  the  streptococcus  into  the  blood  may  be  manifested  in  an 
endocarditis,  pericarditis,  nephritis,  pleuritis,  meningitis,  arthritis,  osseous 
or  pulmonary  infections,  or  other  evidences  of  colonization  of  the  germ  in 
the  various  organs  or  tissues. 

The  onset  of  erysipelas  is  associated  with  a  leukocytosis  of  polymor- 
phonuclear cells,  except  in  malignant  cases  in  devitalized  persons. 

Incubation. — The  period  between  the  introduction  of  the  streptococcus 
and  the  development  of  the  disease  varies  greatly  in  different  cases.  Usually 
the  period  of  incubation  lasts  from  three  to  seven  days. 

Symptoms. — In  the  great  majority  of  cases  erysipelas  affects  the  skin  of 
the  face  about  the  corners  of  the  nose  or  near  the  ear.    A  tingling  of  the 


ERYSIPELAS  191 

skin  is  felt  which  speedily  becomes  an  intense  burning,  and  is  increased 
by  rubbing  or  scratching  the  part.  This  reddened  area  spreads  rapidly 
and  is  characterized  at  the  end  of  twenty-four  hours,  or  before,  by  the  pres- 
ence of  a  shar^  line  of  demarcation,  which  marks  the  advancing  line  of 
inflammation,  a  margin  which  can  often  be  felt  as  a  slightly  indurated  and 
raised  edge.  Sometimes  the  inflammatory  process  projects  well-defined 
areas  of  extension  into  the  healthy  skin.  Palpation  of  the  diseased  skin 
also  reveals  the  fact  that  it  is  hot  and  somewhat  brawny  and  tender.  The 
color  of  the  part  is  not  a  bright  red,  but  is  dusky  in  hue.  The  swelling  of  the 
face  when  well  developed  is  sufficient  to  render  the  patient  unrecognizable, 
and  the  eye,  or  eyes,  may  be  completely  closed  by  the  infiltration  of  the  eye- 
lids. The  ears  when  involved  become  swollen  to  an  extraordinary  degree 
and  the  skin  seems  very  tense  and  indurated.  Not  infrequently  blebs  or 
blisters  form  over  the  inflamed  area. 

After  the  early  stage  of  onset  it  has  been  my  experience  that  patients 
rarely  complain  very  greatly  of  pain  and  burning. 

The  amount  of  systemic  disturbance  varies  very  much  in  different  cases. 
In  those  who  have  previously  been  in  moderate  health  the  local  lesion  and  the 
degree  of  systemic  disturbance  may  be  so  slight  as  to  be  scarcely  noticeable. 
The  patient  may  complain  of  a  slight  chilliness,  the  pidse  may  be  slightly 
accelerated,  and  the  temperature  raised  one  or  two  degrees.  In  other 
cases  in  which  vital  resistance  is  poor  and  the  infecting  germ  virulent  in 
form,  the  symptoms  just  described  are  very  severe  in  degree,  so  that  rigors, 
high  fever,  a  rapid  pulse,  delirium,  and  great  prostration  may  be  present. 
In  still  other  cases,  not  so  common,  when  by  reason  of  great  diminution  of 
vital  powers  the  genei-al  health  has  been  greatly  undermined,  as  in  advanced 
diabetes  or  Bright's  disease,  the  disease  attacks  the  patient  so  vigorously 
that  he  sinks  beneath  its  onset  without  having  enough  stamina  to  resist  the 
infection,  and  may  pass  into  semi-coma  or  even  convulsions  followed  by 
collapse  due  to  the  apparent  exacerbation  of  the  underlying  malady  by  the 
secondary  infection.  In  rare  instances  the  part  involved  may  become 
gangrenous  and  death  follow  from  sepsis  and  exhaustion. 

In  cases  of  ordinary  severity  the  fever  lasts  about  five  days  and  ends 
by  crisis. 

One  attack  of  erysipelas  does  not  protect  but  rather  predisposes  the 
patient  to  another. 

Under  the  name  erysipelas  migrans  a  form  of  the  disease  is  met  with 
in  which  the  disease  spreads  from  part  to  part  and,  in  the  course  of  its 
wandering,  may  affect  successively  almost  the  entire  surface  of  the  body. 

Complications  and  Sequelae. — When  erysipelas  attacks  individuals  who 
are  greatly  impaired  in  health  the  results  are  often  grave,  not  only  because 
the  onset  of  erysipelas  is  dangerous  in  itself,  but  because  it  is  an  indication 
in  many  cases  of  a  grave  disease,  hitherto  unrecognized,  which  may 
speedily  cause  the  death  of  the  patient  by  an  exacerbation.  Thus  the  devel- 
opment of  erysipelas  in  cases  of  chronic  Bright's  disease  not  only  means 
that  the  renal  lesion  has  resulted  in  poor  resistance,  but  in  addition  the  task 
of  eliminating  the  toxins  of  the  new  malady  may  so  overwhelm  the  kidneys 
that  they  may  cease  to  perform  their  function. 


192  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Again  in  cases  of  greatly  impaired  health  the  inflammatory  process  goes 
on  to  suppuration  and  the  deeper  tissues  become  filled  with  pus,  forming 
the  phlegmonous  form  of  the  disease.  In  other  instances  septic  embolism 
occurs  in  the  lungs,  brain,  kidneys,  hver,  and  spleen. 

A  focus  of  erysipelatous  inflammation  also  results  sometimes  in  the  pro- 
duction of  ulcerative  endocarditis  or  even  purulent  pleuritis  or  pericarditis, 
but  these  complications  probably  are  of  less  common  occurrence  than  has 
been  thought.  In  1674  cases  of  erysipelas  collected  by  Anders  from  the 
records  of  five  large  hospitals  and  from  private  practice,  endocarditis 
occurred  only  once,  and  pericarditis  not  at  all.  Pleurisy  was  present  in 
seven  cases.  Roger,  of  Paris,  did  not  have  a  single  case  either  of  endo- 
carditis or  pericarditis  in  957  cases,  and  only  one  case  of  pleurisy. 

In  2631  cases  of  erysipelas  croupous  pneumonia  is  said  to  have  occurred 
in  17  cases,  and  the  catarrhal  form  in  2.  Of  these  cases  957  occurred  in  the 
practice  of  Roger,  of  Paris,  and  the  remaining  1674  were  collected  by  Anders, 
and  represent  chiefly  the  statistics  of  five  large  American  hospitals. 

Prognosis. — The  prognosis  in  a  case  of  erysipelas  depends  largely  upon 
the  general  state  of  the  patient.  As  already  stated  the  presence  of  grave 
visceral  disease,  as  of  the  liver  or  kidneys,  renders  it  very  dangerous,  but  in 
the  great  majority  of  cases,  when  it  occurs  in  otherwise  healthy  persons,  the 
outlook  is  very  favorable.  Anders'  statistics  give  the  mortality  at  7  per  cent, 
for  hospitals  and  4  per  cent,  for  private  practice.  When  it  recurs  frequently 
or  develops  in  different  parts  of  the  body  consecutively,  it  may  cause  death 
by  exhaustion,  but  in  nearly  all  these  cases  there  is  a  chronic  malady  as  a 
predisposing  cause. 

Treatment. — ^The  treatment  of  erysipelas  is  local  and  systemic.  If  the 
bowels  are  not  active  they  should  be  freely  moved  by  a  dose  of  2  grains  of 
calomel  followed  in  twelve  hours  by  a  saline  purge  such  as  a  Seidlitz  powder 
or  a  half-ounce  of  Rochelle  salts.  As  soon  as  the  bowels  have  been  evacuated 
thoroughly  the  patient  should  receive  10  minims  of  the  tincture  of  the 
chloride  of  iron,  well  diluted  with  pure  water,  every  three  or  four  hours,  or 
30  minims  four  times  a  day.  The  excess  of  water  protects  the  stomach 
from  being  disordered  by  the  drug  and  also  aids  in  flushing  the  kidneys, 
the  activity  of  which  prevents  the  accumulation  of  toxic  material  in  the  body. 
The  diet  should  be  as  easily  digested  and  as  nutritious  as  possible,  in  order 
that  the  vital  resistance  of  the  patient  may  be  maintained,  and  such  foods 
as  eggs,  rare  meats,  broths,  and  milk  should  be  freely  given  if  the  digestion 
of  the  patient  is  capable  of  dealing  with  them.  If  it  is  not,  the  food  should 
be  given  in  small  quantities  every  two  or  three  hours,  and  if  necessary  it 
should  be  predigested  by  a  peptonizing  tablet  or  powder 

The  local  treatment  is  a  very  important  factor  in  these  cases.  For  many 
years  I  have  used  with  excellent  results  an  ointment  of  equal  parts  of 
ichthyol  and  lanolin,  or  lard,  smeared  over  the  inflamed  area  and  the 
adjacent  skin,  and  kept  in  contact  with  the  skin  by  also  smearing  this 
salve  on  a  mask  of  gauze  or  lint  which  is  applied  to  the  part  so  that 
the  medicinal  effect  is  continuous.  By  this  means  the  pain  and  burning  is 
almost  entirely  relieved  and  a  very  definite  and  distinct  influence  for  good 
is  exercised  both  in  curing  the  inflammation  and  preventing  its  spread. 


SEPTICEMIA   AND  PYEMIA  193 

In  cases  in  which  the  general  systemic  state  is  very  much  impoverished 
and  the  vitahty  of  the  patient  is  impaired,  sufficient  quantities  of  a  good 
whiskey  or  brandy  should  be  given  to  sustain  the  flagging  powers.  Moderate 
doses  of  quinine  (about  3  grains  t.  i.  d.)  may  also  be  useful  at  this  time  to 
support  the  system,  but  large  doses  are  useless  and  produce  headache  and 
a  disordered  digestion  without  causing  any  benefit.  If  the  fever  is  excessive 
it  may  be  controlled  by  the  use  of  an  ice-cap  and  cold  sponging  with  friction. 
The  coal-tar  antipyretics  should  never  be  used,  as  they  decrease  vital 
resistance. 

SEPTIOiEMIA  AND  PY-ffiMIA. 

Definition  and  Etiology. — Septicsemia  and  pyaemia  are  terms  which  are 
dependent  upon  antiquated  ideas  of  septic  processes,  and  do  not  strictly 
represent  the  states  they  are  now  used  to  describe.  Septicaemia  originally 
meant  that  putrid  material  was  in  the  blood  and  pyaemia  that  the  blood 
contained  pus.  We  now  know  that  blood  infection  is  due  to  the  presence 
in  it  of  bacteria  (bacterisemia)  or  to  the  entrance  into  this  fluid  of  poisons 
made  by  micro-organisms  not  in  the  circulation  (toxaemia).  The  older 
terms  are  placed  at  the  head  of  this  article  because  they  are  still  commonly 
applied. 

Pyaemia,  as  it  is  understood  to-day,  is  that  state  in  which  bacteriaemia 
is  present  with  associated  septic  foci,  or,  in  other  words,  metastatic 
abscesses.  As  a  rule  these  abscesses  appear  chiefly  in  the  tissues  which  are 
not  far  removed  from  the  seat  of  primary  infection.  But  this  is  by  no  means 
always  true,  for  a  septic  process  in  the  foot  may  cause  metastatic  abscesses 
in  the  lungs,  kidneys,  or  liver. 

Cases  are  not  rarely  seen  in  which  the  patient  is  unable  to  give  any  history 
of  even  a  small  abscess  or  minute  break  in  the  skin  through  which  germs 
may  enter  the  circulation,  and  yet  a  diagnosis  of  septicaemia  or  pyaemia  may 
be  made  even  when  no  point  of  entry  can  be  found. 

The  obscurity  of  most  of  these  cases  depends  upon  our  inability  to  find 
the  portal  of  entry,  which  may  be  the  genito-urinary  organs,  the  facial  or 
cranial  sinuses,  the  middle  ear  or  mastoid,  the  mouth  or  pharynx,  possibly 
the  alimentary  canal,  the  biliary  passages  or  gall-bladder,  an  unrecognized 
appendicitis  or  other  point  of  slumbering  infection  which  may  or  may  not  be 
recognized  during  life  or  determined  with  certainty  even  at  a  postmortem 
examination. 

Pathology  and  Morbid  Anatomy. — The  results  of  septicaemia  are  not  seen 
in  equal  degree  in  all  cases.  In  some  they  may  be  so  slight  as  not  to  be 
readily  recognized,  except  by  careful  bacteriological  or  microscopic  exam- 
ination. In  other  instances  the  secondary  results  are  so  patent  that  the 
most  careless  observer  cannot  fail  to  be  impressed  by  their  character. 
Thus,  it  not  infrequently  is  found  that  septic  infection  is  the  cause  of  a 
severe  inflammatory  process  in  any  one  of  the  serous  membranes,  so  that 
pericarditis,  peritonitis,  meningitis,  or  pleuritis  may  occur.  Septic  inflam- 
mation of  these  parts  results  either  in  a  distinctly  fibrinous  or  serofibrinous 
exudate  or  in  one  which  is  purulent.  The  synovial  membranes  and  other 
13 


194  DISEASES  DUE   TO   A   SPECIFIC  INFECTION 

connective  tissues  of    the   joints  are  frequently  infected,   so   that  septic 
arthritis  develops. 

Examination  of  the  veins  may  reveal  thrombi  near  or  remote  from  the 
primary  seat  of  infection,  and  these  thrombi  may  be  soft  and  even  purulent. 
It  is  important  that  a  clear  distinction  be  made  between  simple  or  bland 
thrombi  and  septic  thrombi.  Emboli  of  the  former  type  cause  infarction 
when  they  plug  terminal  vessels  and  mechanically  disturb  the  circulation, 
whereas  septic  emboli  not  only  plug  the  vessel  and  so  disturb  blood  supply, 
but  as  they  contain  bacteria  they  constitute  new  foci  of  infection. 

Very  intimately  associated  with  the  subject  of  septicemia  and  pyaemia, 
so  called,  are  the  subjects  of  vital  resistance  and  terminal  infection.  By 
vital  resistance  is  meant  that  power,  or  property,  possessed  by  the  living 
body  of  protecting  itself  from  the  various  micro-organisms  which  are  con- 
tinually gaining  access  to  the  system.  This  power  lies  largely  in  the  ability 
of  the  blood  to  exercise  its  so-called  bacteriolytic,  or  bacteria-destroying, 
power,  and  to  the  ability  of  the  cells  of  the  body  to  destroy  invading  micro- 
organisms by  phagocytosis,  and  manufacture  certain  other  antibodies  by 
the  action  of  which  bacterial  toxins  may  be  antagonized,  neutralized,  or 
rendered  inert.  A  number  of  valuable  papers  on  the  presence  of  bacteria 
in  the  blood  have  been  published  within  recent  years  (see  Rosenberger  in 
the  American  Journal  of  the  Medical  Sciences,  January  to  July,  1903,  for 
facts  and  references).  When,  because  of  diminution  of  vital  resistance  the 
invading  pathogenic  micro-organisms  obtain  a  foothold  and  multiply,  we 
have  developed  an  infection.  When  a  patient  suffers  from  some  malady 
which  saps  his  vitaUty  and  so  causes  the  approach  of  death,  even  in  a 
remote  degree,  these  micro-organisms  at  once  attack  his  debilitated  body, 
and  the  patient  now  suffers  from  what  is  called  a  "terminal  infection." 
Very  commonly  this  terminal  infection  is  the  actual  cause  of  death,  so  that 
it  has  been  well  said  that  death  is  "rarely  due  to  the  primary  cause  of  the 
illness." 

Symptoms. — The  symptoms  of  septic  infection  vary  greatly  with  the  par- 
ticular organs  which  may  be  the  seat  of  the  primary  or  secondary  lesions. 
The  manner  of  their  onset  varies  likewise.  In  some  instances  the  earliest 
manifestations  consist  in  a  rigor  or  chill,  more  or  less  severe,  followed  by 
fever^  which  varies  in  its  degree  with  the  severity  of  the  infection  and  the 
vitality  of  the  patient.  The  chill  and  fever  are  followed  usually  by  a  period 
of  normal,  or  nearly  normal,  temperature,  and  this  is  again  followed  by 
chill  and  fever.  In  this  way  the  dominant  symptoms  of  the  case  may  closely 
resemble  the  quotidian  malarial  infection,  a  resemblance  which  is  still 
further  emphasized  by  the  frequent  occurrence  of  a  distinct  siveat  as  the 
fever  falls.    These  sweats  may  be  very  profuse. 

Not  rarely  the  pus  in  the  primary  focus  of  infection  changes  its  char- 
acter, and  becomes  less  healthy  looking.  It  is  thinner  and  more  ichorous, 
that  is,  to  use  a  word  now  rarely  heard,  it  is  no  longer  "laudable  pus." 
The  infection  causes  general  malaise,  rapid  loss  of  weight  and  loss  of  appetite 
with  gastric  distress  and  perhaps  vomiting.  Anwmia  is  rapidly  developed, 
the  skin  of  the  hands  and  face  becomes  not  only  pallid  but  develops  a 
peculiar  cadaveric  hue,  an  appearance  difficult  to  describe,  but  alluded  to 


SEPTICMMIA   AND   PY.EMIA  195 

by  those  of  experience  as  the  "septic  facies."  Sometimes  the  skin  may  be 
shghtly  jaundiced. 

If  the  septic  process  develops  secondarily  in  any  special  organ,  localized 
symptoms  may  at  once  appear,  but  it  is  noteworthy  that  they  do  not  always 
ensue.  Severe  pain  in  the  chest  may  betoken  the  presence  of  a  septic  pleurisy 
or  pneumonia,  or  if  the  pain  develops  in  the  left  side  it  is  often  due  to 
septic  infarction  of  the  spleen.  A  physicial  examination  of  these  organs 
may  reveal  the  typical  signs  of  these  affections. 

As  the  case  progresses  pr.lmcnary  abscess,  empyema,  or  suppuration  of 
the  kidney  follows  as  the  result  of  emboli  in  these  organs.  The  pulse 
becomes  more  and  more  rapid,  the  general  state  more  and  m.ore  feeble, 
and  the  patient  dies  from  general  asthenia  or  from  one  of  the  acute 
complications  just  named. 

There  are  other  cases  in  which  the  onset  of  the  systemic  infection  is  not 
so  pronounced,  the  chill,  fever,  and  sweat  being  absent,  but  in  their  place 
a  rapid  extension  of  the  local  inflammatory  process  with  the  absorption  into 
the  general  system  of  the  poisonous  products  of  the  germ  growth  as  well  as 
the  organisms  themselves.  In  such  cases  the  patient  may  speedily  become 
not  only  feeble,  but  suffer  from  stupor  and  finally  die  unconscious  within 
a  few  days  of  the  beginning  of  the  illness.  These  cases  are  usually  those 
which,  suffering  from  nephritis  or  diabetes,  offer  no  vital  resistance  to 
infection,  and  die  not  only  from  this  cause  but  by  reason  of  rapidly  increas- 
ing evidences  of  the  primary  disease  as  well. 

Still  a  third  class  of  cases  may  be  called  subacute  or  chronic,  and  last  for 
weeks.  Not  rarely  these  cases  tax  the  diagnostic  acumen  of  the  physician 
to  the  utmost.  A  child  was  brought  to  me  in  July  with  the  statement  that 
in  the  previous  March  she  had  acute  articular  rheumatism,  but  no  cardiac 
complications.  The  fever  of  the  disease  in  onset  had  lasted  but  a  short 
time,  and  in  its  place  only  a  slight  evening  rise  of  temperature  took  place. 
The  acute  swelling  of  the  joints  disappeared,  but  they  remained  tender, 
and  the  child  was  unable  to  walk.  There  was  marked  pallor,  a  septic  hue 
of  the  skin,  and  a  large  boil  on  the  buttock  with  smaller  ones  on  other  parts 
of  the  body.  Occasional  attacks  of  vomiting  occurred.  A  diagnosis  of 
chronic  septic  infection  was  made,  and  on  the  child's  death  six  weeks  after 
evidences  of  the  correctness  of  this  view  were  found  in  nearly  every  organ 
of  the  body,  although  in  none  of  them  were  distinct  purulent  foci  discovered. 
Circumstances  prevented  bacteriological  examination  of  the  blood  either 
before  or  after  death. 

Diagnosis. — The  presence  of  chill,  fever,  and  sweat  in  any  case  should 
recall  the  fact  that  these  symptoms  may  be  due  to  sepsis  as  well  as  to  other 
forms  of  infection.  It  must  be  recalled  that  a  history  of  an  infected  wound 
is  not  needful  to  reach  the  conclusion  that  infection  has  occurred,  for  it 
may  take  place  by  a  needle-prick,  or  through  a  small  blister  due  to  a  badly 
fitting  shoe,  or  through  a  break  in  the  mucous  membrane  of  the  alimentary, 
respiratory,  or  genito-urinary  tract.  Typhoid  fever  often  fails  to  cause  death 
of  itself,  but  a  terminal  septic  infection  following  it  may  cause  death.  In 
other  cases  a  fatal  general  infection  follows  gonorrhoea,  and  in  tubercu- 
losis of  the  lungs  the  septic  symptoms  are  due  to  the  pyogenic  organisms 


196  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

which  are  associated  with  the  tubercle  bacilhis,  rather  than  to  that  organism 
itself.  So,  too,  gallstones  with  septic  infection  of  the  gall-bladder  may 
afford  the  opening  for  infection.  Finally,  whenever  a  patient  presents 
acute  arthritis  the  physician  should  think  first  of  sepsis  rather  than  rheu- 
matism, and  when  he  has  a  chill,  fever,  and  sweat  which  does  not  promptly 
yield  to  quinine,  he  should  also  think  of  sepsis  or  tuberculosis. 

Treatment. — The  treatment  of  these  states  consists  first  in  seeking  and 
removing  the  cause  and  in  the  support  of  the  vitality  of  the  patient  by  every 
possible  means,  such  as  fresh  air  and  sunshine,  and  good  food  which  is 
easily  digested  and  absorbed.  Second,  many  cases  are  undouljtedly  aided 
in  combating  infection  by  the  use  of  tonic  doses  (5  grains  t.  i.  d.)  of  cjuinine, 
with  or  without  whiskey.  In  some  instances  well-diluted  whiskey  certainly 
seems  to  benefit  the  patient,  and  it  is  surprising  how  much  can  be  taken 
without  producing  any  signs  of  intoxication.  Great  care  that  doses  large 
enough  to  be  toxic  are  not  given,  for  if  they  are,  the  toxaemia  of  alcohol  aids 
the  toxsemia  of  the  infection.  Full  doses  of  tincture  of  the  chloride  of  iron 
are  valuable.  The  coal-tar  products  are  never  to  be  used,  as  they  decrease 
vital  resistance,  increase  sweating,  and  do  not  give  any  comfort  or  relief. 

If  abscesses  form  they  should  be  opened  and  drained  as  early  as  possible. 

When  bacteriological  tests  reveal  the  presence  of  streptococci  as  the 
cause  of  the  trouble,  antistreptococcus  serum  should  be  used. 


ACUTE  RHEUMATIC  FEVER. 

Definition.— This  disease,  also  known  under  the  name  of  acute  articular 
rheumatism,  or  acute  inflammatory  rheumatism,  is  an  acute  infectious,  non- 
contagious, febrile  malady  characterized  by  acute  inflammation  of  the  syno- 
vial membranes  and  adjacent  tissues  about  the  joints  of  the  extremities. 
It  is  to  be  distinctly  separated  from  the  various  forms  of  septic  arthritis. 

Distribution. — Acute  articular  rheumatism  is  a  disease  which  is  found 
chiefly  in  the  temperate  zone  and  rarely  occurs  in  the  tropics  or  in  the 
far  North.  At  present  we  lack  reliable  statistics  concerning  its  frequency 
because  in  many  countries  its  occurrence  is  not  reported,  and  in  those 
in  which  records  of  the  frequency  of  rheumatism  are  preserved,  so  many 
cases  are  reported  which  are  not  true  acute  articular  rheumatism  that  the 
statistics  are  valueless.  Osier  states  that  he  saw  more  cases  in  IMontreal 
than  in  Philadelphia  and  Baltimore  while  connected  with  hospitals  in  those 
cities.  I  was  firmly  convinced  from  my  experience  in  English  hospitals 
that  the  disease  was  more  prevalent  in  England  than  in  the  United  States,  but 
when  I  came  to  the  study  of  the  statistics  of  the  relative  frequency  of  acute 
rheumatism  in  these  two  countries,  I  found  that  out  of  74,S0S  medical  cases 
in  hospitals  in  London,  there  were  3822  cases  of  acute  rheumatism,  a  per- 
centage of  5.1,  and  out  of  73,839  medical  cases  in  hospitals  in  different 
cities  in  the  United  States,  there  were  4153  cases  of  acute  rheumatism,  a 
percentage  of  5.6.  It  would  seem,  therefore,  that  no  marked  difference  in 
frequency  exists  in  these  parts  of  the  world. 


ACUTE  RHEUMATIC  FEVER 


197 


Etiology. — The  influence  of  season  upon  the  occurrence  of  the  disease  is 
marked.  It  is  more  common  in  the  cool,  damp  months  of  the  year  than  at 
other  times.  In  London  its  greatest  prevalence  is  in  September  and  October, 
whereas  in  Montreal  it  is  most  frequent  in  March  and  April. 

The  influence  of  age  upon  the  frequency  of  the  disease  is  notable.  It 
is  met  with  in  a  very  large  proportion  of  the  cases  between  twenty  and 


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Chart  showing  age  incidence  of  acute  articular  rheumatism,  based  on  4328  cases. 

ihirty-five  years  of  age  and  is  very  rare  in  children  below  five  years.  After 
forty-five  years  it  is  also  rarely  met  with,  comparatively  speaking  (Fig.  38). 
It  must  be  remembered,  however,  that  infection  with  the  specific  organism 
of  this  disease  is  probably  more  frequent  in  adolescents  than  is  commonly 
supposed,  and  it  may  cause  very  mild  arthritic  symptoms  and  yet  make 
a  serious  attack  upon  the  heart. 


198  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Males  are  more  frequently  affected  than  females,  but  this  proportion  is 
reversed  when  the  patient  is  under  twenty  years  of  age,  at  which  time 
females  suffer  more  frequently. 

The  question  of  the  influence  of  heredity  is  still  undecided.  It  is 
probable  that  it  plays  a  very  unimportant  part  in  the  causation  of  the 
malady. 

Of  the  immediate  etiological  factors  we  must  include  exposure  to  damp- 
ness and  cold.  These  influences  are  not  provocative  of  the  disease  unless 
the  specific  micro-organism  is  present,  nor  unless  the  exposure  reduces  the 
vital  resistance  of  the  joints  so  that  the  specific  organism  is  enabled  to 
multiply  and  induce  its  pathological  effects. 

Acute  rheumatic  fever  is  a  disease  which  is  endemic,  but  it  has  periods 
in  which  it  is  distinctly  epidemic.  In  other  words,  it  is  much  more  frequent 
in  some  years  than  in  others. 

There  can  be  no  doubt  that  the  infection  usually  gains  access  to  the 
general  system  through  the  tonsils. 

The  old  theory  of  acute  rheumatism  being  due  to  uric  acid  is  now 
exploded.  The  excess  of  uric  acid  present  in  the  urine  in  this  disease 
is  the  result,  not  the  cause,  of  the  affection. 

Bacteriology. — A  very  large  number  of  investigators  have  endeavored  to 
isolate  the  specific  micro-organism  of  this  disease,  but  until  recently  no  satis- 
factory proof  that  this  had  been  accomplished  was  forthcoming.  About  fifteen 
years  ago  Achalme  asserted  that  he  had  done  this,  and  later  Triboulet  and 
Wassermann  made  similar  claims.  Up  to  the  present  time  it  would  appear 
that  Poynton  and  Paine  have  come  nearer  to  success  in  this  line  of  research 
than  any  of  their  predecessors,  and  Meyer  has  also  carried  out  studies  which 
seem  to  prove  the  correctness  of  their  conclusions.  Still  more  recently 
Walker  and  Beaton  have  further  confirmed  the  correctness  of  the  views  of 
Poynton  and  Paine.  These  last  investigators  believe  it  is  impossible  to 
separate  this  special  organism,  for  which  they  advise  the  name  Micrococcus 
rheumaticus,  from  the  ordinary  streptococcus.  Meyer  succeeded  in  obtaining 
it  in  a  form  which  produced  all  the  lesions  found  in  the  course  of  the  disease, 
and  found  the  same  organism  in  the  sore  throat,  in  the  inflamed  endocardium, 
in  the  pleura,  and  in  the  inflamed  joints  of  persons  attacked  by  this  malady. 
More  recently  still  Poynton  has  further  enforced  his  views.  The  most 
that  we  can  say  at  present  is  that  acute  articular  rheumatism  appears  to 
be  a  streptococcic  infection.  Until,  however,  the  supposed  exciting  cause 
can  with  certainty  be  differentiated  from  the  streptococcus  found  in  other 
lesions,  the  propriety  of  giving  to  it  a  special  name  must  be  regarded  as 
doubtful. 

It  is  a  fact  worthy  of  note  that  the  introduction  of  many  pathogenic 
micro-organisms  into  the  body  will  result  in  endocarditis  and  arthritis,  but 
these  states  are  not  true  acute  articular  rheumatism. 

Morbid  Anatomy. — The  changes  produced  by  an  attack  of  acute  rheumatic 
fever  are  not  pathognomonic.  On  the  contrary,  the  condition  of  the  synovial 
membranes  is  one  of  more  or  less  intense  hypersemia  with  the  effusion  of 
fluid  into  the  surrounding  tissues  and  into  the  joint  itself.  The  synovial 
liquid  is  turbid  and  contains  leukocytes  and  some  small  flakes  of  fibrin. 


ACUTE  RHEUMATIC  FEVER  199 

The  secondary  changes  produced  by  the  disease  are  vegetative  endocarditis, 
acute  pleuritis,  and  pericarditis,  but  there  is  nothing  about  these  lesions 
which  is  pecuhar  to  this  specific  infection.     (See  Endocarditis.) 

Symptoms. — The  symptoms  of  acute  articular  rheumatism  are  usually 
sudden  in  onset.  With  or  without  premonitory  signs  of  illness  the  patient 
awakes  to  find  that  one  or  more  of  his  larger  joints  is  acutely  inflamed 
so  that  any  movement  causes  great  pain,  and  the  part  may  be  so  sensitive 
to  the  touch  as  to  prevent  any  thorough  examination  by  palpation  being 
made. 

The  skin  over  the  affected  part  is  usually  dusky  red  in  hue,  and  quite 
puffy  in  appearance  because  of  the  presence  of  subcutaneous  exudation,  and 
the  inflamed  area  is  much  more  hot  to  the  touch  than  adjacent  tissues. 
Sometimes,  however,  no  local  redness  is  seen,  but  in  its  place  swelling  and 
a  peculiar  sodden  and  hvid  hue  of  the  skin.  With  the  development  of  this 
arthritis  a  distinct  febrile  movement  begins,  and  the  fever  may  reach  102° 
or  103°  on  the  first  day  in  many  cases.  This  level  of  temperature  is  not 
usually  exceeded,  but  the  variations  in  its  course  are  very  marked  in  that 
it  is  subject  to  great  remissions,  particularly  if  the  sweating  is  profuse. 
The  fever  ultimately  falls  by  lysis. 

The  tongue  is  coated,  the  bowels  are  usually  confined,  and  the  skin  is 
hot  and  dry,  or  at  times  bathed  in  a  profuse  sweat.  This  sweat  breaks  out 
in  paroxysms  and  is  exceedingly  acid,  possessing  a  peculiar  acid  odor.  It 
is  probably  an  effect  at  elimination,  but  it  does  not  develop  in  all  cases. 
The  urine  is  nearly  always  scanty  and  concentrated,  highly  acid,  and  on 
standing  deposits  urates  in  excess. 

Acute  articular  rheumatism  is  characterized  by  the  speedy  spread  of  the 
arthritis  to  joints  in  other  parts  of  the  body.  In  some  instances  the  involve- 
ment of  a  second  joint  is  followed  by  diminution  of  the  inflammation  in  the 
joint  first  affected,  but  in  many  instances  the  patient  suffers  from  a  pro- 
gressively developing  arthritis  which  soon  involves  almost  all  the  larger 
joints.  This  fugitive  character  of  the  inflammation,  wandering  from  joint 
to  joint,  is  so  very  characteristic,  that  the  presence  of  a  monoarticular 
inflammation  is  a  point  against  the  disease  being  true  rheumatism.  The 
smaller  joints,  such  as  the  fingers  and  toes,  usually  escape,  but  they  are 
often  apparently  affected  by  reason  of  the  fact  that  the  swelling  of  the 
tissues  extends  from  the  large  joint  above  so  that  it  covers  the  smaller  ones. 
In  other  instances,  however,  the  joints  escape  severe  infection,  and  the 
synovial  coverings  of  the  tendons  suffer  chiefly,  so  that  parts  near  the  joint 
may  be  swollen,  and  the  swelling  is  purely  periarticular.  The  vertebral 
and  clavicular  joints  are  very  rarely  affected. 

There  is  no  form  of  acute  arthritis  which  seems  to  give  the  same  amount 
of  severe  pain  as  does  that  of  this  disease,  and  the  close  of  the  attack  usually 
leaves  the  general  system  of  the  patient  considerably  shattered  because  of 
the  severity  of  his  suffering,  his  marked  anaemia,  and  the  exhaustion  caused 
by  the  sweats  and  the  lack  of  sleep.  The  pain  is  also  peculiarly  trying 
because  the  state  of  the  joints  is  such  that  movement  is  impossible  and  the 
patient  gets  bed-sore  and  bed-frantic. 

In  some  cases  a  subacute  type  of  the  disease  develops  in  which  all  the 


200  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

symptoms,  in  the  joints  at  least,  are  very  mild,  but  these  cases  are  very 
prone  to  manifest  cardiac  complications  later  on.  This  is  particularly  true 
in  children. 

One  attack  usually  predisposes  to  another.  It  certainly  in  no  way  pro- 
tects the  patient  from  subsequent  attacks. 

Duration. — The  disease  may  run  its  course  in  a  week  or  be  continued 
over  a  very  long  period  of  time,  lasting  a  month  and  causing  great  dis- 
couragement of  both  the  physician  and  patient.  In  some  instances,  the 
arthritic  state  merges  by  degrees  into  one  of  chronic  arthritis  without  fever, 
and  the  patient  never  fully  recovers  the  free  use  of  his  joints,  but  this  is 
fortunately  very  rarely  the  case.  Even  when  the  amount  of  inflamma- 
tory exudate  seems  very  large  gradual  and  complete  absorption  usually 
occurs. 

Complications. — The  complications  of  acute  articular  rheumatism  are  the 
means  by  which  it  produces  fatal  results,  and  they  are  most  frequently  found 
in  the  heart  muscle,  in  the  cardiac  valves,  or  in  the  pericardium.  The  infection 
attacks  the  endocardium  with  great  constancy,  and  even  in  those  cases  in 
which  the  arthritic  changes  are  slight,  it  often  plays  the  greatest  havoc  in 
the  heart,  so  that  we  frequently  see  young  persons  with  grave  cardiac 
lesions  who  have  presented  such  mild  articular  symptoms  that  the  pres- 
ence of  rheumatism  has  been  overlooked.  Of  842  cases  of  acute  articular 
rheumatism,  all  of  which  were  first  attacks,  valvular  heart  lesions  were 
present  in  420,  or  50  per  cent.  Of  these  lesions,  390  were  mitral,  16 
aortic,  and  14  mitral  and  aortic. 

The  following  table  arranged  from  the  statistics  of  Church  at  St.  Barthol- 
omew's Hospital  illustrates  not  only  the  frequency  of  cardiac  complications 
but  also  the  age  incidence  as  well: 


Number  of 

Number  in 

which 

Percentage  of 

Age. 

cases. 

heart 

was  affected. 

heart  affection. 

Under  10  years 

25 

20 

80 

10  to  20  years 

244 

170 

69.16 

20  to  30  years 

241 

124 

51.1 

30  to  40  years 

115 

35 

30 

40  to  50  years 

41 

9 

21.39 

Over  50  years 

17 

7 

41.03 

683  365  48  78 

This  table  includes  pericarditis  as  well  as  valvular  lesions. 

It  is  generally  recognized  as  a  fact  that  heart  lesions  arise  less  frequently 
in  the  old  than  in  the  young,  and  therefore  the  percentage  of  41.03  given 
for  cases  over  fifty  in  this  table  is  probably  excessive. 

These  lesions  are  rarely  lethal  during  their  acute  stage.  They  develop 
into  subacute  or  chronic  lesions,  and  days,  weeks,  or  years  after  the  patient 
has  recovered  from  the  acute  illness  become  active  agents  in  destroying  life 
or  incapacitating  him  for  work.  The  reason  for  this  lies  in  a  continua- 
tion of  the  endocarditis,  in  a  subacute  or  chronic  form.,  for  days  or  weeks 
after  the  acute  symptoms  have  passed  by,  with  the  result  that  the  valves 
become  shrunken,  and  so  are  unable  to  perform  their  proper  functions;  or 


ACUTE  RHEUMATIC  FEVER  201 

they  become  glued  together,  and  in  this  way  their  action  is  interfered  with. 
Acute  articular  rheumatism  with  cardiac  complications  may  therefore  cause 
death  many  months  or  years  after  the  acute  attack.     (See  Endocarditis.) 

Pericarditis  is  by  no  means  as  frequent  as  endocarditis.  It  is  usually  of 
the  fibrinous  or  serofibrinous  type,  and  occasionally  it  is  purulent,  particu- 
larly in  the  case  of  children.   In  rarer  instances  a  myocarditis  develops. 

It  is  of  the  greatest  importance  that  the  physician  in  charge  of  a  case 
of  acute  articular  rheumatism  be  continually  on  the  lookout  for  cardiac 
complications.  He  can  do  something  toward  preventing  these  by  following 
the  directions  given  under  Treatment,  and  by  insisting  upon  absolute  rest. 
The  vast  majority  of  cases  of  acute  articular  rheumatism  manifest  some- 
time during  their  course  a  more  or  less  well-defined  mitral  murmur,  and 
sometimes  a  pericardial  friction  sound.  In  many  instances,  instead  of  these 
lesions  increasing  in  severity,  they  disappear  with  the  subsidence  of  the 
joint  symptoms. 

Pidmonary  complications  are  not  exceedingly  common.  Stephen  Mac- 
kenzie found  that  pneumonia,  or  pleurisy,  occurred  in  about  10  per  cent, 
of  3433  cases.  Not  infrequently  slight  pulmonary  congestion  of  the  bases 
occurs. 

The  nervous  complications  in  acute  articular  rheumatism  arise  from 
three  causes:  the  high  fever,  the  profound  toxaemia,  and  the  nervous 
irritation  and  exhaustion  produced  by  many  hours  of  suffering.  Delirium 
is  not  commonly  met  with.  An  active,  noisy  delirium  sometimes  develops 
as  a  result  of  the  administration  of  large  doses  of  the  salicylates.  Such 
mental  disturbance  is  said  to  not  infrequently  complicate  the  development 
of  rheumatic  pericarditis.  Sometimes,  too,  excessively  high  temperature  is 
associated  with  delirium. 

Meningitis  occurs  as  a  very  rare  complication. 

The  relationship  between  chorea  and  rheumatism  is  not  clear.  There 
can  be  no  doubt  that  they  bear  some  relationship  one  to  another,  but  whether 
rheumatism  is  to  be  regarded  as  an  etiological  factor  in  chorea  is  undecided. 

The  skin  lesions  of  acute  articular  rheumatism  consist  chiefly  in  the 
development  of  urticaria  and  erythema.  Purpuric  rashes  sometimes  appear, 
hence  the  somewhat  old-fashioned  term  "purpura  rheumatica ;"  but  it  is 
probable  that  these  extravasations  under  the  skin  are  due  to  an  associated 
infection  rather  than  to  the  rheumatism  itself.  Another  very  interesting 
lesion  occurring  as  a  sequence  of  acute  articular  rheumatism  are  rheumatic 
nodules  which  vary  in  size  from  a  small  pinhead  to  a  large  pea,  and  develop 
chiefly  on  the  hands  and  wrists  and  about  the  elbows  and  knees,  and 
sometimes  upon  the  back  over  the  spine.  They  often  last  for  months,  and 
are  seen  more  frequently  in  children  than  in  adults.  Indeed,  they  are  so 
characteristic  in  children  that  they  may  be  regarded  as  a  positive  sign  that 
rheumatism  has  at  some  time  been  present.  They  are  not,  however,  path- 
ognomonic of  rheumatism  in  all  cases,  for  they  appear  in  gouty  .and  rheu- 
matic subjects  who  have  never  suffered  from  the  acute  form  of  the  disease. 

Diagnosis. — The  diagnosis  of  acute  articular  rheumatism  is  by  no  means 
easy  in  all  cases,  but  the  presence  of  fever  with  progressive  involvement 
of  one  joint  after  another  is  very  indicative.     The  great  difficulty  lies  in 


202  DISEASES  DUE   TO   A    SPECIFIC  INFECTION 

separating  the  various  nearly  related  forms  of  septic  arthritis  from  true 
rheumatism.  If  there  is  present  a  pre-existing  septic  focus  from  which 
septicaemia  may  arise,  the  probability  is  that  the  malady  is  not  the  specific 
disease  we  are  discussing.  Thus,  a  multiple  arthritis,  with  or  without 
fever,  often  follows  or  complicates  gonorrhoea,  and  follows  scarlet  fever, 
typhoid  fever,  and  dysentery,  or  any  disease  which,  by  providing  a  source  of 
infection,  exposes  the  joints  to  the  invasion  of  micro-organisms. 

The  chief  conditions,  aside  from  gonorrhoeal  rheumatism  and  ordinary 
septic  arthritis,  that  we  must  carefully  exclude  are  acute  osteomyelitis, 
which  usually  affects  the  femur,  and  which  if  it  is  not  recognized  early  may 
destroy  the  patient's  life;  monoarticular  inflammation,  which  is  often  due 
to  syphilis,  and  acute  gout,  in  which  case  the  history  of  previous  attacks  of 
pain  in  the  smaller  joints  will  be  present  and  the  inflamed  area  will  prob- 
ably be  in  the  ball  of  the  thumb  or  in  the  joint  of  the  great  toe.  In  children 
an  acute  arthritis  with  little  fever  sometimes  develops  and  soon  suppurates. 
It  is  undoubtedly  due  to  septic  infection.  Finally,  let  it  be  borne  in  mind 
that  the  mere  presence  of  heat,  pain,  swelling  and  fixation,  in  a  joint  should 
not  be  called  acute  articular  rheumatism  until  all  other  possibilities  are 
excluded.  Perhaps  no  more  frequent  error  occurs  than  the  calling  of  all 
forms  of  acute  arthritis  "  acute  rheumatism." 

Prognosis. — Death  very  rarely  ensues  as  a  result  of  acute  articular  rheu- 
matism without  any  complications.  This  is  well  shown  by  the  following 
statistics.  In  8431  cases  of  acute  articular  rheumatism  collected  from 
the  official  reports  of  several  American  and  English  hospitals  there  were 
127  deaths,  which  gives  a  percentage  of  1.5.  From  the  years  1880  to  1903 
1524  cases  were  treated  in  the  Pennsylvania  Hospital  with  only  14  deaths, 
a  mortality  of  0.9  per  cent.  While,  therefore,  acute  rheumatism  rarely  causes 
death  during  its  presence  in  the  active  stage  it  is  nevertheless  true  that  no 
acute  disease  causes  death  so  frequently  in  after  years  because  of  secondary 
changes  in  the  heart. 

Treatment. — The  treatment  of  acute  articular  rheumatism  is  at  times 
eminently  satisfactory  and  at  others  equally  disappointing.  In  a  certain 
proportion  of  cases,  in  which  treatment  fails  to  produce  good  results,  the 
condition  is  perhaps  maintained  by  the  presence  of  associated  infections 
which  help  to  produce  the  arthritis.  ^Yhile  no  true  specific  exists  for  acute 
articular  rheumatism,  the  salicylates  act  in  some  cases  with  a  degree  of 
celerity  which  is  most  gratifying,  and  therefore  they  are  always  to  be 
considered  as  the  most  important  remedies  when  the  physician  is  called 
upon  to  treat  a  case  of  this  disease.  The  chief  objects  of  the  physician 
under  these  circumstances  are  the  alleviation,  modification,  and  shortening 
of  the  disease,  and,  second,  the  protection  of  the  heart  from  the  secondary 
affections  of  its  endocardium,  its  muscle,  and  its  pericardium.  For  the 
relief  of  the  pain  and  of  the  inflammatory  processes  in  the  joints  the  best 
remedy  is  the  salicylate  of  strontium  in  the  dose  of  15  to  20  grains  from 
three  to  six  times  a  day.  It  should  be  given  in  capsules  and  followed  by 
a  copious  draught  of  water  or  milk  to  prevent  it  from  irritating  the  stomach. 
Sometimes  a  few  swallows  of  the  emulsion  of  sweet  almonds  may  be  taken 
to  protect  the  stomach  from  irritation. 


ACUTE   RHEUMATIC  FEVER  203 

If  full  doses  of  the  salicylates,  sufBcient  to  produce  distinct  physio- 
logical symptoms,  such  as  fulness  in  the  head  and  some  deafness,  do 
not  produce  signs  of  improvement  in  the  course  of  five  or  six  days,  they 
will  probably  fail  to  cure,  and  had  better  be  discontinued,  as  after  this 
time  they  are  apt  to  increase  the  discomfort  of  the  patient,  to  disorder 
his  stomach,  and  to  increase  the  sweats.  In  their  place  the  patient  may 
receive  10  minims  of  the  wine  of  colchicum  root  and  15  grains  of  iodide 
of  potassium  three  times  a  day.  While  the  salicylates  are  being  given 
it  is  always  advisable  to  give  not  less  than  40  to  60  grains  of  sodium 
bicarbonate  or  bicarbonate  of  potassium  in  each  twenty-four  hours.  The 
sodium  bicarbonate  seems  to  aid  the  stomach  in  withstanding  the  salicy- 
lates, and  provides  the  body  with  a  certain  amount  of  alkali  which  is 
advantageous. 

Copious  draughts  of  water  are  always  to  be  given  in  rheumatism  for 
the  purpose  of  flushing  the  kidneys. 

For  the  prevention  of  endocarditis  and  pericarditis  from  four  to  six  small 
fly-blisters  may  be  placed  over  the  prsecordium,  and  their  influence  as  pre- 
ventive measures  is  thought  to  be  aided  by  the  free  use  of  the  sodium  bicar- 
bonate just  named.  If  pericarditis  develops  and  the  action  of  the  heart  is  very 
excessive,  small  doses  of  aconite  may  be  cautiously  given  to  act  as  a  cardiac 
sedative.  But  this  drug  is  not  to  be  used  if  the  patient  is  markedly  depressed. 
Sometimes  an  ice-bag  placed  over  the  heart  acts  equally  well. 

The  joints  are  best  treated  by  anointing  them  with  ichthyol  and  lanolin  in 
equal  parts,  applying  an  excess  of  this  ointment,  and  then  wrapping  them  in 
cotton-batting.  When  the  patient  suffers  pain  because  of  the  twitchings  of 
his  muscles,  which  in  turn  move  his  inflamed  joints,  some  relief  and  comfort 
can  be  given  by  applying  a  splint  to  produce  fixation  of  the  joint. 

The  acute  inflammatory  process  in  the  joint  is  usually  severe  enough 
to  make  the  patient  content  to  remain  in  bed.  But  it  not  infrequently 
happens  that  as  the  pain  in  the  joint  diminishes  the  patient  is  most  anxious 
to  get  about  and  return  to  his  usual  pursuits.  Nothing  can  be  more 
dangerous  than  the  pursuance  of  such  a  policy.  A  very  large  proportion 
of  cases  of  valvular  heart  disease  are  due  to  the  fact  that  the  patient  has 
suffered  from  rheumatism,  and  has  returned  to  his  occupation  before  the 
endocarditis  produced  by  the  rheumatic  poison  has  entirely  disappeared. 
For  a  time  he  may  be  able  to  perform  his  customary  duties,  but  the  increased 
labor  thrown  upon  his  heart  by  exercise  causes  a  delay  in  the  healing  of 
the  lesions  in  his  endocardium,  and  as  a  result  he  suffers  from  mitral  stenosis 
or  mitral  regurgitation,  which  sooner  or  later  will  make  him  a  cardiac  invalid. 
Even  if  these  symptoms  are  not  manifested  for  some  time  after  the  attack 
of  rheumatism  has  been  present,  they  may  nevertheless  become  dangerously 
active  when  with  advancing  years  cardiac  compensation  is  lost.  The 
physician  should  therefore  impress  upon  every  patient,  with  acute  articular 
rheumatism,  who  insists  upon  rising  as  soon  as  he  feels  well,  the  fact  that 
he  is  taking  his  life  in  his  hands  by  so  doing.  Even  after  all  articular 
symptoms  are  passed  by,  the  patient  who  has  had  this  disease  should  remain 
in  his  bed  for  at  least  two  or  three  weeks,  and  this  advice  holds  good  even  if 
during  the  attack  no  signs  of  an  endocardial  murmur  have  been  manifest. 


204  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


CHOLERA. 

Definition. — The  word  cholera  when  strictly  applied  is  used  to  designate 
a  disease  which  is  characterized  by  profuse  serous  purging,  cramps, 
vomiting,  and  extreme  prostration,  and  which  is  due  to  an  infection 
of  the  bowels  by  the  specific  micro-organism  of  this  disease,  called  the 
Spirillum  cholerce  asiaticoe,  which,  as  it  is  often  broken  into  short,  curved 
rods,  is  frequently  incorrectly  termed  the  "comma  bacillus."  When  it  is 
desired  to  indicate  that  the  true  disease  is  present  the  term  "Asiatic  cholera" 
is  used  to  distinguish  the  malady  from  other  forms  of  serous  diarrhoea  of 
a  severe  type,  such  as  cholera  morbus  or  cholera  infantum. 

History. — Prior  to  1817  cholera  was  confined  to  certain  parts  of  India  and 
never  infected  districts  far  removed  from  them.  It  is  probable  that  the  dis- 
ease has  occurred  for  many  centuries,  but  it  is  a  noteworthy  fact  that,  unlike 
most  epidemic  diseases  of  pronounced  characteristics  and  high  mortality, 
no  clear  description  of  its  presence  was  placed  on  record.  Since  1817, 
when  an  epidemic  of  unusual  severity  broke  out  in  India,  it  has  been  known 
to  be  constantly  present  in  endemic  form  in  some  parts  of  that  country,  and 
it  has  from  time  to  time  been  carried  thence  along  well-travelled  routes 
by  pilgrims  and  travellers,  or  by  their  possessions,  until  many  parts  of  the 
earth  removed  thousands  of  miles  from  the  original  focus  have  suffered 
from  it.  Seven  distinct  invasions  of  Europe  have  occurred  since  1817,  and 
the  last  one  from  1891  to  1895.  The  disease  was  first  introduced  into 
America  by  emigrants  who  landed  in  Quebec  and  New  York  early  in  the 
decade  of  1830  to  1840. 

Distribution. — The  geographical  area  of  origin  has  already  been  described. 
The  disease  may  occur  in  any  part  of  the  world  to  which  the  specific  germ 
may  be  conveyed. 

Etiology. — The  cause  of  epidemic  cholera  is  the  spirillum  which  was  first 
isolated  by  Koch.  It  is  spiral  shaped  or  assumes  the  form  of  segments  of 
a  spiral,  or  short  curved  rods  and  S  forms. 

The  degree  of  curve  varies  greatly;  sometimes  the  organism  is  almost 
straight,  at  other  times  it  forms  a  partial  circle.  Bizarre  forms  also  occur. 
It  is  active,  motile,  and  flagellate.  The  bodies  described  by  Hueppe  as 
Spores  have  not  been  so  considered  by  other  observers. 

Cholera  is  distinctly  a  water-borne  disease  in  the  vast  majority  of  epidemics. 
The  specific  organism  gains  access  to  the  body  through  contaminated  drinking 
water  or  soiled  food.  In  the  Hamburg  cholera  epidemic  of  1892,  about  18,000 
persons  were  stricken,  and  of  this  number  8000  died.  In  the  city  of  Altona, 
which  is  really  a  part  of  Hamburg,  and  which  also  derives  its  drinking  water 
from  the  Elbe,  there  were  only  about  500  cases  of  cholera  in  a  population  of 
150,000.  Hamburg  had  no  filtration  plant  at  the  time,  while  Altona  had  a 
sand  filtration  plant.  It  is  only  by  water  and  food  that  cholera  can  be 
transmitted,  except  that  if  choleraic  stools  are  desiccated,  and  the  dust  is 
blown  on  food  or  into  the  mouth,  it  is  conceivable  that  the  infection  may 
occur.  Aside  from  the  rarity  with  which  this  accident  takes  place,  the  fact 
that  the  bacillus  speedily  dies,  when  dried,  militates  against  it  being  active 


CHOLERA  205 

under  these  circumstances.  A  more  possible  and  indeed  probable  method 
by  which  the  infecting  agent  may  reach  the  food  is  its  carriage  by  flies, 
for  in  the  body  of  the  common  house-fly  the  specific  organism  may  exist  for 
twelve  days. 

Hot  weather  favors  the  spread  of  the  disease.  As  in  all  infectious  maladies, 
all  causes  which  decrease  vital  resistance,  such  as  alcoholism,  exposure,  con- 
valescence from  other  diseases,  and  even  profound  mental  depression,  dis- 
tinctly increase  the  susceptibility  of  the  patient. 

Prevention. — It  is  evident  from  what  has  been  said  that  there  is  no  reason 
why  cholera  cannot  be  prevented,  and  it  may  be  said  of  deaths  from  cholera, 
as  it  is  said  of  deaths  from  typhoid  fever,  that  every  one  is  preventable  if  proper 
care  is  taken  to  destroy  all  the  specific  organisms  the  moment  they  escape 
from  the  body  of  a  patient  suffering  from  the  malady.  That  they  are  not 
destroyed  in  cholera  is  all  the  more  to  be  condemned  by  reason  of  the  fact 
that  they  escape  only  in  the  stools,  whereas  in  typhoid  fever  the  specific 
bacillus  escapes  by  the  urine,  the  skin,  and  perhaps  the  saliva.  The  cholera 
spirillum  is  exceedingly  susceptible  to  bactericides  and  particularly  to  acids, 
under  favorable  circumstances  succumbing  to  such  weak  acids  as  vinegar. 

All  dejecta  from  cholera  patients  should  be  destroyed  by  heat  or  by  the 
action  of  chlorinated  lime,  or  formaldehyde,  or  of  corrosive  sublimate,  con- 
tact with  a  solution  of  which  should  be  complete  and  prolonged  for  at  least 
one  hour,  for  in  the  latter  instance  the  mercury  salt  may  combine  with  the 
albumin,  or  be  decomposed  by  the  gases  in  the  stools. 

During  the  presence  of  the  disease  nonfood  should  be  taken  in  the  raw 
state,  and  it  should  be  cooked  immediately  before  it  is  eaten,  in  order  that 
there  may  l)e  no  time  for  it  to  become  infected  after  it  is  cooked.  With  these 
precautions  the  danger  to  physicians  and  nurses  is  reduced  to  a  minimum. 
When  there  is  a  possibility  of  negligence,  a  valuable  prophylactic  is  the  use  of 
dilute  sulphuric  acid  in  the  dose  of  5  to  10  drops  in  water  three  times  a  day 
after  food.  This  does  good,  by  reason  of  the  fact  that  dilute  acids  kill  the 
comma  bacillus,  and  again  because  this  acid  acts  as  an  astringent  remedy 
in  diarrhoea.  Care  should  be  taken  during  an  epidemic  that  bad  food  and 
exposure  are  avoided,  as  this  may  prepare  the  way  for  infection. 

Through  the  researches  of  Haffkine  in  India,  it  would  seem  that  it  is  possible 
to  immunize  human  beings  against  cholera,  but  this  plan  of  inoculation  is  of 
no  value  when  the  disease  has  once  developed. 

During  the  years  1894  and  1895  Haffkine  inoculated  3951  individuals 
with  his  anticholera  vaccine.  Of  this  number,  33,  or  a  little  less  than  1  per 
cent.,  contracted  the  disease,  whereas,  of  9335  individuals  who  were  uninocu- 
lated  and  similarly  exposed  to  the  infection,  210,  or  2.24  per  cent.,  were 
stricken.    These  observations  were  made  in  India. 

In  July,  1902,  an  epidemic  of  cholera  broke  out  in  the  prefecture  of 
Nagasaki,  Japan,  and  preventive  inoculations  were  at  once  begun.  Of 
21,334persons  who  were  inoculated,  110  contracted  the  disease.  In  previous 
epidemics  the  number  of  persons  aftected  ran  well  up  into  the  thousands, 
but  it  is  but  fair  to  state  that  in  this  epidemic  only  741  cases  occurred  in 
that  prefecture  among  the  uninoculated.  As  the  number  of  uninoculated 
inhabitants  is  not  stated,  we  cannot  judge  of  the  real  value  of  the  plan. 


206  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Haffkine's  conclusions  as  to  the  result  of  anti  cholera  inoculations  are  as 
follows : 

1.  The  inoculation  produces  an  effect  within  four  days. 

2.  During  these  four  days  a  difference  in  susceptibility  shows  itself  in  favor 
of  the  inoculated. 

3.  After  the  expiration  of  the  four  days  and  during  a  period  of  at  least 
fourteen  months,  a  high  degree  of  resistance  to  attack  is  observed  in  the 
inoculated. 

4.  The  proportion  of  deaths  to  cases  is  not  influenced  by  the  inoculation. 
Pathology  and  Morbid  Anatomy. — After  death  from  cholera  postmortem 

rigidity  comes  on  very  rapidly,  and  is  persistent  to  such  a  degree  that  dis- 
tortions of  the  limbs  and  body  may  be  present.  In  typical  cases  the  entire 
body  appears  shrunken  and  wasted  and  the  dependent  portions  rapidly 
become  livid.     Not  rarely  a  postmortem  rise  of  temperature  takes  place. 

When  the  body  is  incised  the  tissues  are  found  to  be  devoid  of  their  normal 
moisture,  and  the  blood  in  the  great  vessels  is  thick  and  dark  in  hue. 
The  stomach  is  empty,  its  mucous  membrane  is  congested,  and,  in  some 
instances,  ecchymoses  may  be  present. 

The  chief  changes  are  to  be  found,  however,  in  the  lower  part  of  the 
small  bowel.  Its  mucous  membrane  is  boggy  or  sodden,  and  covered  by  a 
glutinous  material  which  is  readily  detached.  Not  rarely  the  mucous  mem- 
brane is  stripped  off  in  patches  or  shed  in  flakes.  These  changes  may 
extend  as  high  as  the  duodenum,  and  in  the  lower  ileum  Peyer's  patches 
and  the  solitary  glands  are  found  to  be  swollen  and  congested.  There 
may  be  present  a  diphtheritic  exudate,  which  is  adherent  in  part,  and  in 
part  is  fleecy  or  flocculent  in  appearance.  Deeper  ulcerations  and  perfora- 
tions are  exceptional.  Hemorrhages  may  also  be  found  in  the  mucous  mem- 
brane at  this  place. 

Notwithstanding  the  active  purgation,  the  large  bowel  in  cholera  is  not 
as  much  altered  as  is  the  ileum,  the  only  change,  as  a  rule,  being  an  acute 
catarrh  of  the  mucous  membrane. 

It  is  important  to  the  student  to  recall  the  fact  that  cholera  is  character- 
ized by  changes  in  the  smaU  bowel,  whereas  dysentery  is  chiefly  characterized 
by  changes  in  the  colon. 

The  intestines  are  contracted,  their  coats  thickened,  and  the  peritoneum 
possesses  a  peculiar  rosy  hue.  The  mesenteric  glands  are  enlarged  and 
infiltrated. 

Granular  changes  in  the  large  glandular  viscera  are  present  in  a  certain 
percentage  of  cases,  and  a  complicating  nephritis  is  occasionally  seen.  The 
kidneys  may  be  enlarged  and  the  vessels  congested.  Under  the  micro- 
scope the  uriniferous  tubules  are  seen  to  be  filled  with  granular  casts,  but 
the  tufts  are  not  materially  changed.  The  great  loss  of  fluid  by  the  serous 
discharges  and  the  lessened  absorption  of  liquids  causes  concentration  of 
the  blood  and  greatly  interferes  with  the  excretion  of  poisons  by  the  kidneys. 

The  liver  is  not  enlarged  but  rather  shrunken,  and  its  cells  show,  under 
the  microscope,  cloudy  swelling,  with  patches  of  fatty  degeneration.  The 
spleen  is  usually  small.     The  heart  is  flaccid  and  the  lungs  shrunken. 

The  cholera  organism  is  found  in  immense  numbers  in  the  contents  of  the 


CHOLERA  207 

bowels  and  in  the  discharges  of  patients  suffering  from  this  disease,  but, 
unKke  the  typhoid  bacillus,  it  is  not  usually  widely  disseminated  through  the 
body  (Figs.  39  and  40). 

Fig.  39 


X 


Comma  bacilli  in  the  fundus  of    a  gland  of  Lieberkuhn  in  the  small  bowel  in  a  case  of 
Asiatic  cholera.      (Kast  and  Rumpler.) 

Fig.  40 


A" 


« 
m 


«,„  ^  *>  '%^..: 


%  ^   c  * 


4^ 


» 


4 


^^       t  ''..    ^_.      ,.  .'■-.,    A  .'      "V-, 


^^;  T*"^' 


Comma  bacilli  in  the  intestinal  contents.      (Kast  and  Rumpler.) 

Symptoms.— The  symptoms  of  cholera  develop  in  from  a  few  hours  to  ten 
days  after  infection  has  occurred.  The  average  period  of  incubation  is 
usually  three  to  six  days. 

The  earliest  symptoms,  aside  from  a  feeling  of  depres.sion,  is  the  onset  of 
watery  diarrhoea,  which  may  be  associated  with  pain.     The  patient  suffers 


208  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

from  the  weakness  and  depression  characteristic  of  ordinary  watery  diarrhoea, 
and  if  the  passages  are  very  profuse  tliere  may  be  great  feebleness  and  even 
collapse.  In  the  majority  of  cases,  however,  the  onset  of  the  disease  is  more 
abrupt  than  that  just  described.  With  almost  no  indication  of  impending 
illness  the  patient  is  seized  by  active  vomiting  and  purging,  by  severe  cramps 
in  the  extremities  and  trunk,  and  passes  into  collapse.  The  stools,  as  soon 
as  all  the  ordinary  intestinal  contents  have  been  washed  out,  are  rice-water 
in  character;  that  is,  on  standing  they  separate  into  two  layers,  the  upper 
clear  and  opalescent,  the  lower  full  of  flakes  of  mucus  and  exfoliated 
necrotic  mucosa. 

The  amount  of  serum  lost  by  the  purging  is  very  large,  and  it  is  expelled 
with  considerable  force.  Because  of  the  large  quantities  of  fluid  lost  by  this 
means  the  urine  becomes  scanty  and  suppressed.  This  loss  of  fluid,  com- 
bined with  the  changes  in  the  kidneys,  results  in  urasmia,  which,  of  course, 
aids  greatly  in  increasing  the  toxoemia  of  the  disease.  The  vomiting  is  not 
only  violent,  but  persistent  retching  may  greatly  exhaust  the  patient.  The 
cramps  in  the  muscles  are  due  to  the  rapid  abstraction  of  fluid  from  their 
tissues  and  perhaps,  in  part,  to  the  toxaemia  of  the  disease. 

In  about  half  the  cases  recovery  begins  to  take  place  at  this  stage  by  a 
gradual  modification  of  the  symptoms,  but  if  the  patient  is  too  ill  to  recover, 
the  second  stage,  or  that  of  collapse  and  profound  asthenia,  now  develops. 
This  stage  may  last  from  a  few  hours  to  two  days.  As  it  proceeds  the  patient 
becomes  so  feeble  that  the  respirations  become  shallow.  The  fluid  stools 
pass  from  the  bowel  involuntarily,  escaping  rather  by  relaxation  of  the 
sphincter  than  by  the  conscious  act  of  the  patient.  Feeble  attempts  at 
emesis  may  still  persist,  and  the  cramps  may  be  more  severe  than  before. 

As  the  exhaustion  deepens  the  -pidse  becomes  a  mere  thread  at  the  wrist, 
and  may  even  be  imperceptible  in  the  great  vessels.  The  heart  sounds 
become  more  and  more  indistinct,  and  occasionally  soft  murmurs  are 
heard. 

The  face  now  bears  the  Hippocratic  expression,  the  nose  is  pinched  and 
pointed,  the  eyes  sunken  and  surrounded  by  dark  rings,  the  mouth  is  partly 
open,  the  teeth  covered  with  sordes,  the  skin  of  the  entire  body  is  livid  and 
often  bedewed  with  a  cold  sweat.  The  voice  is  whispering ,  the  thirst  exces- 
sive, and  the  mind  clouded.  Toward  the  close  of  life  stupor  or  coma  merci- 
fully relieves  suffering.  Finally,  with  a  continued  fall  of  bodily  temperature, 
death  takes  place. 

When  the  stage  of  reaction  develops,  before  these  grave  symptoms  threaten 
death,  the  pulse  becomes  a  little  stronger,  the  passages  are  less  frequent  and 
less  copious,  and  the  respirations  grow  deeper.  Bodily  heat  is  gradually 
restored,  and  the  patient  recovers,  unless  some  of  the  complications  men- 
tioned farther  on  ensue. 

Variations  from  the  Ordinary  Course. — The  patient  may  have  so  mild  an 
infection  as  to  be  but  slightly  ill  and  never  forced  to  go  to  bed.  In  other 
instances  the  serous  diarrhoea  is  excessive,  but  the  urine  is  not  suppressed, 
and  the  general  debility  does  not  become  marked.  These  cases  are  some- 
times called  cases  of  "  cholerine."  They  may  speedily  recover  or  rapidly 
proceed  to  the  fully  developed  malady.    In  still  another  class  the  toxaemia  of 


CHOLERA  209 

the  disease  exceeds  all  other  symptoms.  The  diarrhoea  may  be  absent,  and 
the  patient,  overwhelmed  by  the  poison^  sinks  into  unconsciousness  and 
death.    This  is  called  "  cholera  sicca." 

The  degree  of  shipor  varies  greatly.  In  some  patients  the  mind,  at  the 
well-developed  stage  of  the  disease,  is  remarkably  clear;  in  other  instances 
it  is,  almost  from  the  first,  stupid  from  toxjemia. 

In  some  instances  high  fever  develops.  This  is  a  very  unfavorable  sign. 
In  others  an  urticaria  or  erythema  is  seen. 

Complications  and  Sequelae. — Aside  from  the  grave  complication  of  urinary 
suppression  followed  by  unemia,  the  profound  infection  may  result  in  local- 
ized gangrene  of  the  .toes  and  fingers.  (Edema  of  the  lungs  often  causes 
death,  and  infectious  arthritis  and  parotitis  may  develop.  Profound  weak- 
ness and  feebleness  may  persist  for  a  long  time  in  convalescence,  and  second- 
ary nephritis  may  ultimately  cause  death. 

Diagnosis. — The  diagnosis  of  cholera  is  not  difficult  if  the  well-developed 
type  of  the  disease  is  present,  but  in  the  early  stages,  or  in  the  aberrant  forms 
just  described,  the  determination  of  the  cause  of  the  illness  may  not  be  easy. 
True  cholera  is  to  be  separated  from  cholera  nostras  or  cholera  morbus, 
but  in  the  presence  of  an  epidemic  of  Asiatic  cholera  this  may  be  im.possible 
without  bacteriological  tests,  for  severe  cholera  morbus  may  not  only  be 
manifested  by  purging  and  vomiting,  but  by  collapse  as  well,  and  even  cramps 
may  appear  in  the  more  severe  types.  Cholera  must  also  be  separated  during 
an  epidemic  from  the  profuse  watery  purging  sometimes  met  with  in  cases 
of  Bright's  disease,  when  the  purging  is  due  to  an  effort  at  elimination 
Various  poisons  may  also  cause  choleraic  diarrhoea,  notably  antimony. 
Indeed,  it  is  impossible  to  separate  acute  antimonial  poisoning  from  cholera 
during  an  epidemic  of  the  latter  disease,  because  the  symptoms  are  identical. 
Nothing  but  a  chemical  analysis,  on  the  one  hand,  or  a  bacteriological  test, 
on  the  other,  can  determine  this  question. 

It  is  important  to  remember  that  while  the  presence  of  the  spirillum  of 
cholera  is  characteristic  of  cholera,  that  inability  to  discover  it  in  the  dis- 
charges is  not  positive  proof  that  cholera  is  not  present,  because  in  rare 
instances  it  may  be  temporarily  undemonstrable.  A  very  valuable  method 
of  diagnosis  is  the  test  of  agglutination  of  cholera  bacilli  by  the  blood  of  the 
patient  in  a  manner  similar  to  that  of  the  Widal  test  in  typhoid  fever. 

Prognosis. — The  prognosis  in  cholera,  whenever  the  symptoms  are  well 
developed,  is  always  grave,  for  the  mortality  in  most  epidemics  is  about  50 
per  cent.  In  the  old  and  very  young  the  outlook  is  worse  than  in  a  well- 
developed  person  in  the  prime  of  life. 

There  are  three  facts  aside  from  the  severity  of  the  disease  which  increase 
the  gravity  of  the  prognosis  very  materially,  namely,  alcoholism,  renal  dis- 
ease, and  disease  of  the  liver.  In  addition,  it  must  be  remembered  that  any 
pre-existing  disease  which  decreases  vital  resistance  increases  the  gravity  of 
the  case. 

In  respect  to  the  disease  itself,  it  may  be  said  that  abruptness  of  onset, 

early  hebetude,  and  rapid  development  of  signs  of  collapse  are  the  three 

facts  that  promise  evil  tendencies.     If  to  these  is  added  renal  inactivity, 

pulmonary  consolidation,  or  an  abnormally  low  temperature,  the  case  is  to 

14 


210  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

be  regarded  as  almost  hopeless.  Contrariwise,  there  are  several  signs  of 
good  omen,  namely,  the  presence  of  a  good  pulse  and  the  maintenance  of 
bodily  heat,  the  return  of  a  fecal  color  to  the  stools,  and  the  absence  of  the 
great  emaciation  and  wasting  which  severe  cases  usually  manifest. 

Treatment. — Tiie  three  most  important  details  in  the  treatment  of  cholera 
are  the  control  of  the  diarrhoea,  the  maintenance  of  strength,  and  the  con- 
servation of  body  heat.  All  persons  who  have  any  tendency  to  diarrhoea 
during  a  cholera  epidemic  should  at  once  be  treated  by  astringent  mixtures, 
which  should  be  increased  in  their  efficiency  by  the  addition  of  a  few  drops 
of  sulphuric  acid.  By  this  method  of  treatment  the  development  of  cholera 
can  be  probably  prevented  in  a  considerable  number  of  persons.  The  use 
of  an  astringent  and  acid  substance  like  sulphuric  acid  is  far  more  advan- 
tageous than  the  employment  of  opium,  because  the  acid  is  destructive  to 
the  comma  bacihus,  and  it  does  not  interfere  with  other  functions  of  the 
body  as  does  opium.  If  the  diarrhoea  is  already  active  10  to  15  drops  of 
aromatic  sulphuric  acid,  with  double  that  quantity  of  spirit  of  camphor, 
should  be  administered,  well  diluted  with  water  or  with  brandy,  every 
three  hours,  and  counterirritation  in  the  form  of  a  mustard  plaster  or  sina- 
pisms or  capsicum  drafts  should  be  applied  over  the  abdomen.  If  these 
cannot  be  obtained  a  turpentine  stupe  may  be  used  with  advantage. 

It  seems  scarcely  necessary  to  add  that  even  in  mild  cases  the  patient 
should  be  kept  in  bed  and  the  greatest  possible  amount  of  rest  enforced.  If 
vomiting  is  an  active  symptom  it  may  be  necessary  to  avoid  all  medication 
by  the  mouth  and  give  stimulants  hypodermically.  Under  these  circum- 
stances a  grain  of  camphor  dissolved  in  sterilized  olive  oil  may  be  given  by 
means  of  the  hypodermic  needle  every  eight  hours.  Such  a  method  of  treat- 
ment will  usually  do  much  toward  the  maintenance  of  active  circulation,  but 
should  the  circulation  fail  the  physician  must  employ  not  only  the  camphor 
injections  named,  but  give  brandy  and  strychnine  hypodermically,  and 
more  important  still,  for  the  purpose  of  compensating  for  the  loss  of  much 
fluid  by  the  bowel,  hypodermoclysis  should  be  resorted  to.  It  is  best  to 
employ  "concentrated  sterile  saline,"  one  ounce  of  which  when  added  to 
a  quart  of  pure  water  makes  normal  salt  solution.  But  if  this  cannot  be 
obtained  ordinary  common  salt  in  the  proportion  of  a  drachm  to  the  pint 
may  be  injected  by  hypodermoclysis.  This  fluid  should  of  course  be  first 
sterilized  by  boiling,  and  the  injection  should  be  made  slowly,  the  fluid 
being  at  the  temperature  of  100°.  It  is  quite  remarkable  how  rapidly  the 
thirsty  tissues  will  absorb  this  fluid,  which  not  only  compensates  for  the 
loss  by  purging,  but  also  aids  in  overcoming  suppression  of  urine  by  sup- 
plying the  bloodvessels  with  fluid.  There  can  be  no  doubt  that  hypoder- 
moclysis is  a  most  valuable  life-saving  measure  in  the  treatment  of  this 
disease. 

The  body  heat  should  be  maintained  by  the  application  of  hot  bottles 
about  the  patient,  particularly  at  his  extremities,  and  when  the  temperature 
seems  to  be  falling  and  the  skin  has  a  tendency  to  be  relaxed  and  bedewed 
with  sweat  a  hypodermic  injection  of  y^o"  to  y^o"  o^  ^  grain  of  atropine 
is  advantageous.  This  injection  should  be  into  the  trunk  rather  than  into 
one  of  the  extremities,  since  if  the  circulation  is  poor  it  will  be  absorbed 


CHOLERA  211 

more  rapidly  from  the  body  than  from  an  arm  or  the  leg.  Thirst  is  to  be 
allayed  by  giving  fluids  to  the  patient  in  small  quantities  frequently,  but 
large  draughts  of  water  are  disadvantageous.  Sometirnes  barley-water  or 
soda-water  is  retained  better  than  plain  water.  For  the  relief  of  the  cramps 
gentle  rubbing  of  the  extremities  with  chloroform  liniment,  or  ammonia 
liniment,  may  be  employed,  but  the  severity  of  this  symptom  is  usually 
modified  by  the  use  of  the  camphor  and  the  subcutaneous  saline  injections. 

To  aid  in  the  restoration  of  renal  activity  a  hot  compress  may  be  placed 
under  the  loins. 

During  the  last  outbreak  of  cholera  in  Europe  salol  was  employed  by  a 
large  number  of  physicians  with  excellent  results,  its  employment  being  based 
upon  the  fact  that  if  it  is  added  to  an  alkaline  solution  of  pancreatic  juice 
it  rapidly  destroys  this  cholera  bacillus.  As  an  illustration  of  its  value  it  may 
be  stated  that  Hehir  treated  88  cases  with  corrosive  sublimate  with  a  mor- 
tality of  44.7  per  cent.,  and  11  cases  with  salol  with  no  deaths;  while  Gon- 
zalez lost  only  3  out  of  53  patients  when  he  employed  salol.  Similar  statis- 
tics from  other  parts  of  the  world  might  be  quoted  indicating  its  very  great 
value. 

Under  the  leadership  of  Cantani  the  following  treatment  by  injection 
has  also  become  popular,  it  being  necessary  to  give  it  in  large  quantities 
not  only  for  the  purpose  of  irrigating  the  large  bowel,  but  if  possible 
getting  it  into  the  small  bowel  as  well;  for  it  is  in  the  small  bowel  that 
the  micro-organism  of  the  disease  exists  in  largest  number.  The  fluid 
employed  by  Cantani  consists  of  infusion  of  chamomile  flowers,  2000 
parts;  tannic  acid,  10  parts;  gum  arable,  30  parts;  and  laudanum,  2  parts. 
The  object  in  using  tannic  acid  is  not  only  to  obtain  its  astringent  influ- 
ence, but  also  because  in  the  strength  of  1  per  cent,  it  inhibits  the  growth 
of  intestinal  micro-organisms,  and,  Cantani  thinks,  also  neutralizes  the 
poisons  formed  by  these  bodies.  Lustig  treated  117  cases  of  cholera  in  this 
way  with  34  deaths  and  193  cases  by  other  methods  with  146  deaths.  Care 
must  be  employed  in  giving  these  injections  that  the  fluid  is  introduced  into 
the  bowel  slowly,  the  buttocks  of  the  patient  being  slightly  elevated  and  his 
body  turned  slightly  to  the  left.  Any  tendency  to  bearing  down  on  the  part 
of  the  patient  is  to  be  avoided  by  diverting  his  attention  from  the  injection 
and  by  momentarily  stopping  its  flow  when  he  feels  the  desire  to  expel  the 
fluid.  The  fountain  syringe  containing  the  fluid  should  not  be  hung  or  held 
more  than  eighteen  inches  above  the  anus.  If  the  fluid  flows  in  under  this 
gentle  pressure,  very  large  quantities  may  be  retained,  and  Cantani  asserts 
that  it  will  find  its  way  through  the  ileocsecal  valve  and  flush  the  smaller 
bowel.  Such  a  passage  through  this  valve  in  the  healthy  intestine  is,  I 
believe,  impossible,  but  it  is  stated  that  in  the  relaxation  of  the  muscular 
fibres  produced  by  cholera  its  passage  is  by  no  means  difficult. 

When  collapse  is  threatened  or  present  the  fluid  injected  should  be  as  hot 
as  105°,  and  the  fluid  in  the  bag  may  be  at  110°  or  115°,  as  it  loses  much 
heat  in  flowing  slowly  through  the  tube.  If,  on  the  other  hand,  hyper- 
pyrexia is  present,  cool  water  should  be  employed. 

As  a  rapidly  acting  diffusible  stimulant  in  conditions  of  marked  collapse 
Hoffmann's  anodyne  in  the  dose  of  a  drachm  every  hour  may  ge  given  hypo- 


212  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

dermically  or  by  the  mouth  with  shaved  ice.  A  drachm  of  spirit  of  cam- 
phor may  also  be  used  with  advantage  for  this  purpose.  Aromatic  spirit  of 
ammonia  may  also.be  given  by  the  mouth,  but  is  not  so  valuable. 


YELLOW  FEVER. 

Definition. — Yellow  fever  is  an  acute  infectious  disease  occurring  chiefly 
in  tropical  or  semi-tropical  regions,  and  characterized  by  fever,  yellow  dis- 
coloration of  the  skin,  black  vomit  in  some  cases,  and  a  tendency  to  oozing 
hemorrhages  from  the  mucous  membranes.  The  early  development  of 
albuminuria  is  also  a  noteworthy  symptom. 

History,  Etiology,  and  Prevention. — The  earliest  history  of  yellow  fever 
records  its  occurrence  among  the  followers  of  Columbus,  and  before  that 
time  it  never  attacked  Europeans.  It  is,  therefore,  a  disease  indigenous  to 
the  Western  Hemisphere.  As  early  as  1648  the  inhabitants  of  St.  Kitts 
and  in  1655  those  of  Jamaica  were  attacked  by  it. 

Since  then  yellow  fever  has  devastated  North  and  South  America  many 
times.  It  has  extended  its  ravages  all  the  way  from  Quebec  to  Montevideo, 
and  on  the  western  coast  of  the  Western  Hemisphere  has  been  almost  equally 
widely  distributed.  In  the  latter  part  of  the  eighteenth  century  it  destroyed 
10  per  cent,  of  the  population  of  Philadelphia.  On  more  than  one  occasion  it 
has  brought  military  expeditions  to  defeat  by  the  frightful  mortahty  which 
it  has  caused  amongst  the  troops.  During  the  French  expedition  to  Hayti, 
in  1802,  22,000  out  of  25,000  men  died  from  it  in  one  season,  and  the  various 
attempts  which  were  made  by  Spain  to  subjugate  Cuba  were  practically 
frustrated  by  the  mortality  from  yellow  fever  among  the  Spanish  troops. 
Davidson  states  that  out  of  a  population  of  9000  persons  at  Gibraltar  in 
1800  only  28  escaped  infection.  In  1878  the  financial  loss  in  the  Mississippi 
Valley  produced  by  a  single  epidemic  amounted  to  over  SI 5, 000,000. 

For  one  hundred  and  fifty  years  Havana  was  recognized  as  the  focus 
in  which  yellow  fever  was  practically  constantly  present,  and  from  this  focus 
many  portions  of  the  civilized  world  were  again  and  again  infected.  It  was 
not  until  the  United  States  Army  took  possession  of  Havana  and  its  medical 
officers  instituted  sanitary  measures  that  any  real  attempt  was  made  to  dis- 
cover the  means  of  propagation  of  yellow  fever  or  to  limit  its  development 
in  that  city.  When  the  brave,  skilful,  and  scientific  labors  of  these  officers 
were  completed  one  of  the  most  brilliant  medical  discoveries  in  the  history 
of  the  world  was  announced. 

Under  proper  sanitary  directions  the  death  rate  in  Havana  fell  from  91  and 
a  fraction,  under  Spa,nish  rule  in  1898,  to  33  and  a  fraction  in  1899  under 
American  rule,  to  24^  in  1900,  and  to  22  and  a  fraction  in  1901,  but  there 
was  not  a  simultaneous  diminution  in  the  frequency  or  mortality  of  yellow 
fever.  Indeed,  at  that  period  there  was  an  actual  increase  in  the  disease 
notwithstanding  the  fact  that  all  other  maladies  were  decreasing.  It  was 
under  these  circumstances  that  a  commission  was  appointed  by  the 
Surgeon-General  of  the  United  States  Army  for  the  purpose  of  studying 
yellow  fever.     The  chairman  of  the  commission  was  the  late  Dr.  Walter 


YELLOW  FEVER  213 

Reed,  a  major  in  the  United  States  Army,  and  associated  with  him  were 
acting  assistant  surgeons  James  Carroll,  Jesse  W.  Lazear,  and  Aristides 
Agramonte. 

The  medical  profession  should  never  cease  to  do  honor  to  the  members 
of  this  commission,  which  faced  one  of  the  most  horrible  and  fatal  diseases 
with  the  greatest  bravery,  and  thereby  have  succeeded  in  saving  the  lives  of 
hundreds  of  thousands  of  individuals.  Dr.  Lazear,  who  was  one  of  the  most 
enthusiastic  members  of  the  commission,  allowed  himself  to  be  bitten  by  an 
infected  mosquito.  He  was  not  infected  by  this  bite,  but  several  days  after 
he  was  accidentally  bitten,  and  lost  his  life  from  the  consequent  attack  of 
yellow  fever.  Another  member.  Dr.  Carroll,  allowed  himself  to  be  bitten, 
was  also  attacked  by  the  disease,  and  narrowly  escaped  death. 

The  fact  that  Ross  and  others  had  proved  that  the  transmission  of  malarial 
fever  was  by  the  mosquito,  and  that  Dr.  Carlos  Finlay,  a  physician  of 
Havana,  a  graduate  of  the  Jefferson  Medical  College,  of  Philadelphia,  had 
asserted  as  long  ago  as  1881  that  certain  species  of  mosquito  in  Havana 
was  guilty  of  transmitting  yellow  fever  from  person  to  person,  led  the  Army 
Board  to  direct  their  attention  to  the  investigation  of  this  question,  and 
they  soon  found  that  if  a  female  mosquito  of  the  species  Stegomyia  fasciata 
were  allowed  to  bite  a  yellow  fever  patient  during  the  first  three  days  of  the, 
disease,  and  then,  from  twelve  to  twenty  days  later,  permitted  to  bite  a  non- 
immune, the  latter  almost  invariably  developed  yellow  fever. 

That  the  disease  is  never  carried  by  fomites  was  also  proved  by  these 
investigators,  who  had  a  number  of  young  non-immunes  sleep  for  twenty 
consecutive  nights  in  a  room  which  was  hung  with  articles  soiled  by  black 
vomit,  bloody  fecal  discharges,  and  urine,  from  fatal  and  other  cases  of  yellow 
fever.  These  persons  also  packed  and  unpacked  these  articles  night  and 
morning  from  boxes  in  which  they  were  placed.  Other  non-immunes  actually 
slept  in  garments  and  between  sheets  that  had  covered  fatal  cases  of  yellow 
fever,  but  in  not  a  single  instance  was  the  disease  contracted,  although  as 
soon  as  these  non-immunes  were  exposed  to  mosquitoes  several  of  them 
developed  yellow  fever. 

The  practical  result  of  proving  that  the  mosquito  is  the  cause  of  the 
transmission  of  the  infection  has  been  the  complete  clearance  of  Havana  of 
yellow  fever.  All  cases  of  yellow  fever  were  protected  by  mosquito  netting 
so  that  miosquitoes  could  not  carry  infection  from  them  to  others.  All 
pools  and  gutters  containing  water  upon  which  mosquitoes  could  breed 
were  removed,  and  the  destruction  of  mosquitoes  was  carried  on  actively, 
with  the  result  that  it  was  possible  in  a  year  to  diminish  the  number  of 
deposits  of  mosquito  larvae  in  the  city  of  Havana  from  26,000  to  300.  As 
a  result,  the  death  rate  from  malaria  fell  from  344  in  1900  to  151  in  1901, 
and  up  to  July,  1902,  it  was  only  47;  while  the  diminution  in  the  number 
of  mosquitoes  caused  so  great  a  decline  in  the  prevalence  of  yellow  fever 
that  by  September  28,  1901,  new  cases  ceased  to  occur  in  Havana.  Since 
that  time,  according  to  Dr.  Gorgas,  of  the  United  States  Army,  from 
whose  reports  much  of  this  information  is  taken,  not  a  single  case  has 
originated  in  that  city,  until  the  latter  part  of  1905,  when  relaxed  vigilance 
allowed  the  disease  again  to  reappear. 


214  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

The  conclusions  of  the  commission  are  so  important  that  they  are  given 
verbatim : 

1.  The  mosquito — Stegomyia  fasciata — serves  as  the  intermediate  host 
for  the  parasite  of  yellow  fever. 

2.  Yellow  fever  is  transmitted  to  the  non-immune  individual  by  means 
of  the  bite  of  the  mosquito  that  has  previously  fed  on  the  blood  of  those 
sick  with  this  disease. 

3.  An  interval  of  about  twelve  days  or  more  after  contamination  appears 
to  be  necessary  before  the  mosquito  is  capable  of  conveying  the  infection. 

4.  The  bite  of  the  mosquito  at  an  earlier  period  after  contamination  does 
not  appear  to  confer  any  immunity  against  a  subsequent  attack. 

5.  Yellow  fever  can  also  be  experimentally  produced  by  the  subcutaneous 
injection  of  blood  taken  from  the  general  circulation  during  the  first  and 
second  days  of  this  disease. 

6.  An  attack  of  yellow  fever,  produced  by  the  bite  of  the  mosquito  con- 
fers immunity  against  a  subsequent  attack  of  the  non-experimental  form 
of  this  disease. 

7.  The  period  of  incubation  in  thirteen  cases  of  experimental  yellow 
fever  has  varied  from  forty-one  hours  to  five  days  and  seventeen  hours. 

8.  Yellow  fever  is  not  conveyed  by  fomites,  and  hence  disinfection  of 
clothing,  bedding,  or  merchandise,  supposedly  contaminated  by  contact 
with  those  sick  with  this  disease,  is  unnecessary. 

9.  A  house  may  be  said  to  be  infected  with  yellow  fever  only  when  there 
are  present  within  its  walls  contaminated  mosquitoes  capable  of  conveying 
the  parasite  of  this  disease. 

10.  The  spread  of  yellow  fever  can  be  most  effectually  controlled  by 
measures  directed  to  the  destruction  of  mosquitoes,  and  the  protection  of 
the  sick  against  the  bites  of  these  insects. 

11.  While  the  mode  of  propagation  of  yellow  fever  has  now  been  defi- 
nitely determined,  the  specific  cause  of  this  disease  remains  to  be  discov- 
ered. 

^  Prophylaxis. — Attention  has  already  been  called  to  the  fact  that  the  infec- 
tious agent  of  yellow  fever  is  conveyed  by  mosquitoes  from  patient  to  patient. 
It  is  therefore  essential  that  all  cases  of  yellow  fever  should  be  kept  under 
mosquito  netting  so  that  they  may  not  be  bitten  by  mosquitoes,  and  it  is 
also  wise  for  those  who  are  well  to  protect  themselves  at  night  from  mos- 
quitoes by  similar  means.  For  screening  those  who  are  ill,  a  gauze  of  not 
less  than  twenty  meshes  to  the  inch  should  be  used,  otherwise  the  mosquito 
may  pass  through  it.  An  active  crusade  against  all  mosquitoes  and  the 
destruction  of  their  breeding-places  should  also  be  instituted. 

Pathology  and  Morbid  Anatomy. — One  of  the  most  marked  changes  pro- 
duced in  the  body  by  the  infection  of  yellow  fever  is  that  which  takes  place 
in  the  blood.  Many  of  the  red  cells  are  crenated  and  some  of  the  white 
cells  are  granular.  Free  haemoglobin,  hsemin,  and  hsematin  are  found  in  it 
owing  to  the  destruction  of  the  red  corpuscles. 

The  heart  is  soft  and  flabby,  and  minute  ecchymoses  in  its  muscular  tissue 
may  be  present.  The  pericardium  may  contain  an  excess  of  blood-stained 
fluid,  and  its  membrane  may  be  dotted  with  petechise. 


YELLOW  FEVER  215 

The  stomach  shows  changes  with  great  constancy.  It  usually  contains 
black  fluid  due  to  altered  exuded  blood;  its  mucous  lining  is  congested  in 
patches  and  is  marked  by  ecchymosis  or  even  softened.  When  placed 
under  the  microscope  sections  of  the  stomach  show  the  bloodvessels  engorged 
and  their  walls  undergoing  fatty  degeneration.  The  intestinal  canal  also 
contains  broken-down  blood  passed  from  the  stomach,  and  its  contents  may 
be  acid.  Fatty  degeneration  of  Peyer's  patches  and  the  glands  of  Lieber- 
kiihn  is  present. 

The  liver  is  often  paUid  or  yellow  in  hue,  and  its  cells  also  may  undergo 
fatty  change.  Councilman  states  that  associated  with  these  signs  of  fatty 
degeneration  areas  of  necrosis  can  be  demonstrated  in  every  case  that  comes 
to  autopsy. 

As  in  many  acute  and  severe  infections,  the  kidneys  show  signs  of  acute 
diffuse  nephritis  with  fatty  degeneration  of  the  cells  lining  the  tubules. 

Small  hemorrhagic  spots  are  sometimes  found  in  the  meninges  of  the 
brain  and  cord,  and  fatty  degeneration  of  the  cells  of  the  solar  plexus  has 
been  described. 

Symptoms. — A  very  noteworthy  fact  in  connection  with  the  symptom- 
atology of  yellow  fever  is  that  in  a  majority  of  cases  its  onset  is  most  abrwpt. 
There  may  be,  for  a  few  hours  before  the  well-defined  symptoms  show 
themselves,  a  sense  of  malaise  and  headache  or  vertigo.  The  first  symptom 
of  prominence  is  the  appearance  of  a  rigor,  or  rigors,  which  may  be  moderate 
or  severe,  but  Bemiss  states  that  chills  are  rare.  In  addition  the  patient 
suffers  from  severe  lumbar  and  muscular  pains,  headache  and  eyeache,  and 
marked  pallor.  There  is  often  epigastric  distress.  In  children  the  disease 
may  be  ushered  in  by  convulsions. 

After  the  stage  of  onset  the  skin  of  the  face  becomes  flushed  and  turgid ; 
the  mind  may  wander,  but  as  the  disease  develops  it  is  usually  remarkably 
clear  and  alert,  so  that  the  patient  watches  those  about  him  with  the  same 
degree  of  attention  as  is  often  seen  in  acute  peritonitis.  The  expression  is 
anxious.  The  temperature  rapidly  rises  so  that  it  reaches  its  acme  of  from 
103°  to  107°  by  the  end  of  twenty-four  or  thirty-six  hours. 

If  the  case  is  a  very  mild  one  the  febrile  movement  may  cease  as  early  as 
the  end  of  the  flrst  day  or  on  the  morning  of  the  second  day,  but  usually 
the  acme  of  the  temperature  is  maintained  for  from  two  to  three  days, 
during  which  time  there  may  be  slight  morning  and  evening  variations. 
In  cases  which  are  moderately  severe  the  fever  usually  begins  to  fall  after 
this  time  and  reaches  a  point  near  the  normal  in  from  twenty-four  to 
seventy-two  hours.     That  is,  the  fall  is  by  lysis. 

After  the  temperature  has  reached  normal,  that  is  when  the  stage  of 
remission  about  to  be  described  has  become  well  marked,  a  secondary  fever 
develops  which,  like  that  of  the  stage  of  onset,  lasts  from  two  to  three  days  and 
falls  by  lysis.     In  cases  which  are  likely  to  be  fatal  this  fall  may  not  occur. 

The  respiration  and  pulse  rate  are  at  first  increased  in  frequency  and  the 
individual  pulse  beat  is  increased  in  volume,  but  these  circulatory  condi- 
tions speedily  undergo  a  marked  change  with  the  approach  of  the  period  of 
remission.  On  the  second  or  third  day,  even  if  the  temperature  remains 
as  high  as  before,  the  pulse  rate  begins  to  fall,  or  falls  even  while  the  tern- 


216  DISEASES   DUE    TO   A    SPECIFIC   IXFECTIOX 

perature  is  still  rising,  so  that  a  pulse  rate  which  early  in  the  onset  was 
as  high  as  110  may  now  be  as  low  as  75.  . 

After  the  fever  begins  to  fall  owing  to  the  beginning  of  convalescence  the 
pulse,  as  in  many  cases  of  ordinary  catarrhal  jaundice,  may  fall  still  farther 
till  it  reaches  45  a  minute.  It  is  the  slowing  of  the  pulse  in  the  stage  of  onset, 
while  the  temperature  is  still  high,  that  is  particularly  worthy  of  note. 

The  tongue  is  covered  with  a  white  fur  save  at  its  edges,  which  are 
red;  the  bowels  are  constipaied,  and  there  may  be  epigastric  distress  fol- 
lowed by  the  vomiting  of  acid  mucus. 

The  urine  is  scanty  and  it  may  be  distinctly  albuminous  as  early  as  the 
third  day.  This  early  albuminuria  is  considered  by  yellow-fever  experts  to 
be  a  very  important  aid  to  diagnosis. 

By  the  third  day  a  very  marked  remission  in  the  symptoms  may  occur. 
The  pains  and  aches,  the  rapid  pulse,  the  high  temperature,  and  the  flushing 
of  the  face  all  become  modified.  The  gastric  symptoms  abate,  but  the  con- 
junctivae may  begin  to  be  jaundiced  and  the  skin  of  the  body  may  also  begin 
to  show  a  yellow  hue.  This  is  the  critical  period  of  the  disease,  for  the 
patient  is  now  "at  the  parting  of  the  ways."  One  path  leads  to  rapid 
recovery  with  marked  amelioration  of  all  the  s}Txiptoms;  the  other  leads, 
after  a  remission  of  from  twelve  to  forty-eight  hours,  to  a  recurrence  of  all 
the  dangerous  symptoms  in  an  aggravated  form. 

If  the  way  is  evil  there  is  prcecordial  and  epigastric  distress,  persistent 
vomiting  of  clear  liquid  mth  flakes  of  brown  reddish-looking  material,  which 
speedily  increases  in  amount  until  the  well-known  black  vomit  presents 
itself.  The  urine  is  more  scanty  and  more  albuminous  than  ever,  and  the 
general  state  of  the  patient  is  that  of  profound  illness.  The  temperature 
in  some  cases  rises  as  it  did  in  the  stage  of  onset,  but  it  may,  and  this  sign 
is  of  grave  import,  fall  below  normal.  Even  yet  it  is  possible  for  recovery 
to  occur  by  a  gradual  amelioration  of  all  the  symptoms,  but  usually  the 
symptoms  continually  get  worse.  The  grave  depression  increases,  the 
yellow  skin  develops  a  greater  degree  of  yellowness,  and  petechise  are 
formed.  The  vomiting  of  black  material  is  more  severe  and  profuse,  and 
hemorrhages  may  occur  from  other  mucous  membranes  than  that  of  the 
stomach.  The  scene  closes  with  hiccough,  profound  asthenia,  subsultus 
tendinum,  the  Hippocratic  face,  and  in  exhaustion  and  coma,  due  in  part 
to  the  direct  effect  of  the  infection  and  in  part  to  the  uraemia  produced 
by  the  intense  renal  lesions. 

While  these  may  be  considered  the  symptoms  of  yellow  fever  in  many 
cases,  in  others  they  are  very  different.  In  the  so-called  apoplectiform  type 
the  patient  is  seized  with  vertigo,  stupor,  unconsciousness,  and  convulsive 
attacks.  He  speedily  becomes  more  and  more  deeply  depressed,  his  circula- 
tion fails,  the  bowels  and  bladder  are  involuntarily  emptied,  and  with  the 
development  of  multiple  hemorrhagic  extravasations  he  dies. 

In  another  severe  type  the  symptoms  are  algid,  the  patient  speedily  pass- 
ing into  profound  collapse  with  a  subnormal  temperature  and  profuse  hemor- 
rhages, death  coming  on  in  a  few  hours.  In  still  another  type  the  violent 
vomiting,  purging,  and  collapse  may  cause  the  case  to  resemble  one  of 
cholera. 


YELLOW   FEVER  217 

Diagnosis. — It  is  stated  by  all  physicians  of  experience  that  in  some  cases 
it  is  almost  impossible  to  make  a  diagnosis  of  yellow  fever  in  its  early  stages, 
chiefly  because  it  has  few  pathognomonic  signs,  and  these  are  of  value  only 
when  associated  and  not  when  they  appear  singly.  Again,  many  cases  of 
yellow  fever  pursue  a  very  aberrant  course,  so  that  several  days  elapse  before 
the  diagnosis  can  be  made. 

Yellow  fever  must  be  separated  from  dengue,  pernicious  malarial  fever, 
from  malarial  haemoglobinuric  fever,  and  from  relapsing  fever.  The  dif- 
ferentiation of  yellow  fever  from  dengue  has  given  rise  to  much  bitter  con- 
troversy, and  even  at  the  present  time  physicians  of  wide  experience  with 
both  maladies  are  by  no  means  agreed  about  the  separation  of  these  diseases 
in  their  early  stages. 

Guiteras  asserts  that  there  are  three  notable  symptoms  of  yellow  fever 
which  are  of  service  in  this  connection.  First,  the  facial  expression  of  the 
yellow-fever  patient  is  characteristic  because  in  no  other  disease  is  it  so 
flushed,  the  eyes  so  injected,  nor  the  conjunctiva  so  icteroid  after  a  few  hours 
of  illness.  Second,  the  development  of  albuminuria  as  early  as  from  the  first 
to  the  third  day,  wdiich  may  be  transient  and  slight,  or  persistent  and  pro- 
fuse. The  third  differential  point  is  the  change  in  the  pulse  already  noted 
as  occurring  on  the  second  or  third  day  of  the  disease  during  the  continu- 
ance of  fever. 

The  jaundice  of  dengue  rarely  appears  as  early  as  the  third  day. 

The  history  of  the  patient  as  to  exposure,  the  presence  of  the  sestivo-autum- 
nal  parasite  in  the  blood,  and  the  enlarged  spleen  of  malarial  infection  point 
to  pernicious  malarial  fever.  A  porter-colored  urine,  the  blood  infection, 
and  the  enlarged  liver  point  to  hfemoglobinuric  fever,  while  the  discovery  of  the 
spirillum  of  Obermeier  in  the  blood  will  demonstrate  the  presence  of  relap- 
sing fever.  (See  Relapsing  Fever.)  While  all  these  facts  may  aid  greatly  in 
distinguishing  yellow  fever,  it  is  not  to  be  forgotten  that  the  absence  of  some 
of  them  does  not  prove  that  the  yellow  fever  is  not  present.  Thus  in  some 
cases  the  albuminuria  does  not  appear  very  early,  in  others  the  failure  to  dis- 
cover the  eestivo-autumnal  parasite  may  be  due  to  the  lack  of  skill  of  the 
observer  or  to  the  well-known  difficulty  of  its  discovery  even  by  the  most 
practised  observers.  xA.gain,  it  is  possible  for  the  malarial  parasite  to  be 
present  when  yellow  fever  is  present,  the  two  diseases  existing  simultaneously. 

Prognosis  and  Mortality. — In  a  disease  which  is  so  variable  in  its  manifesta- 
tions, prognosis  must  always  be  guarded.  If  the  febrile,  gastric,  and  renal 
symptoms  are  mild  in  the  stage  of  onset,  the  outlook  is  more  favorable  than 
if  they  are  severe.  If  the  period  of  remission  is  not  well  marked  and  hemor- 
rhagic tendencies  are  well  developed,  the  prognosis  is  bad. 

The  mortality  varies  very  greatly  in  different  epidemics,  as  already  shown 
in  the  discussion  of  the  history  of  the  disease.  Sometimes  it  is  as  low 
as  15  per  cent.,  again  as  high  as  85  per  cent.  It  is  apt  to  be  lower  in 
private  than  in  hospital  practice.  Some  authors  have  made  the  interesting 
statement  that  the  mortality  is  in  inverse  ratio  to  the  morbidity.  The  average 
mortality  may  be  stated  at  about  30  per  cent.  Thus,  in  25,220  cases  of 
yellow  fever  occurring  in  the  West  Indies,  Central  and  South  America, 
Mexico,  and  the  United  States,  8020  cases  were  fatal,  a  percentage  of  31.8. 


^218  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Treatment. — In  the  treatment  of  yellow  fever  it  is  essential  that  the  patient 
shall  have  a  plentiful  supply  of  fresh  air  and  sunshine,  with  absolute  rest  and 
proper  sanitary  surroundings.  Bad  hygienic  surroundings  always  greatly 
increase  the  mortality  of  the  disease. 

As  soon  as  the  patient  is  suspected  to  be  suffering  from  yellow  lever,  he 
should  be  put  to  bed  and  required  to  remain  there  until  convalescence 
has  been  completed,  for  physical  and  mental  unrest  distinctly  predispose 
the  patient  to  a  fatal  issue.  During  the  whole  period  of  the  disease  the 
patient  should  not  be  allowed  to  sit  up  in  bed,  since  sudden  cardiac  failure 
may  occur.  All  the  food  and  medication  should  be  given  to  the  patient 
when  in  the  recumbent  position,  and  the  contents  of  the  bowels  and 
bladder  emptied  into  a  bed-pan.  The  patient  should  be  lightly  covered, 
and  the  use  of  heavy  blankets  or  quilts  should  be  discouraged. 

Cleanliness  of  the  mouth  should  be  carefully  maintained,  since  otherwise 
softening  and  ulceration  of  the  gums  not  infrequently  occur. 

Active  medication  for  the  treatment  of  the  disease  itself  is  unwise.  The 
physician  should  give  only  remedies  when  they  are  very  distinctly  indicated, 
as  for  the  relief  of  a  failing  heart,  with  the  hope  of  increasing  the  activity  of 
the  kidneys  and  for  the  prevention  of  profound  asthenia.  In  some  portions 
of  the  world  where  yellow  fever  frequently  occurs,  it  is  customary  to  employ 
hot  mustard  foot-baths  and  even  hot  packs  during  the  early  stages  of  the 
disease,  but  they  are  unwise  after  the  malady  is  once  well  developed.  For 
the  relief  of  the  fever  cool  sponging  with  alcohol  and  water,  or  even  with 
ice-water,  may  be  employed,  an  ice-bag  being  applied  to  the  head.  The 
employment  of  the  coal-tar  products  is  never  advisable,  and  they  are  particu- 
larly contraindicated  when  the  depression  is  marked.  Many  practitioners 
have  employed  emetics  in  the  early  stages  of  yellow  fever,  but  these  are 
certainly  not  required  unless  it  is  known  that  the  patient's  stomach  is 
overloaded  with  food,  when  10  to  20  grains  of  ipecac  may  be  given. 

Many  years  ago  former  Surgeon-General  Sternberg  advised  the  employ- 
ment of  bicarbonate  of  soda,  corrosive  sublimate,  and  water  in  the  treatment 
of  yellow  fever,  but,  although  this  method  of  treatment  has  been  widely 
employed,  it  has  now  largely  gone  out  of  use,  although  large  quantities  of 
bicarbonate  of  soda  are  given  freely  by  many  practitioners  as  a  matter  of 
routine. 

As  in  most  infectious  diseases,  the  bowels,  if  constipated,  should  be  moved 
by  means  of  calomel,  which  in  turn  may  be  followed  by  one  of  the  saline 
purges  or  by  castor  oil.  Purgation  may  be  resorted  to  every  twenty- 
four  or  forty-eight  hours,  in  order  to  keep  the  bowels  thoroughly  evacuated. 
To  aid  the  purgatives  and  for  the  purpose  of  washing  toxic  materials  from 
the  large  intestines,  copious  irrigations  of  the  colon  with  normal  salt  solu- 
tion are  advisable.  The  patient  should  be  urged  to  drink  freely  of  water 
in  order  to  flush  the  kidneys,  and  alkaline  mineral  waters,  such  as  Vichy, 
Apollinaris,  or  Seltzer,  or  plain  water,  to  which  bicarbonate  of  soda  has 
been  added  in  small  quantities,  may  be  used  with  advantage  to  neutralize 
the  acidity  of  the  gastric  contents  and  to  act  as  diuretics. 
.  For  the  arrest  of  excessive  vomiting,  cocaine  has  been  highly  recommended, 
but  there  is  no  reason  to  believe  that  it  exercises  any  better  anti-emetic  prop- 


PLAGUE  219 

erties  in  this  disease  than  in  other  diseases  in  which  vomiting  is  present.  One 
or  2  minims  of  creosote  or  carbohc  acid  are  equally  valuable. 

For  the  purpose  of  stimulating  the  heart  and  circulatory  system,  digitalis 
in  the  dose  of  5  minims  of  the  tincture,  or  strychnine  in  the  dose  of  -^-j^  of 
a  grain,  or  caffeine  in  the  dose  of  1  or  2  grains,  may  be  given  three  or  four 
times  a  day,  and  if  collapse  is  threatened  the  strychnine  may  be  given 
hypodermically  with  atropine,  or  Hoffmann's  anodyne  may  be  given  by  the 
mouth  or  by  the  hypodermic  needle.  Strong,  black  coffee  may  also  be 
employed  by  the  mouth  or  by  the  rectum,  for  the  purpose  of  rallying  the 
patient. 

For  persistent  hiccough,  sipping  very  hot  water  is  often  advantageous. 

From  the  beginning  to  the  end  of  the  attack  it  is  the  duty  of  the  physician 
to  carefully  watch  the  condition  of  the  kidneys  by  making  daily  examinations 
of  the  urine,  since  uraemia  is  one  of  the  greatest  dangers  which  can  beset  the 
patient.  After  the  kidneys  have  once  become  so  inactive  that  the  urine 
is  exceedingly  scanty  it  is  often  absolutely  impossible  to  stimulate  them  to 
activity,  whereas  much  can  be  done,  if  from  the  very  first,  renal  activity  is 
maintained.  For  this  purpose  calomel  may  be  given  as  a  diuretic  in  the  dose 
of  2  or  3  grains  every  few  hours  for  one  or  two  days  at  a  time,  or  one  of  the 
diuretic  potassium  salts,  such  as  the  citrate  or  acetate,  in  large  amounts  of 
water.  Hypodermoclysis  with  normal  salt  solution  may  be  employed.  Renal 
congestion  may  be  overcome  by  the  application  of  mustard  plasters  and  dry 
cups  over  the  kidneys. 

During  the  acute  stage  of  the  illness  the  condition  of  the  stomach  is  such 
that  the  administration  of  food  is  almost  impossible,  but  milk  diluted  one- 
half  with  Vichy  water  or  with  water  containing  bicarbonate  of  sodium  may 
be  given. 

During  convalescence  the  greatest  possible  care  must  be  exercised  that  the 
patient  does  not  take  food  in  too  large  quantities.  No  solid  food  should  be 
permitted  before  the  end  of  a  week,  and,  if  the  patient  has  been  very  ill,  not 
for  two  weeks.  In  the  mean  time  the  diet  should  consist  of  partially  pepton- 
ized milk,  milk-toast,  broths,  and  eggs. 

As  in  all  exhausting  diseases,  the  physician  must  insist  upon  the  patient 
remaining  in  bed  until  the  heart  muscle  has  entirely  recovered  from  the 
profound  depression  of  the  disease.  Bitter  tonics,  such  as  iron,  quinine, 
and  strychnine,  may  be  given. 


PLAGUE  (BUBONIC  PLAGUE). 

Definition. — Plague  is  an  acute,  specific,  infectious,  and  contagious  dis- 
ease caused  by  the  Bacillus  pestis.  It  occurs  in  widespread  epidemics,  is 
characterized  by  fever,  inflammation  of  various  glandular  groups,  and  pro- 
found depression.  The  course  of  the  disease  is  exceedingly  rapid  and  the 
mortality  extremely  high. 

History  and  Distribution. — In  ancient  times  plague  occurred  in  pandemics, 
spreading  over  the  whole  known  world.  Most  of  the  old  world  epidemics 
about  the  beginning  of  the  Christian  era  have  been  described  as  plague  on 


220  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

wholly  insufficient  evidence.  Hirsch  dates  the  first  recognizable  epidemic  in 
the  second  century  B.C.  Following  this,  historical  descriptions  do  not  satis- 
factorily identify  the  disease  until  the  pandemic  which  persisted  for  nearly 
sixty  years,  during  which  time  it  ravaged  the  whole  of  Europe  (a.d.  542). 
Following  this  epidemic,  known  in  history  as  the  plague  of  Justinian,  the 
disease  appeared  from  time  to  time,  but  only  twice  to  so  great  a  degree. 
The  first  of  these  two  extensions  was  during  the  fourteenth  century;  the 
second,  known  as  the  Great  Plague  of  London,  began  in  1664  and  lasted 
until  1679.  During  the  first  year  of  this  epidemic  one-sixth  of  the  total  popu- 
lation of  London  perished.  The  advance  of  sanitary  science  since  that  time 
has  gradually  forced  plague  out  of  Europe  and  limited  the  area  of  its 
extension.  During  the  last  three  decades  it  has  lingered  in  Southeastern 
Europe. 

We  are  now  in  the  presence  of  what  must  be  considered  a  world-wide 
extension  of  the  disease,  limited  only  by  effective  preventive  measures. 
The  present  epidemic  began  in  Hong  Kong  in  1894.  In  1896  it  reached  the 
Presidency  of  Bombay,  and,  in  the  ten  years  following,  it  has  spread 
through  nine  British  provinces  and  fifty-one  native  States,  the  cases  increas- 
ing in  spite  of  all  restrictive  efforts.  It  is  estimated  that  to  the  middle  of 
the  year  1903  two  million  persons  have  perished  in  the  Deccan  since  the 
beginning  of  the  outbreak.  In  the  city  of  Bombay  over  one  hundred  thou- 
sand persons  have  died,  and  in  the  Presidency  of  Bombay  alone  during 
January,  1903,  the  deaths  averaged  eight  thousand  weekly.  Later,  the 
disease  appeared  in  Japan,  Madagascar,  and  South  Africa.  It  obtained 
a  temporary  foothold  in  Glasgow,  Lisbon,  and  Oporto.  In  1900  it  reached 
Sydney,  Australia.  On  the  American  continent  it  appeared  in  Brazil  and 
the  Argentine  Republic.  In  1899  it  established  a  foothold  in  San  Francisco, 
in  which  city  rigorous  measures  have  limited  it  to  a  very  great  degree. 
During  the  year  1902  the  disease  appeared  in  Peru,  Mexico,  and  Alaska. 

Etiology. — Plague  is  caused  by  a  specific  micro-organism  discovered  by 
Kitasato  and  Yersin  in  1894,  during  the  epidemic  in  Hong  Kong.  This 
organism  is  a  short,  oval,  non-motile,  coccobacillus  resembling  the  bacillus 
of  chicken  cholera.  It  occurs  singly,  joined  in  pairs,  and  occasionally  in 
long  chains.  It  is  found  in  large  numbers  in  the  pus  of  plague  buboes  and 
in  smaller  numbers  in  the  viscera  and  blood.  It  has  been  cultivated  from 
all  the  accessible  tissues  of  the  body  during  hfe,  and  from  all  the  excretions 
except  the  sweat.  It  has  also  been  recovered  from  the  floors  and  soil  in  the 
houses  of  patients  sick  with  plague. 

The  bacillus  stains  with  all  the  ordinary  staining  reagents  and  is  decolor- 
ized by  Gram's  method.  It  takes  up  the  stain  much  more  strongly  at  its 
poles.  Sometimes  a  capsule  is  observed,  but  there  is  no  spore  formation. 
It  grows  best  at  the  body  temperature  and  on  all  the  ordinary  media.  In 
fluid  culture  media,  overlaid  with  a  film  of  bland  cocoanut  oil,  the  bacillus 
grows  in  the  form  of  long  stalactites  hanging  from  this  oily  layer  that  are 
considered  characteristic  of  this  organism.  Its  viability  is  rather  low.  If 
kept  moist  and  cool,  it  may  keep  alive  and  virulent  for  months,  but  if  dried 
at  the  room  or  body  temperature  it  dies  in  from  three  to  four  days.  Exposure 
to  direct  sunlight  destroys  it  in  a  few  hours.    The  bacillus  is  pathogenic  for 


PLAGUE  221 

nearly  all  domestic  animals.  Indeed,  most  of  them  are  subject  to  plague 
and  aid  in  its  dissemination.  Sheep,  calves,  pigs,  ducks,  and  fowls  readily 
contract  the  disease,  and  the  bacilli  may  be  recovered  from  their  viscera 
and  excretions.  The  disease  also  occurs  in  bats,  and  the  common  rat  is 
peculiarly  susceptible  to  it.  The  great  mortality  among  rats,  preceding 
and  often  signalizing  an  epidemic  of  plague,  is  an  observation  that  was 
well  known  to  the  ancients. 

The  Chinese  Ions  ago  recognized  the  association  between  the  death  of 
the  rats  in  a  house  and  the  development  of  plague  a  few  days  later.  Fin- 
ally, the  fleas  that  infest  rats  and  the  flies  in  infected  houses  also  serve  to 
carry  the  contagion. 

The  method  of  conveyance  to  man  has  been  established  with  a  fair  degree 
of  certainty.  Inoculation  experiments  in  man  and  animals  have  shown 
that  when  virulent  bacilli  are  introduced  into  the  tissues  plague  develops. 
Thus  at  Cairo  in  1835  plague  blood  was  used  to  inoculate  two  criminals, 
but  though  they  developed  the  disease  both  recovered.  The  list,  too,  of 
physicians  and  laboratory  workers,  who  have  contracted  the  disease  from 
accidental  inoculation  and  dissection  wounds,  is  a  large  one.  Among  them 
may  be  mentioned  Whyte,  who,  in  1802,  infected  himself  and  perished, 
and  Aoyama  and  his  assistants  who  contracted  plague  from  dissection 
wounds. 

In  1898  three  deaths  occurred  in  Vienna  as  a  result  of  laboratory  inocula- 
tions, one  in  1899  in  Lisbon,  and  one  in  1902  in  Berlin,  while  thirteen  cases 
resulting  from  accidental  inoculations  in  postmortem  examinations  have 
been  collected  in  India. 

For  a  time  it  was  believed  that  man  was  infected  by  inhalation  of  the 
germ,  by  swallowing  it  on  infected  food,  and  by  direct  inoculation.  That 
infection  takes  place  through  air  and  food  has  not  been  substantiated. 
The  disease  enters  through  the  skin,  by  direct  infection  through  slight 
wounds  or  abrasions,  or  through  the  bite  of  suctorial  insects.  It  has  been 
shown  that  rats  sufi^er  more  intensely  perhaps  than  any  other  animal  from 
plague.  The  rats  are  infested  with  fleas,  which  are  also  infected,  and  the 
disease  is  transmitted  from  rat  to  rat  and  finally  from  rat  to  man  by  the  bite 
of  these  insects.  There  has  been  some  conflict  of  opinion  as  to  whether 
the  fleas  of  plague-infected  rats  would  bite  man.  To  settle  this  question 
Tidswell  examined  the  fleas  from  a  number  of  rats  and  found  five  varieties, 
of  which  four  were  known  to  attack  man. 

The  possibility  of  infection  taking  place  directly  into  wounds  and  abra- 
sions from  infected  soil  must  be  admitted.  Calvert  reports  an  interesting 
case  where  the  disease  was  acquired  in  sexual  intercourse,  and  one  case 
where  the  bite  of  an  infected  rat  caused  a  fatal  infection.  Direct  trans- 
mission from  patient  to  patient,  while  always  possible,  occurs  very  rarely. 
This  is  borne  out  by  the  observations  in  Bombay,  Hong  Kong,  and  other 
places,  that  cases  are  extremely  rare  among  the  physicians,  nurses,  quar- 
antine guards,  and  disinfection  laborers,  who  are  constantly  in  intimate 
contact  with  plague  cases. 

The  disease  principally  attacks  the  poorer  classes  of  the  native  popula- 
tion, those  who  live  in  the  slums  under  poor  hygienic  surroundings.    Lack 


222  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

of  personal  cleanliness  and  deficient  light  and  ventilation  in  living  rooms 
are  predisposing  causes. 

Frequency. — Plague  affects  all  ages  and  both  sexes  equally.  Neither 
geographical  location,  character  of  soil,  nor  elevation  have  any  influence  on 
its  spread.  It  prevails  at  all  seasons  of  the  year,  although,  generally  speaking 
it  is  least  active  in  the  seasons  of  greatest  heat  or  cold. 

Epidemics  begin  slowly.  The  common  history  is  that  in  the  beginning 
a  few  isolated  cases  develop,  the  epidemic  slumbering  along  in  this  way  for 
a  year  or  more  before  rapid  extension  takes  place.  It  declines  in  the  same 
way.  Not  only  do  the  number  of  cases  grow  less,  but  their  virulence  notably 
diminishes.  It  creeps  slowly  from  town  to  town,  following  the  routes  of  travel. 
Its  extension  from  one  country  to  another  over  sea  is  due  to  the  presence  of 
infected  rats  on  the  ships  plying  between  them.  Thus  the  epidemic  in  Peru 
was  shown  to  have  spread  from  the  rats  on  a  ship  carrying  grain  from  India. 

Symptoms. — Clinically  plague  may  be  divided  into  four  varieties: 

1.  Bubonic  plague,  pestis  bubonica,  malignant  adenitis. 

2.  Septicaemic  plague,  pestis  siderans. 

3.  Pneumonic  plague. 

4.  Larval  plague,  pestis  minor,  pestis  ambulans. 

Bubonic  Plague. — ^This  is  by  far  the  commonest  type,  averaging  80  per 
cent,  of  all  cases.  The  incubation  period  varies  from  two  to  eight  days, 
averaging  four  days. 

The  attack  begins  with  fever,  lassitude,  severe  headache,  and  pain  in  the 
limbs.  Rigors  may  or  may  not  be  present,  but  vomiting  is  usual  in  this 
stage.  There  is  drowsiness,  vertigo,  and  extreme  anxiety.  After  lasting 
from  twelve  to  twenty-four  hours,  fever  begins  and  the  temperature  ri^es 
rather  quickly  to  103°  to  107°.  There  is  now  hurried  pulse  and  respira- 
tion. The  face  is  heavy,  swollen,  and  flushed;  the  tongue  is  coated  with 
a  heavy  black  fur;  the  teeth  are  covered  with  sordes.  Vomiting  is  often 
persistent  and  diarrhoea  may  develop.  The  patient  is  most  profoundly 
depressed,  the  depression  being  out  of  all  proportion  to  the  duration  of  the 
disease,  and  a  low  muttering  delirium  is  present.  Death  may  occur  in  this 
stage,  accompanied  by  convulsions  and  collapse  or  by  urcemic  coma  with 
total  suppression  of  urine. 

In  from  twenty-four  to  seventy  hours — that  is,  from  the  third  to  the 
fifth  day  of  the  disease — the  characteristic  glandular  swellings  develop. 
The  glands  involved  are  in  the  groin  in  60  per  cent,  of  the  cases,  the 
axilla  in  35  per  cent.,  and  the  neck  and  angle  of  the  jaw  in  5  per  cent. 
The  buboes  are  usually  single  and  are  much  more  common  on  the  right 
side  than  on  the  left.  Occasionally  they  are  bilateral,  rarely  multiple.  In 
size  they  vary  from  a  pigeon 's  egg  to  the  size  of  a  fist.  They  are  frequently 
painful  and  always  exquisitely  tender. 

Coincident  with  the  development  of  the  buboes,  small  areas  of  gangrene 
of  the  skin,  carbuncles,  or  generalized  pustular  skin  lesions  may  develop. 

The  buboes  increase  in  size  for  three  or  four  days  and  then  become 
stationary.  In  a  small  proportion  of  cases  gradual  resolution  takes  place. 
In  the  larger  proportion  softening  and  suppuration  occur  and  the  bubo  is 
opened  or  ruptured  and  discharges  a  foul-smelling  pus.    At  this  stage  free 


PLAGUE  223 

suppuration  is  usually  a  good  omen.  If  the  pus  continues  scanty  and 
sanious  the  disease  remains  virulent. 

In  free  suppuration  the  bacilli  disappear  from  the  pus  in  a  very  few  days 
and  convalescence  is  rapidly  established.  In  the  cases  that  terminate  favor- 
ably a  marked  amelioration  is  observed  with  the  development  of  the  gland- 
ular swelling,  and  usually  about  the  seventh  day  the  temperature  falls  and 
the  profound  depression  disappears. 

Septicemic  Plague. — In  this  form  the  symptoms  are  much  more  severe 
and  the  stage  of  bubo  formation  is  lacking.  That  is,  there  is  no  one  gland 
or  group  of  glands  conspicuously  involved,  but  the  whole  glandular  system 
is  engorged  and  swollen.  The  essential  difference  seems  to  lie  in  that  the 
infection  is  more  severe  either  quantitatively  or  qualitatively.  There  is 
a  marked  bacterisemia.  Clinically,  these  cases  differ  from  the  former  in 
the  more  profound  depression,  more  moderate  fever  (100°  to  102°),  and 
the  greater  tendency  to  hemorrhages. 

Pneumonic  Plague. — This  form  begins  suddenly  with  rigors  and  all  the 
symptoms  of  acute  'pulmonary  inflammation.  Respiration  is  rapid  and 
labored  and  there  is  a  painful  harassing  cough.  So  far  the  symptoms 
resemble  an  ordinary  lobar  pneumonia.  The  sputum,  instead  of  being 
scanty,  tenacious,  and  of  the  usual  prune-juice  color,  is  copious,  watery, 
and  spotted  and  streaked  with  bright  blood.  Physical  examination  shows 
areas  of  consolidation  scattered  throughout  the  lungs.  An  entire  lobe  is 
rarely  involved.  This  form  of  the  disease  is  the  most  fatal  of  all,  patients 
rarely  surviving  after  the  third  day.  In  these  cases,  too,  although  it  is  not 
clinically  apparent,  postmortem  examinations  show  general  involvement 
of  the  glandular  system.  Pneumonic  plague  is  more  common  in  children 
than  in  adults,  and  at  the  beginning  of  epidemics  than  at  the  end. 

Hemorrhages  occur  in  all  the  various  clinical  types  of  plague,  more  com- 
monly perhaps  in  the  septicsemic.  They  appear  in  the  skin  as  petechioe  and 
ecchymoses.  There  may  be  epistaxis,  hcematuria,  and  hemorrhage  from 
the  stomach  or  bowel.    Haemoptysis  is  a  very  sinister  symptom. 

The  urine  is  diminished  and  commonly  contains  large  quantities  of  albu- 
min with  more  or  less  kidney  structure.  Albuminuria  is  never  absent  in 
severe  or  fatal  cases. 

The  blood  changes  are  not  characteristic.  There  is  a  marked  leuko- 
cytosis, varying  from  20,000  to  50,000,  with  moderate  reduction  of  the 
haemoglobin. 

Relapses  occur  in  a  small  percentage  of  cases  and  are  always  grave.  Con- 
valescence may  be  very  much  prolonged  by  indolent  ulcers  and  burrowing 
sinuses  at  the  seat  of  the  buboes. 

Larval  Plague,  Pestis  Minor. — Cases  of  this  type  occur  in  all  epidemics 
and  are  very  common  toward  their  close.  In  larval  plague  the  typical 
buboes  develop  with  few  prodromata.  The  constitutional  reaction  may  be 
very  mild,  the  fever  is  slight,  and  the  patient  is  but  little  annoyed  by  the 
disease.  Some  epidemics  are  characterized  by  large  proportions  of  such 
cases. 

Prophylaxis. — ^Personal  prophylaxis  should  be  directed  in  the  first  place 
to  avoiding  too  close  contact  with  plague  cases.     Nurses  and  physicians 


224  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

should  remain  as  short  a  time  as  possible  in  their  immediate  vicinity. 
Wounds,  abrasions,  and  skin  eruptions  on  the  limbs  should  be  carefully 
guarded,  particularly  against  a  germ-carrying  finger-nail.  Tight  leggings 
or  gaiters  should  be  worn  to  prevent  the  bite  of  fleas.  These  measures 
combined  with  personal  cleanliness,  a  good  water  supply,  and  abundant 
ventilation  are  efficient. 

The  general  measures  to  be  taken  for  the  prevention  of  plague  are,  first, 
strict  attention  to  sewage,  water,  ventilation,  and  cleanliness  of  dwellings; 
second,  the  extermination  of  rats  and  mice.  This  has  been  tried  on  a  large 
scale  by  trapping  and  poisoning.  Quarantine  has  never  been  an  effective 
check  to  this  disease. 

The  danger  from  contact  is  not  very  great.  Exposed  persons  should  be 
disinfected,  given  a  prophylactic  inoculation,  have  their  clothing  destroyed, 
and  then  be  released.  The  quarters  in  which  a  plague  patient  has  lain 
should  be  thoroughly  scraped,  disinfected,  and  repainted  or  whitewashed. 
Better  still,  when  practical,  they  should  be  burned.  The  evacuations  and 
bedding  of  the  sick  should  be  cremated 

In  spite  of  the  most  stringent  prophylactic  measures,  plague  is  very  diffi- 
cult to  control.  As  a  matter  of  fact,  where  it  has  once  attained  even  a 
slight  foothold  it  has  not  been  successfully  eradicated  by  any  of  these 
measures.  Witness  the  cases  in  San  Francisco,  where  after  several  years  of 
effort  the  disease  still  persisted.  It  seems  likely  that  the  most  we  can  expect 
with  our  present  means  is  to  hold  the  disease  in  check. 

Protective  Inoculation. — Haffkine  introduced  a  prophylactic  inocula- 
tion against  plague.  His  method  has  been  modified  by  Lustig  and  recently 
by  Besredky.  Briefly,  these  methods  consist  in  injection  of  plague  cultures 
killed  by  heat.  Extensive  experience  has  shown  that  these  inoculations 
confer  an  immunity  against  plague,  beginning  in  twenty-four  hours  and 
lasting  from  three  to  four  months.  Recent  studies  seem  to  show  that,  given 
during  the  period  of  incubation,  they  have  the  power  to  abort  the  disease 
in  many  cases.  This  system  of  protective  inoculation  was  being  tried  on 
an  extensive  scale  in  the  Punjab,  when  a  very  deplorable  accident  cut  the 
experiment  short.  After  more  than  100,000  persons  had  been  inoculated 
without  untoward  results,  nineteen  men  received  their  injection  from  the 
same  package,  developed  tetanus  on  the  fifth  day,  and  all  died.  This  unfor- 
tunate affair  practically  stopped  prophylactic  work  in  India  by  greatly 
increasing  the  aversion  the  natives  had  always  shown  to  it. 

Pathological  Anatomy.  —  The  visceral  lesions  of  plague  are  constant 
and  uniform.  Punctate  hemorrhages  appear  not  only  on  the  skin,  but 
throughout  the  whole  gastrointestinal  tract.  They  are  found  on  the  peri- 
toneum, pleura,  and  pericardium,  as  well  as  in  the  capsules  of  the  spleen, 
kidney,  and  liver.  The  cerebrospinal  system  is  congested  and  there  is  an 
increase  of  its  fluid.  The  liver  and  kidneys  are  hypersemic  and  the  spleen 
very  much  enlarged.  In  pneumonic  cases  the  bronchi  are  injected  and 
swollen  and  there  are  small  areas  of  consolidation  scattered  throughout 
the  lung.  The  pleural  cavities  frequently  contain  moderate  quantities  of 
seropus. 

The  glandular  system  shows  constant  involvement.  In  the  bubonic  form  the 


PLAGUE  225 

glands  appear  on  section  as  large,  diffused  masses,  with  extensive  hemorrhages 
into  their  substance.  This  appearance  is  not  confined  to  one  group  of 
glands,  but  extends  along  the  lymphatic  trunk  and  invades  the  glands  in 
the  immediate  proximity  to  the  main  buboes. 

Microscopically,  intense  hyperyemia  with  hyperplasia  is  found  not  only 
in  the  glandular  but  also  in  the  periglandular  structure.  Before  the  glands 
break  down  the  bacillus  pestis  is  found  alone;  after  suppuration  is  estab- 
lished other  organisms  are  found  with  it. 

In  the  septicsemic  and  pneumonic  cases,  or  in  those  cases  dying  before 
marked  bubo  formation  has  taken  place,  the  gross  changes  in  the  lymph- 
atic system  are  not  so  apparent,  but  there  is  always  enlargement  of  one 
or  more  groups  of  glands  or  slight  tumefaction  and  congestion  of  the 
entire  lymphatic  system.  The  pathological  process  is  identical  in  all 
the  types,  only  that  in  the  bubonic  form  the  intensity  of  the  affection  is 
expended  on  one  gland  or  group  of  glands,  while  in  the  other  form  the 
adenitis  and  lymphangitis  are  diffuse. 

Diagnosis. — In  the  presence  of  plague  in  epidemic  form  the,  rapid  onset 
of  the  disease,  the  profound  depression,  the  glandular  swelling  can  hardly 
suggest  anything  else  than  this  disease.  The  identification  of  the  bacillus 
pestis  in  the  blood,  in  fluid  from  the  buboes,  or  in  the  sputum  assures  the 
diagnosis.  Inoculations  and  culture  experiments  are  important  in  the 
early  stages  of  an  epidemic  with  large  numbers  of  atypical  cases  of  plague. 
The  best  routine  method  of  diagnosis  is  the  microscopic  examination  of  a 
drop  or  two  of  the  fluid  obtained  from  the  buboes  by  means  of  a  hypodermic 
syringe.  The  few  drops  of  bloody  lymph  collected  in  this  manner  contain 
large  numbers  of  bacilh.  The  diagnosis  of  the  pneumonic  form  can  only 
be  made  by  demonstrating  the  micro-organism  in  the  sputum. 

Prognosis. — Varying  in  different  epidemics,  the  average  mortality  runs 
from  70  per  cent,  to  95  per  cent.  The  variations  depend  on  the  stage  of 
the  epidemic,  the  proportion  of  pestis  minor  cases,  and  the  race  and  hygienic 
conditions  of  the  patients.  In  the  Hong  Kong  epidemic  the  average  mor- 
tality was  93  per  cent,  among  the  Chinese,  77  per  cent,  among  the  Indians, 
60  per  cent,  among  the  Japanese,  and  18  per  cent,  among  the  Europeans. 
This  gradation,  as  Manson  has  remarked,  is  "in  general  correspondence  with 
the  social  and  hygienic  conditions  with  these  different  nationalities." 

The  influence  of  the  type  of  the  disease  on  mortality  is  shown  in  the  follow- 
ing figures  from  an  analysis  of  13,145  cases.  In  the  bubonic  cases  the  mortality 
was  77.25  per  cent.,  in  the  pneumonic  cases  96.69  per  cent.,  and  in  the  sep- 
ticsemic  cases  89.62  per  cent. 

The  number  of  the  buboes  and  their  location  has  no  bearing  on  the  mor- 
tality. Visceral  hemorrhages  are  always  unfavorable  symptoms,  while  free 
suppuration  of  the  buboes  must  be  considered  as  a  very  favorable  omen. 

Pregnancy  complicating  plague  is  also  very  unfavorable.  Abortion 
invariably  occurs  and  death  is  almost  certain. 

Treatment. — ^Treatment  of  plague  is  wholly  symptomatic.    For  the  fever, 

headache,  and  dehrium  nothing  is  so  effective  as  cold  sponging.     Cantlie 

recommends  initial  purging  with  calomel  in  large  doses,  followed  by  salines. 

This  remedy  frequently  checks  vomiting  and  permits  nourishment  to  be  taken. 

15 


226  DISEASES  DUE   TO   A    SPECIFIC  INFECTION 

For  the  pain  and  restlessness  there  is  no  remedy  so  effective  as  mor- 
phine, given  hypodermicahy,  in  small  doses.  In  the  profound  depression 
and  collapse,  diffusible  stimulants  are  indicated;  ammonia  to  the  nose, 
mustard  to  the  skin,  and  ether  or  camphor  subcutaneously.  Alcohol  should 
be  given  freely,  particularly  in  a  septicsemic  form. 

Suppuration  of  the  buboes  should  be  hastened  by  poultices  and  hot 
fomentations.  When  fluctuation  occurs  they  should  be  opened  freely  and 
dressed  antiseptically. 

Thomson  reports  excellent  results  in  the  epidemic  in  Hong  Kong  from  the 
internal  use  of  carbolic  acid  in  large  doses.  He  gave  144  grains  daily  in 
doses  of  12  grains  every  two  hours  in  a  mixture  of  syrup  of  orange  and 
chloroform-water.  One  patient  took  over  2500  grains  of  pure  carbolic  acid 
before  his  blood  was  free  from  plague  bacilli.  Beyond  a  few  cases  of  car- 
boluria  no  toxic  symptoms  developed.  He  considers  this  the  most  hopeful 
method  at  our  disposal. 

Yersin,  Calmette,  and  Borrell  have  developed  an  antitoxic  serum  by  the 
injection  of  ascending  doses  of  cultures  killed  by  heat  into  susceptible 
animals.  Experimentally,  plague  in  animals  has  been  arrested  by  this 
means.  Clinically  the  results  with  the  antitoxic  sera  have  been  most  con- 
tradictory. While  they  have  not  entirely  fulfilled  the  hope  that  they  first 
seemed  to  hold  out,  later  experience  in  this  direction  is  more  encouraging. 
The  antitoxin  needs  further  study,  and  particularly  needs  standardization. 


CLIMATIO  BUBO. 

Definition. — Climatic  bubo,  tropical  bubo,  tropical  adenitis  (non-venereal), 
is  a  subacute  inflammation  of  the  lymphatic  glands  of  the  groin,  attended 
by  a  fever  remitting  in  type  and  persisting  from  three  to  four  weeks.  The 
disease  is  widely  distributed  in  tropical  climates.  It  occurs  on  the  coast  of 
Africa  and  Asia,  and  is  common  enough  in  the  Philippines,  Japan,  Malaya, 
the  West  Indies,  and  the  Mediterranean. 

The  disease  commonly  affects  individuals  living  together  under  the  same 
hygienic  conditions,  as  sailors  and  soldiers,  and  occurs  in  small  epidemic 
outbreaks.  There  is  some  evidence  to  show  that  its  origin  is  due  to  the 
entrance  of  bacterial  infection,  either  through  minute  wounds  in  the  legs 
and  genitals  or  the  bites  of  insects.  It  has  been  described  as  due  to  tropical 
heat  and  to  paludism,  as  a  sequel  to  dysentery,  and  even  as  a  form  of  bubonic 
plague  (pestis  minor).  Bacterial  evidence  disposes  of  the  last  theory,  but 
in  the  presence  of  epidemic  plague  these  cases  demand  careful  study. 

Symptoms. — They  begin  with  moderate  swelling,  redness,  and  tenderness 
of  the  inguinal  or  crural  glands  of  one  or  both  sides.  At  the  outset  there 
is  usually  a  chill,  fever  of  a  remitting  type,  headache,  and  backache.  The 
buboes  slowly  increase  until  they  attain  the  average  size  of  a  hen's  egg, 
after  which  the  fever  gradually  diminishes.  After  persisting  from  one  to 
two  months  or  longer  they  gradually  disappear.  In  the  large  majority  of 
cases  the  inflammation  is  limited  to  the  gland  structure  proper.  The  peri- 
glandular tissues  and  skin  are  not  involved  and  there  is  very  little  pain  or 


DYSENTERY  227 

tenderness.  In  from  3  per  cent,  to  5  per  cent,  of  all  cases  the  inflammation 
spreads  to  the  periglandular  tissues.  The  skin  becomes  adherent  over  the 
glands  and  they  finally  suppurate.  In  these  cases  the  constitutional  symp- 
toms are  intensified  and  the  pain  and  tenderness  are  very  great.  The 
abscesses  tend  to  burrow  freely.  After  a  period  of  free  suppuration  deep, 
sharp-edged,  indolent,  painful  ulcers  remain.  The  average  duration  of  the 
suppurating  cases  is  from  two  to  three  months. 

Treatment. — -The  febrile  condition  is  not  severe  enough  to  demand  special 
treatment.  Iodine  and  ichthyol  may  be  apphed  to  the  skin  over  the  gland, 
and,  after  acute  symptoms  subside,  mercurial  ointment  and  elastic  pressure 
should  be  used.  When  suppuration  takes  place  the  gland  must  be  laid 
open.  Rife  advises  calomel  as  a  dusting-powder  to  control  the  severe  pain 
in  the  chronic  ulcers. 

DYSENTERY. 

Definition. — Dysentery  is  a  condition  characterized  by  diarrhoea,  abdom- 
inal pain,  and  the  presence,  as  a  rule,  of  considerable  quantities  of  mucus 
in  the  stools.  When  the  condition  becomes  chronic  it  is  often  interrupted 
by  periods  in  which  constipation  supplants  the  diarrhoea.  Dysentery  is  to 
be  separated  from  the  diarrhoea  due  to  indigestion  and  to  catarrh  of  the 
small  bowel  by  the  facts  that  tenesmus  is  usually  marked,  the  lesions  are, 
primarily  at  least,  in  the  large  bowel,  and  the  stools  are,  in  the  early  part  of 
the  attack,  rather  scanty  and  consist  of  mucus  and  blood. 

It  is,  moreover,  to  be  distinctly  understood  that  dysentery  is  not  a  single 
disease,  but  that  this  term  is  applied  to  the  conditions  and  symptoms  which 
develop  as  the  result  of  several  distinct  causes,  although  at  present  there  is 
much  confusion  as  to  the  causes  of  the  various  forms.  Strictly  speakirg, 
amoebic  dysentery  should  be  classed  among  the  diseases  due  to  animal 
parasites,  but  it  is  best,  from  the  clinical  standpoint,  to  discuss  it  here. 

At  the  present  time  at  least  four  well-defined  types  of  dysentery  are 
recognized,  namely,  that  which  is  known  as  bacillary  dysentery,  which  is 
due  to  infection  with  the  specific  bacillus  of  Shiga,  or  a  bacillus  nearly 
related  to  it.  Second,  amoebic  dysentery,  intestinal  amoplicsis  (Musgrove 
and  Clegg),  which  is  due  to  the  Amoeba  dysenterice.  This  form  is 
found  in  all  parts  of  the  world,  but  is  much  more  frequent  in 
the  tropics,  from  whence  most  of  the  cases  seen  in  this  country 
come.  Strong,  of  the  United  States  army,  reports  561  cases  of  amoebic 
dysentery  out  of  1328  cases  of  dysentery  in  his  service.  Third,  catarrhal 
dysentery,  which  is  apparently  not  due  to  a  definite  infection,  but  to  acute 
congestion  of  the  mucous  membrane  of  the  colon;  and  finally,  fourth, 
diphtheritic  dysentery,  which  is  not  due  to  the  Klebs-Loeffler  bacillus,  but 
is  characterized  by  a  yellowish  exudate  on  the  mucous  folds  of  the  bowel 
with  areas  of  ulceration  and  necrosis.  A  form  of  catarrhal  dysentery  some- 
times also  develops  as  the  result  of  renal  disease. 

History  and  Etiology. — Epidemics  of  dysentery  have  occurred  since  the 
earliest  times,  and  Herodotus  mentions  one  which  attacked  the  army  of 
Xerxes  in  the  year  480  B.C.     During  the  first  part  of  the  Christian  era  the 


228  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

disease  raged  in  France,  Germany,  and  England.   It  has  existed  in  Europe  in 
pandemic  form  on  at  least  two  occasions,  namely,  in  the  years  1538  and  1779. 

In  the  year  1729  an  epidemic,  in  which  5000  persons  died,  occurred 
in  Holland,  Friesland,  Guilders,  and  Liege.  More  than  2000  of 
Napoleon's  soldiers  died  from  it  during  the  expedition  to  Egypt,  and 
4000  cases  occurred  in  the  English  army  during  the  Crimean  xvar. 
About  one-fourth  (288,000)  of  all  cases  of  sickness  among  the  soldiers  of  the 
War  of  the  Rebellion  were  said  to  be  cases  of  dysentery.  In  the  year  1890  an 
epidemic  broke  out  in  the  province  of  Tuhuoka,  Japan.  This  province 
had  a  population  of  1,231,387,  of  which  25,272  were  attacked.  Of  these 
25,272  cases  4742  proved  fatal.  Smaller  but  equally  fatal  epidemics  of  the 
disease  have  repeatedly  occurred  on  crowded  ships  and  in  periods  of  famine. 
Further  than  this  it  has  long  been  recognized  that  this  epidemic  form  of 
dysentery  was  distinctly  infectious,  and  it  can  even  be  spread  from  one  con- 
tinent to  another  by  infected  ships,  as  in  the  great  outbreak  in  the  United 
States  from  1846  to  1856,  when  it  was  probably  conveyed  by  emigrants 
from  Ireland,  where  the  disease  was  rampant.  More  recently  an  instance 
of  ship  conveyance  of  the  disease  has  been  reported  from  the  New  Hebrides. 
Davidson  states  that  in  the  decade  of  1841  to  1851  no  less  than  50,019 
persons  died  in  the  Irish  workhouses  from  dysentery. 

Marshy  lands  seem  to  have  a  pronounced  predisposing  influence.  Water 
which  has  been  contaminated  by  those  who  are  ill  with  the  disease  is  an 
important  factor  in  its  spread.  Alilk  and  solid  food  may  also  carry  the 
infection. 

Dysentery  in  its  various  forms  is,  in  a  large  proportion  of  cases,  the 
result  of  bad  sanitation  both  as  to  surroundings  and  diet.  It  is  much  less 
frequent  at  present  than  in  times  past,  and  rarely  ravages  modern  insti- 
tutions or  armies  as  it  did  fifty  years  ago. 

Epidemic  dysentery  being  exceedingly  prevalent  in  Japan  in  1897,  Shiga, 
a  Japanese  investigator,  became  interested  in  its  bacteriological  study,  and 
isolated  from  the  stools  of  36  patients  suffering  from  this  disease  a  shghtly 
motile  bacillus  having  rounded  ends  and  decolorizing  by  Gram's  method. 
When  brought  into  contact  with  the  blood  serum  of  patients  suffering 
with  dysentery  this  bacillus  usually  agglutinates  (as  does  the  typhoid  bacillus 
m  the  Widal  test),  although  in  a  few  mild  cases  the  reaction  fails  to  take 
place.  Flexner,  Strong,  Kruse,  Vedder  and  Duval,  ^^allard,  JMusgrave, 
Craig  and  Dopter,  Spronck,  Rosenthal,  and  other  investigators  have  isolated 
in  such  cases  organisms  which  they  consider  closely  related  to  or  identical 
with  the  one  observed  by  Shiga,  and  which  they  believe  to  be  the  cause  of 
acute  epidemic,  sporadic,  and  institutional  dysentery. 

Recently  (1902)  Duval  and  Bassett  have  obtained  a  similar  organism 
from  the  stools  of  children  suffering  from  dysentery  or  the  summer  diarrhoea 
of  infants.  Still  more  recently  (1903)  Wolf  stein.  Park,  Dunham,  and  Carey 
have  not  only  confirmed  these  findings,  but  have  shown  that  at  least  two 
bacilli  are  present  in  cases  of  cholera  infantum  and  dysentery.  One  of 
these  corresponds  to  Shiga's  bacillus,  but  they  believe  that  in  all  probability 
several  closely  allied  pathogenic  bacilli  will  be  found  responsible  in  different 
epidemics.    The  bacilli  are  found  in  numbers  proportionate  to  the  severity 


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Amoebse  from  Cases  of  Dysentery  and  Enteritis.     (Roemer.) 


DYSENTERY  229 

of  the  illness,  but  often  are  not  demonstrable  in  the  stools  until  the  latter 
are  typical  of  the  disease,  and  usually  only  after  the  lapse  of  five  to  seven 
days  of  illness.  Chantemesse  and  Widal  assert  that  a  bacillus  which  they 
found  in  the  stools  of  five  dysentery  patients,  and  which  they  also  recovered 
from  the  mesenteric  glands  and  intestinal  wall  of  a  patient  who  died  of 
dysentery,  is  identical  with  the  Shiga  bacillus,  and  as  their  observations 
were  made  in  1888,  ten  years  before  Shiga  published  the  results  of  his  work, 
they  claim  priority  of  discovery.  In  France  and  Italy  it  is  generally  con- 
ceded that  they  were  the  first  to  find  a  specific  organism  in  cases  of  dysentery. 

Our  recognition  of  the  presence  of  amoebce  in  cases  of  dysentery  dates 
from  1859,  when  Lambl  first  discovered  an  amoeba  in  the  stools  of  this  type 
of  diarrhoea.  Later  the  parasite  was  studied  by  Losch  (1875)  and  Kartulis, 
but  it  was  not  until  Osier  (in  1890),  Councilman,  and  Lafleur  (1891)  reported 
upon  its  presence  in  several  cases  of  dysentery,  and  in  the  past  decade,  that 
it  ^ceived  the  attention  that  it  deserves.  Leukart  has  placed  the  Amoeba 
dysenterice  in  the  class  of  rhizopoda  of  the  Protozoa.  Schandinn  calls  it 
Entamoeba  histologica  or  Entamoeba  dysenterioe. 

The  Amoeba  dysenteries  is  a  spheroidal  cell,  four  or  eight  times  the  size  of 
the  red  blood  cell.  It  consists  of  two  parts,  an  internal  part  called  the 
endosarc,  or  endoplasm,  and  an  external  part  called  the  ectosarc,  or  ecto- 
plasm. These  two  parts  cannot  always  be  clearly  recognized  when  the 
organism  is  at  rest,  but  they  are  easily .  identified  when  motion  is  present. 
The  endosarc  makes  up  the  greater  part  of  the  body  and  its  granules  may 
be  fine  or  coarse.  In  this  portion  several  vacuoles  are  not  rarely  found 
and  a  distinct  nucleus  is  discernible  when  the  organism  is  stained.  As  in 
ordinary  amoebae  the  Amoeba  dysenterioe  often  contains  foreign  bodies  such 
as  red  blood  cells,  and  even  bacteria.  The  pseudopod,  or  arm,  which  is 
protruded  from  the  amoeba  when  it  is  engaged  in  amoeboid  movement,  is 
of  the  hyaline  ectosarc.     (See  Plate  IV.) 

In  addition  to  this  particular  amoeba  other  forms  have  been  described 
by  Quincke  and  Roos  and  other  writers.  One  of  these  is  much  larger  than 
that  just  described,  called  the  Amoeba  intestini  vulgaris,  which  is  not  capable 
of  producing  dysentery  in  man.  The  other  is  the  Amoeba  colimitis,  which  is 
pathogenic  for  man.  It  also  is  far  larger  than  the  amoeba  coli  of  Losch — that 
is,  the  Amoeba  dysenterioe  of  Councilman  and  Lafleur.  The  latter  parasite  is 
found  in  the  stools  of  acute  and  chronic  dysentery,  in  the  floors  of  the  intes- 
tinal ulcers,  and  in  the  secondary  abscesses  which  it  is  prone  to  produce. 

It  is  to  be  distinctly  understood  that  two  distinct  types  of  infectious  dysen- 
tery exist,  one  due  to  the  bacillus  of  Shiga  and  one  to  the  Amoeba  dysenterioe 
Indeed,  a  third  division  due  to  the  Balantidium  coli  may  be  made  Savalier 
has  collected  75  cases  of  this  character  and  our  own  Strong  has  reported 
others. 

Amoebic  dysentery  may  occur  at  any  age  from  infancy  to  senility,  but  it 
is  most  common  between  twenty  and  thirty  years  of  age.  It  is  much  more 
common  in  men  than  in  women.  Thus,  in  119  cases  reported  by  Futcher  108 
were  males. 

Prevention.— Dysentery  in  all  its  forms  is  to  be  prevented  by  the  use  of 
boiled  water  and  cooked  foods,  by  the  establishment  of  proper  drainage, 


230  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

and  by  the  avoidance  of  cold  and  wet.  Persons  who  are  subject  to  catarrh 
of  the  colon  and  rectum  should  wear  a  flannel  binder.  When  the  disease 
develops,  the  stools  of  the  patient  should  be  thoroughly  destroyed  and  the 
greatest  care  exercised  that  the  food  and  drink  of  the  healthy  are  not 
contaminated  by  his  discharges. 

Frequency. — Until  very  recently  it  was  generally  supposed  that  amoebic 
dysentery  was  the  type  of  the  disease  most  commionly  met  with  in  the 
United  States,  but  now  that  Shiga's  bacillus  has  been  found  in  many  cases 
of  sporadic  and  epidemic  diarrhoea  in  this  country  it  must  be  regarded  as 
the  less  frequent  form  of  the  two.  Indeed,  it  would  seem  probable  that 
many  of  the  cases  hitherto  regarded  as  catarrhal  are  due  to  this  bacillus. 
(See  also  Cholera  Infantum.) 

Pathology  and  Morbid  Anatomy. — In  bacillary  dysentery,  when  death  has 
occurred  in  the  first  week,  the  autopsy  reveals  the  mucous  membrane  of 
the  colon  to  be  intensely  corrugated  and  swollen,  so  that  its  natural  rugosities 
are  greatly  emphasized,  while  over  them  is  spread  an  easily  detached  layer 
of  superficial  epithelium,  which  has  undergone  necrotic  changes.  Numerous 
spots  of  ecchymosis,  or  hemorrhage,  into  the  mucous  membrane  are  often 
present,  but  ulcers  are  not  found,  although  the  necrotic  process  just  named 
may  be  so  severe  that  a  superficial  gangrene  may  be  present.  When  the 
inflammation  is  very  intense  the  whole  thickness  of  the  bowel  wall  may  be 
indurated,  and  even  the  visceral  peritoneum  may  be  infected.  In  some 
instances  an  associated  inflammation  of  the  small  bowel  is  present,  some-, 
what  similar  changes  being  present  in  its  coats. 

Shiga  described  the  morbid  process  of  acute  bacillary  dysentery  as  a 
catarrhal  inflammation  proceeding  to  hemorrhagic,  diphtheritic,  or  ulcerative 
inflammation.  Kruse  also  observed  diphtheritic  membranes  in  eight  cases 
which  came  to  autopsy,  and  Flexner  recognizes  the  tendency  to  their 
formation,  although  he  did  not  find  any  in  the  cases  which  he  examined 
postmortem  in  the  Philippines. 

Craig  has  reviewed  the  morbid  anatomy  of  chronic  cases  of  infectious  or 
bacillary  dysentery,  recognizing  follicular,  diphtheritic,  and  gangrenous  stages. 
In  the  first  the  coats  of  the  colon  usually  are  thickened,  and  the  follicles,  par- 
ticularly of  the  caecum,  ulcerated.  The  mucosa  is  of  a  gray-slate  color,  and 
shows  patches  of  acute  congestion ;  the  gut  is  narrowed,  but  there  are  areas 
of  dilatation.  The  ulcers  appear  at  the  summit  of  the  follicles  as  minute, 
ragged  erosions.  Later  the  necrotic  areas  extend,  and  their  margins  appear 
stamped  out,  but  undermined.  The  ulcers  measure  ^  to  |  cm.,  but  may 
attain  diameters  of  1.5  cm.  and  extend  to  the  submucosa  or  muscular  layer. 
Cicatrized  and  open  ulcers  may  be  found  together.  In  the  diphtheritic 
stage,  which  may  be  implanted  on  the  follicular,  the  colon  is  grayish  or 
greenish-blue,  marked  by  red  or  dusky-brown  areas  and  greatly  thickened. 
The  mucosa  becomes  necrotic,  exfoliates  in  masses  or  irregular  patches 
composed  of  granular  detritus,  leukocytes,  and  innumerable  bacteria.  Ulcer- 
ation practically  always  accompanies  the  formation  of  the  membrane.  The 
gangrenous  stage  seems  but  an  intensification  of  the  diphtheritic.  The 
serosa  is  more  affected,  and  matted  adhesions  are  the  rule.  The  necrotic 
colon  is  easily  torn,  greenish-black,  and  marked  by  inky-black  areas.    The 


DYSENTERY  231 

ileocsecal  region  is  sacculated,  and  the  sigmoid  flexure  and  rectum  dark 
olive-green  in  color.  Tumefied,  purulent  elevations  show  through  the  serous 
coat.  Internally  the  mucosa  shows  an  indescribable  admixture  of  necrotic 
or  gangrenous  lesions,  with  purulent  suffusion  of  all  the  coats  of  the  colon. 
In  each  of  the  foregoing  forms  parts  of  the  mucosa  escape,  and  these  manifest 
more  or  less  catarrhal  inflammation.  The  protean  manifestations  of  bacillary 
dysentery,  both  acute  and  chronic,  are  so  influenced  by  the  pathogenicity  of 
the  infecting  organism,  the  activity  of  mixed  or  associated  infection,  suscept- 
ibility of  the  patient,  duration  of  the  process  and  other  factors  that  an  exact 
description  is  impossible. 

The  noteworthy  difference  between  the  lesions  produced  in  children  and 
adults  by  the  Bacillus  dysenterice  is  that  in  the  former  the  solitary  and  agmin- 
ated  lymphatic  tissues  are  much  more  commonly  and  more  severely  affected 
than  in  adults. 

The  lesions  of  amcebic  dysentery  are  quite  different  from  those  of  bacillary 
dysentery.  In  the  first  place  the  ulceration  is  confined  almost  entirely  to 
the  large  intestine,  although  the  lower  part  of  the  small  intestine  may  be 
slightly  affected.  The  submucous  tissues  become  infiltrated  and  swollen 
in  patches,  which  project  above  the  level  of  the  normal  mucous  membrane. 
These  infiltrated  areas  undergo  necrosis  and  slough  away,  leaving  ulcers 
which  may  be  superficial  or  deep,  and  which  may  extend  as  far  as  the 
peritoneal  coat  of  the  intestine,  but  perforation  is  rare.  They  are  often 
very  large  and  extend  laterally  as  well  as  downward.  The  edge  of  the  ulcer 
may  be  undermined  and  the  floor  honeycombed.  Not  rarely  the  extension 
laterally  takes  place  under  the  mucosa  or  dissects  the  muscle  coat  so  that 
there  is  only  a  small  opening  to  a  large  area  of  necrotic  tissue.  Occasionally 
the  submucosa  is  necrotic  without  evident  superficial  lesions.  The  amoehce 
are  found  in  the  ulcers  in  the  neighboring  lymph  spaces  and  sometimes  in 
the  bloodvessels  of  the  part,  but  there  is  an  extraordinary  lack  of  pus  when 
the  severity  of  the  necrotic  process  is  considered. 

When  recovery  takes  place  fibrous  tissue  covered  by  epithelium  closes  the 
spaces  made  by  the  ulcers,  and  as  these  scars  contract  strictures  may 
develop.  The  colon  becomes  thickened  and  it  may  be  adherent  to  the 
adjacent  structures  and  uneven  contractions  form  pockets  in  which  the 
parasites  may  linger  after  apparent  clinical  recovery.  The  appendix  may 
be  involved. 

The  changes  in  the  liver  in  amcebic  dysentery  consist  of  two  alterations. 
The  first  are  multiple  areas  of  local  necrosis,  and  secondly  abscess,  either 
single  or  multiple.  The  single  abscesses  are  usually  large  and  in  the  con- 
vexity of  the  right  lobe,  or  else  in  the  concavity  of  the  liver  where  it  lies 
nearest  the  large  bowel.  Roux  has  collected  639  cases  of  amoebic  abscess 
of  the  liver.  Of  these,  435,  or  70.8  per  cent.,  were  in  the  right  lobe;  85,  or 
13.3  per  cent.,  were  in  the  left  lobe,  and  2,  or  0.3  per  cent.,  were  in  the 
lobus  Spigelia.  The  multiple  abscesses  are  usually  small  and  widely  scat- 
tered and  often  near  the  surface.  It  is  noteworthy  that  these  so-called 
abscesses  do  not  contain  true  pus  unless  secondary  infection  with  pus 
organisms  has  occurred.  They  are  composed  of  a  grumous  material  made 
up  of    a  thick,  coarse,  irregular    reticulum,  in   the  meshes  of    which  lie 


232  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

the  semi-fluid  contents.  As  the  area  increases  in  size  the  fluid  becomes  red- 
dish, brownish,  greenish-yelloWj  or  chocolate  color,  and  is  mixed  with  pieces 
or  shreds  of  broken-down  hepatic  tissue.  Amoebae  may  be  found  in  the 
contents  of  these  cavities. 

Abscess  of  the  liver  due  to  the  Amoeba  dysenterioe  nearly  always  develops 
in  the  first  few  weeks  of  the  disease.  Occasionally  one  of  the  larger 
abscesses  ruptures  into  the  right  lung.  (See  Complications.)  Boston  has 
collected  statistics  of  2340  cases  of  amoebic  dysentery.  Of  these,  486,  or  20  per 
cent.,  suffered  from  hepatic  abscess.  (See  Hepatic  Abscess.)  The  percentage 
varies  from  60  per  cent.  (Kartulis)  to  21  per  cent.  (Councilman  and  Lafleur.) 

A  valuable  contribution  to  the  subject  of  the  associated  lesions  of  dysentery 
has  been  made  by  Craig,  of  the  United  States  Army  Medical  Staff.  Analyzing 
120  cases  of  dysentery,  of  which  60  were  of  the  bacillary  and  60  of  the  amoebic 
type,  he  found  that  in  nearly  every  instance  the  autopsy  revealed  an  increase 
in  the  cerebrospinal  fluid  and  oedema  of  the  brain.  In  the  amoebic  cases  an 
intense  congestion  of  the  cerebral  vessels  was  also  present,  and  in  50  per 
cent,  minute  capillary  hemorrhages  were  present.  In  the  bacillary  cases,  on 
the  other  hand,  the  brain  seemed  unduly  ansemic.  In  the  respiratory  system 
bronchopneumonia  is  the  most  common  lesion  in  the  bacillary  disease.  Craig 
believes  that  fully  60  per  cent,  of  the  cases  of  dysentery  seen  in  the  San 
Francisco  Military  Hospital  have  coincident  nephritis,  and  of  the  120  cases 
already  cited  no  less  than  101  had  this  condition,  usually  of  the  parenchyma- 
tous type.  More  cases  of  nephritis  occur  in  the  amoebic  than  in  the  bacillary 
type. 

In  the  acute  catarrhal  form  there  is  a  free  production  of  mucus  which 
coats  the  surface  of  the  lower  bowel,  chiefly  in  the  sigmoid  flexure  and 
rectum.  This  mucus  is  filled  with  exfoliated  epithelium,  some  of  which  has 
undergone  fatty  degeneration.  Not  infrequently  blood  cells  are  present  in 
the  mucus.  When  the  inflammatory  process  is  severe,  marked  congestion 
and  infiltration  of  the  mucous  membrane  and  submucosa  may  be  present, 
and  even  a  purulent  and  superficial  ulceration  may  occur. 

The  diphtheritic  type  is  characterized  by  congestion  of  the  mucous  mem- 
brane and  the  development  upon  its  surface  of  a  false  membrane.  The 
connective  tissue  under  it,  and  between  the  glands,  is  infiltrated  and  filled 
with  fibrin  and  pus.  In  cases  in  which  the  process  is  very  active,  the  inflam- 
mation may  reach  not  only  the  muscular  coats,  but  even  the  peritoneal  coat. 
The  area  covered  by  the  false  membrane  varies  greatly  in  different  cases. 
In  some  only  the  rectal  mucous  membrane  is  affected,  in  others  a  con- 
tinuous exudate  covers  the  entire  colon,  and  in  still  others  it  appears  in 
scattered  patches.  If  the  process  is  severe  healing  takes  place  by  sloughing 
of  the  necrotic  tissues,  which  may  reach  to  the  deeper  layers  of  the  bowel, 
leaving  ulcers  which  gradually  undergo  cicatrization,  or  the  ulcers  remain 
granulating  surfaces  for  months  and  only  heal  under  direct  treatment. 

Symptoms. — ^The  symptoms  of  all  the  various  forms  of  dysentery  are 
closely  similar.  The  onset  is  usually  sudden,  or  it  may  develop  in  the  course 
of  a  gradually  increasing  diarrhoea,  which  at  flrst  is  thought  to  be  an  ordinary 
attack  of  looseness  of  the  bowels.  The  patient  suffers  from  wretchedness, 
which  is  thought  to  be  the  result  of  the  intestinal  disorder,  and  often  has, 


DYSENTERY  233 

In  the  earliest  stages,  a  considerable  degree  of  griming  fain.  The  initial 
diarrhea  soon  sweeps  the  bowels  clean  of  their  normal  contents,  and  as 
soon  as  this  is  accomplished  the  stools  become  scanty  and  consist  largely 
of  mucus  which,  not  rarely,  contains  blood.  The  griping  pain  increases  in 
violence,  and  there  is  marked  tenesmus  which  often  causes  the  patient  to 
break  out  in  a  profuse  sweat.  The  rectal  irritation  causes  a  constant  desire 
to  go  to  stool,  which  is  not  satisfied  by  the  small  evacuation  that  occurs. 
At  first  the  constant  irritation  of  the  anus  may  cause  spasm  of  the  sphincters, 
but  later  when  the  disease  is  severe  the  sphincter  ani  may  become  relaxed, 
and  even  rectal  prolapse  may  ensue.  The  centres  in  the  spinal  cord  con- 
trolling the  bladder  become  reflexly  irritated  and  difficult  urination  may 
add  to  the  suffering  of  the  patient. 

It  is  manifest  that  such  symptoms  must  speedily  cause  grave  systemic 
disturbance  by  reason  of  the  loss  of  nutritive  material,  the  constant  pain, 
the  loss  of  sleep  and  straining,  and  so  the  pulse  soon  becomes  rapid  and 
feeble,  and  the  patient  rapidly  emaciates  not  only  because  of  the  reasons 
just  cited,  but  also  because  the  local  lesion  in  the  bowels  soon  results  in 
general  systemic  infection,  either  with  the  specific  cause  of  the  attack  or 
with  other  micro-organisms  which  gain  access  to  the  general  system  through 
the  diseased  intestinal  wall. 

The  tongue  is  very  foul  and  the  secretions  of  the  mouth  scanty. 

If  the  disease  persists  the  scanty  mucous  stools  may  be  supplanted  by 
more  profuse  serous  discharges,  which  are  often  reddish  in  hue,  and  seem  to 
contain  small  particles  of  flesh  (probably  bloody  mucus  and  mucous  mem- 
brane). This  fluid  is  highly  albuminous.  The  debility  and  emaciation  of 
the  patient  speedily  becomes  profound,  as  the  loss  of  fluid  and  albumin 
continues.  Whether  the  stools  are  mucous  or  serous,  they  are  fetid  and  have 
an  odor  which  is  quite  characteristic. 

In  that  form  of  dysentery  called  bacillary  the  fever  at  first  may  rise  as 
high  as  103°,  but  in  the  amoebic  form  the  temperature  is  usually  not  greatly 
disturbed  unless  secondary  abscess  develops.  It  rarely  rises  above  102°, 
and  may  be  subnormal  after  the  stage  of  onset. 

When  the  infection  with  Shiga's  bacillus  is  very  virulent,  death  from 
toxaemia  and  exhaustion  may  occur  as  early  as  the  fourth  day,  but,  on  the 
other  hand,  the  case  may  last  for  much  longer  periods  before  the  fatal  result 
ensues.  There  is  sometimes  met  a  subacute  form,  which  lasts,  in  a  modified 
type,  for  weeks  or  even  months. 

Cases  of  amoebic  dysentery  may  be  divided  into  three  types :  (a)  A  mild 
form  in  which  the  general  health  remains  good,  although  the  number  of 
stools  may  vary  from  two  to  six  in  a  day.  (b)  A  moderately  severe  form  in 
which  the  general  health  is  greatly  impaired  and  there  is  much  loss  of 
flesh,  with  an  evening  rise  of  temperature  and  frequent  stools,  (c)  A  very 
severe  type  is  met  with  in  which  the  prostration  and  loss  of  weight  are 
extreme,  the  stools  are  bloody  and  very  frequent,  and  the  extremities 
cold.  In  all  these  cases  the  patient  may  without  any  apparent  cause  pass 
to  better  or  worse  with  extraordinary  speed. 

Amoebic  dysentery  may  cause  death  in  a  few  days  or  last  for  weeks,  and 
may  cause  death  finally  by  the  secondary  abscesses  in  the  liver.    Free  hem- 


234  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

orrhages  from  the  bowel  may  also  occur  in  this  form,  and  perforation  from 
deep  ulcers  is  recorded.  A  chronic  form  of  amoebic  dysentery  also  exists 
which  lasts  for  months  and  has  temporary  periods  of  constipation.  These 
periods  of  constipation,  if  abscess  does  not  develop,  give  the  patient  an 
opportunity  to  be  nourished,  and  so  he  may  be  able  to  retain  strength 
and  flesh. 

In  the  acute  catarrhal  form  of  dysentery  there  may  be  fever  at  onset  and 
scybalous  masses  will  often  be  found  mixed  with  the  mucus  which  is  expelled. 
After  an  illness  of  from  four  to  seven  days  the  quantity  of  blood  in  the 
stools  is  decreased,  and  they  become  less  frequent.  Marked  abdominal 
tenderness  over  the  course  of  the  large  bowel  is  usually  present  in  all  cases. 

In  the  acute  diiphtheritic  form  the  patient  is  usually  extremely  ill  from 
the  very  first.  The  systemic  depression  is  marked  and  profound  adynamia 
is  quickly  developed.  The  belly  is  diste?uled  and  painful  upon  pressure. 
Bloody  mucus  is  not  uncommonly  absent  from  the  stools.  Just  as  in  the 
other  forms  so  in  this,  a  subacute  or  chronic  type  is  met  with  in  which  the 
abdominal  signs  are  mild  and  the  number  of  stools  a  day  are  as  low  as 
four  or  five. 

Complications  and  Sequelae. — Perforation  of  the  bowel  has  already  been 
named  as  a  possible  sequel  of  the  amoebic  form  of  the  disease.  In  other 
instances  a  localized  peritonitis  develops,  and  as  the  result  of  infection  of 
the  tissues  about  the  colon  a  perityphlitis  or  periproctitis  comes  on.  Rupture 
of  an  hepatic  abscess  is  a  very  frequent  occurrence.  The  pus  finds  its  way 
through  the  diaphragm  into  the  right  lung  or  right  pleural  space-  Rarely 
it  has  burst  into  the  duodenum  and  even  into  the  vena  cava,  or  backward 
and  downward  along  the  psoas  muscle,  or  into  the  kidney.  Even  the  peri- 
cardium and  the  bladder  may  be  perforated.  Strong  has  called  attention 
to  the  occurrence  of  profuse  intestinal  hemorrhage. 

In  many  epidemics  of  dysentery  there  is  associated  mild  or  severe  malarial 
infection  which  renders  the  case  diflScult  of  treatment  in  that  two  infections 
have  to  be  controlled  simultaneously.  Septic  arthritis,  pericarditis,  and 
endocarditis  sometimes  occur  as  terminal  infections.  (See  Pathology  and 
Morbid  Anatomy.) 

Diagnosis. — The  diagnosis  that  the  patient  has  acute  inflammation  of  the 
large  bowel,  and  is  therefore  suffering  from  dysentery  in  one  of  its  forms, 
is  easily  made  if  the  symptoms  just  described  are  present.  It  is  not, 
of  course,  so  easy  to  determine  which  of  the  several  forms  of  dysentery  is 
present.  The  bacillary  form  is  separated  from  the  amoebic  variety  by  the 
presence  of  marked  fever,  which  is  usually  absent  in  the  latter  disease;  by 
the  discovery  of  the  specific  bacillus  in  the  stools,  which  discovery,  however, 
requires  special  training  in  searching  for  it;  and  by  the  agglutination  test 
of  the  baciUus  with  the  patient's  blood  serum,  which,  as  in  the  case  of  the 
Widal  test  of  the  blood  in  typhoid  fever,  gives  us  such  valuable  informa- 
tion. This  reaction  is  uncertain  in  the  first  week,  often  positive  after  the 
sixth  day,  but  in  some  cases  it  does  not  occur  for  two  weeks.  For  this 
reason  it  does  not  possess  great  diagnostic  importance  in  the  early  stages 
of  the  disease.  To  be  of  value  it  must  take  place  in  a  dilution  of  1 :  200. 
The  percentage  of  positive  reactions  according  to  Rosenberger  is  80.2  per  cent. 


DYSENTERY  235 

The  amoebic  variety  can  only  be  recognized  during  life  by  finding  the 
amoeba  in  the  stools.  This  requires  some  practice  and  skill.  The  small  pieces 
of  blood-stained  mucus  are  the  parts  in  which  the  organism  is  to  be  sought  for, 
first  with  a  low-power  and  then  with  a  high-power  lens.  (See  Plate  IV.)  The 
light  coming  through  the  instrument  should  be  stopped  down  by  an  appro- 
priate diaphragm.  Several  negative  examinations  do  not  exclude  amoebic 
dysentery,  and  particularly  in  chronic  cases  it  is  necessary  to  make  repeated 
examinations.  In  such  cases  acute  exacerbations  may  afi^ord  stools  relatively 
rich  in  amoebae  even  when  intercurrent  examinations  have  been  negative 
several  times.  The  stools  should  be  as  fresh  as  possible,  unmixed  with 
urine,  and,  if  not  warm,  the  slide  examined  should  be  warmed  gently  or 
placed  on  a  warm  stage  so  as  to  induce  movements  of  the  amoebse.  If  an 
organism  which  possesses  active  amoeboid  movement  is  discovered  and  if 
it  contains  several  red  blood  cells  the  diagnosis  is  practically  assured. 

When  examining  the  stools  it  is  essential  to  bear  in  mind  that  a  multitude 
of  intestinal  bacteria  are  also  present  and  that  various  parasites  other  than 
the  specific  amoeba  may  be  present.  Thus,  the  Trichomonas  intestinalis  and 
the  Cercomonas  intestinalis  are  often  found.  Thayer  has  recorded  a  case  in 
which  the  Strongyloides  intestinalis  was  present  as  an  additional  parasite. 

The  diphtheritic  form  is  to  be  suspected  if  from  the  first  the  patient 
seems  profoundly  adynamic.  Typhoid  fever  is  to  be  separated  from  dysen- 
tery by  the  fever,  the  rose  rash,  and  the  Widal  test. 

Prognosis. — The  prognosis  in  dysentery  depends  to  some  extent  upon  the 
variety  of  infection  which  is  present,  and  upon  the  hygienic  surroundings 
and  vitality  of  the  patient,  for  even  the  mildest  types  may  be  fatal  if  the 
patient  receives  bad  food  and  is  exposed  to  excessive  heat  or  cold  or  wet. 
When  the  bacillus  of  Shiga  is  the  cause  the  prognosis  in  acute  cases  must 
always  be  most  guarded,  both  as  to  the  recovery  and  the  duration  of  the 
illness.  The  mortality  varies  greatly  in  difl^erent  epidemics  in  different 
parts  of  the  world.  Thus  in  Japan,  Shiga  found  it  varied  from  22  to  55 
per  cent.  In  this  country  the  mortality  has  been  as  low  as  3  per  cent. 
The  general  state  of  emaciation  and  depression  must  always  be  con- 
sidered. If  the  stools  contain  gangrenous  sloughs,  the  outlook  is  of 
course  very  grave;  and  if  hiccough,  great  nervous  depression,  and  low 
delirium  develop,  the  outlook  is  probably  fatal. 

In  the  amoebic  type  the  development  of  abscess  in  the  liver  of  course 
adds  very  greatly  to  the  gravity  of  the  case ;  but  even  when  amoebic  abscess  is 
present  and  ruptures  into  the  lung,  it  is  possible  for  recovery  to  take  place, 
if  proper  surgical  measures  of  relief  are  undertaken. 

Even  the  most  urgent  cases  may,  when  apparently  near  to  death,  recover, 
but  convalescence  is  protracted. 

According  to  Duncan  prognosis  can  be  based,  to  some  extent  at  least,  on 
the  character  of  the  stools.  He  believes  a  good  result  can  be  foreshadowed 
in  those  cases  in  which  are  passed  mucus  with  minute  fecal  lumps,  stained 
or  not  with  blood,  and  in  which  the  blood  and  mucus  disappear,  after  which 
the  ordinary  fecal  characters  will  soon  manifest  themselves. 

The  prognosis  is  of  evil  omen,  according  to  Sir  Joseph  Fayrer:  (a) 
in  the  cases  in  which  pulpy  stools  without  blood  or  mucus  are  passed; 


236  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

(6)  where  fluid  fecal  matter  is  from  time  to  time  passed  throughout  the 
illness,  the  prognosis  is  unfavorable,  inasmuch  as  these  characters  of  the 
stools  show  the  disease  to  be  extensive,  and  affecting  chiefly  the  upper  part 
of  the  large  as  well  as  in  some  cases  part  of  the  small  intestine;  (c)  where 
the  stools  in  conjunction  with  the  symptoms  that  are  laid  down  as  character- 
izing the  true  amoebic  dysentery  are  present,  the  prognosis  is  again  unfavor- 
able, on  account  of  the  high  mortality  that  is  said  to  attend  this  form  of 
the  disease;  (d)  the  prognosis  is  of  the  worst  possible  character  where  the 
stools  consist  of  blackish-red  or  blackish  fluid  with  a  horribly  putrescent 
odor,  and  of  bits  of  gangrenous  tissue.  Duncan  has  never  seen  a  patient 
passing  this  character  of  stool  recover. 

Treatment. — So  far  as  diet  is  concerned  it  is  self-evident  that  the  food 
should  consist  of  those  substances  which  are  readily  digested  and  absorbed 
from  the  stomach  and  the  duodenum,  in  order  that  as  small  a  residue  as 
possible  may  pass  on  downward  into  the  large  bowel.  Milk,  which  is  so 
universally  resorted  to  in  the  treatment  of  all  forms  of  diarrhoea,  is  not 
always  as  useful  a  form  of  nutriment  as  it  is  thought  to  be;  for  not  uncom- 
monly it  will  be  found  that  when  milk  is  taken  it  remains  undigested,  or 
forms  curds  which  are  indigestible  because  of  the  feeble  secretion  of  digestive 
juice.  These  curds  pass  through  the  bowels  and  afford  pabulum  for  micro- 
organisms which,  in  turn,  are  injurious  to  the  mucous  membrane.  If  it 
is  given,  it  should  certainly  be  diluted  freely  with  lime-water,  barley-water, 
or  Vichy  water,  or  else  it  should  be  peptonized  in  order  that  its  digestion 
may  be  readily  performed;  and  it  is  of  vital  importance  in  this  connection 
that  it  should  be  given  in  small  quantities,  frequently,  rather  than  in  large 
quantities.  SoHd  food  is,  of  course,  contraindicated,  but  semi-solid  foods 
like  milk-toast,  the  digestion  of  which  is  aided  by  pancreatin  or  taka-diastase, 
and  a  very  soft-boiled  egg.  will  often  prove  a  better  diet  than  one  which  is 
more  liquid,  but  less  nourishing,  since  the  physician,  in  the  presence  of 
dysentery,  is  faced  by  two  opposing  factors;  on  the  one  hand  a  feeble  diges- 
tion, and  on  the  other  hand  the  necessity  of  supporting  vitaUty  to  the 
highest  possible  point  by  the  administration  of  proper  foodstuffs. 

The  treatment  of  the  condition  itself  may  be  divided  into  three  methods, 
and  each  one  of  these  plans  finds  ardent  advocates  among  those  of  the  pro- 
fession who  have  had  sufficient  experience  to  make  us  feel  that  their  opinions 
are  of  value. 

The  ipecac  plan  may  be  considered  among  the  first  of  these,  and  it  cannot 
be  doubted  that  physicians  in  tropical  countries  have  found  it  of  benefit  in 
so  large  a  number  of  cases  that  it  is  impossible  to  consider  that  they  have 
been  mistaken  in  their  chnical  observation.  As  Dr.  Woodhull,  late  Assistant 
Surgeon-General  of  the  U.  S.  Army,  has  said,  the  one  remedy  which,  properly 
used,  is  as  conspicuous  in  dysentery  as  quinine  is  in  malaria  is  ipecacuanha. 
He  gives  the  following  directions  for  its  use: 

"The  stomach  must  be  empty  and  the  patient  recumbent.  About  twenty 
minutes  before  giving  the  ipecac  it  is  well  to  paint  the  epigastrium,  not 
the  whole  abdomen,  with  tincture  of  iodine,  or  to  apply  a  mild  sinapism 
sufficiently  to  induce  gentle  counterirritation.  This  precaution,  however, 
may  sometimes  be  omitted,  or  may  be  deferred  until  the  medicine  has  been 


DYSENTERY  237 

taken.  Ten  or  15  minims  of  laudanum  may  be  given,  always  on  an 
empty  stomach,  to  be  followed  in  ten  or  twelve  minutes  by  from  15  to  30  or 
more  grains  of  ipecac  in  pill  form,  or  as  a  paste,  with  a  very  small  quantity 
of  water.  No  food  or  fluid  should  be  taken  for  at  least  four  hours,  and 
recumbent  rest  should  be  strictly  maintained.  If  the  ipecac  is  administered 
in  pill  or  capsule  the  laudanum  may  be  mixed  with  it  instead  of  given 
previously.  One  scruple  of  ipecac  and  1  grain  of  opium  can  be  made  into 
four  pills,  or  the  laudanum  can  be  put  in  the  pills.  When  pills  are  used 
they  should  be  freshly  made.  Or  20  grains  of  ipecac  can  be  suspended 
in  2  fluidrachms  of  water  with  a  few  drops  of  an  aromatic  to  disguise  the 
taste.  It  is  never  advisable,  on  account  of  the  popular  idea  associated  with  it, 
to  disclose  the  name  of  the  medicine,  and  the  patient  should  be  warned  to 
resist  any  inclination  to  vomit.  The  size  of  the  dose  should  be  in  proportion 
to  the  gravity  of  the  case.  Just  as  in  severe  colic  very  large  doses  of  opium 
are  tolerated,  and  in  pernicious  fever  enormous  quantities  of  quinine  are 
indicated,  so  in  dysentery  surprisingly  large  doses  of  ipecac  are  well  borne, 
although  the  magnitude  of  the  dose  should  bear  some  relation  to  the  severity 
of  the  disease.  With  a  little  experience,  that  relation  will  soon  be  deter- 
mined. Sixty  grains  is  not  a  maximum  dose  for  an  adult,  but  with  ordinary 
acute  dysentery  from  15  to  25  grains  at  a  time  should  suffice.  If  the  first 
or  any  subsequent  dose  is  rejected,  which  rarely  happens  if  these  rules  are 
carefully  followed,  it  is  to  be  repeated  after  a  short  interval.  The  retching 
or  vomiting  of  exhaustion  or  the  restlessness  of  delirium  is  no  bar,  but 
rather  an  inducement  to  this  treatment;  and  small  children  or  delicate 
women  can  take  it  with  impunity  in  proportionate  amounts. 

"The  common  course  in  acute  dysentery  is,  first,  the  relief  of  pain,  next 
the  subsidence  of  fever,  and  then  the  cessation  of  the  bloody  discharges. 
The  usual  sign  that  recovery  is  at  hand  is  a  painless,  copious,  semi-fluid 
evacuation,  much  the  color  of  the  ipecacuanha  powder,  not  black  as  has 
been  stated.  The  medicine  then  may  be  reduced  or  entirely  suspended. 
In  acute  cases  these  results  will  follow  very  quickly.  In  chronic  dysentery 
complete  recovery  may  be  delayed  or,  indeed,  may  fail  of  absolute  attain- 
ment, but  great  amelioration  may  be  confidently  anticipated.  That  the 
powder  should  be  pure  and  comparatively  fresh  is  always  essential." 

The  second  method  of  treatment  is  the  purgative  flan,  which  has  come 
forward  largely  within  the  last  few  years,  probably  because  of  increasing 
experience  on  the  part  of  American  and  English  surgeons  in  the  Philippines 
and  in  South  Africa.  Clinical  evidence  is  rapidly  accumulating  which  proves 
beyond  all  doubt  that  in  a  certain  proportion  of  cases  of  acute  dysentery 
the  employment  of  sulphate  of  magnesium  combined  with  aromatic  sulphuric 
acid  is  a  most  advantageous  method.  The  bowels  are  first  thoroughly 
moved  with  Epsom  salts  or  with  Rochelle  salts,  and  then  aromatic  sulphuric 
acid  is  given  freely,  so  that  it  will  exercise  its  well-known  astringent  or 
constipation  influence.  This  plan  is  a  more  rational  one  than  that  which 
concerns  the  employment  of  ipecac,  in  that  it  is  a  well-known  fact  that  the 
micro-organisms  which  are  commonly  found  in  the  intestines  in  dysenteric 
cases  are  destroyed  or  rendered  inert  by  an  acid  medium,  and  it  has  long 
been  known  by  the  profession  that  the  administration  of  sulphuric  acid  is 


238  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

apt  to  produce  an  acid  reaction  of  the  stools,  so  that  its  beneficial  influence 
in  dysentery  does  not  rest  alone  upon  its  astringent  effect,  but  upon  its 
power  to  destroy  the  infecting  micro-organisms,  just  as  its  use  in  Asiatic 
cholera  meets  the  double  indication  of  restraining  diarrhoea  and  destroying 
the  comma  bacillus. 

The  third  plan  of  treatment  consists  in  the  administration  of  intestinal 
antiseptics,  of  which  perhaps  bismuth  salicylate,  benzonaphthol,  and  salol 
have  been  most  commonly  employed.  Theoretically,  it  is  easy  to  conceive 
that  these  substances  may  be  advantageous,  but  practical  experience  has 
shown  that  they  fail  to  exercise  the  degree  of  antiseptic  influence  with  which 
they  are  credited,  and  they  are  not  of  sufficient  importance  to  justify  their 
employment  to  the  exclusion  of  the  ipecac  or  saline  methods  which  have 
just  been  described.  The  employment  of  calomel  and  corrosive  sublimate 
with  good  results  in  these  cases  rests  upon  the  fact  that  they  increase  the 
activity  of  the  liver,  both  in  destroying  toxic  material  and  in  secreting 
bile. 

Without  doubt  local  treatment  by  high  intestinal  irrigations  is  of  very 
great  value.  Copious  clysters  which  will  reach  far  up  into  the  descending 
and  transverse  colon  are  necessary.  In  a  number  of  instances  the  writer 
found  that  injections  of  sulphocarbolate  of  zinc,  in  the  proportion  of  20 
grains  to  the  pint,  have  produced  very  satisfactory  results,  the  zinc  acting 
both  as  an  astringent  and  antiseptic.  Other  practitioners  have  employed 
copious  injections  of  weak  solutions  of  nitrate  of  silver  of  the  strength  of 
1  drachm  to  4  pints.  The  tenesmus  which  is  frequently  associated  with 
the  dysenteric  condition,  or  on  the  introduction  pf  the  soft  rectal  tube,  can 
sometimes  be  avoided  by  the  use  of  a  10  grain  iodoform  suppository  used 
half  an  hour  before  the  injection  is  to  be  given.  This  suppository,  by  its 
local  anaesthetic  effect,  is  of  service,  and  I  have  thought  that  the  absorption 
of  the  iodine  from  it  was  also  advantageous. 

The  method  of  giving  the  intestinal  lavage  is  of  considerable  importance. 
It  should  not  be  given  with  a  Davidson  or  other  pumping  syringe,  but 
always  by  means  of  a  fountain  syringe  or  surgical  irrigator.  The  hydro- 
static pressure  employed  should  never  be  greater  than  two  or  three  feet, 
and  it  is  much  better  that  the  injection  should  be  gently  given,  so  that  it 
takes  fifteen  or  twenty  minutes  to  find  its  way  up  into  the  intestine,  than 
that  it  should  be  delivered  forcibly  enough  to  produce  angry  contractions 
of  the  bowel,  which  will  cause  great  agony  and  so  much  irritation  that  the 
treatment  makes  the  patient  worse. 

Where  great  irritability  of  the  bowel  exists  it  is  probably  better  to  employ 
two  rubber  catheters  side  by  side,  one  being  for  the  intake  and  the  other 
for  the  outflow,  since  in  this  way  great  distention  of  the  bowel  is  avoided. 
In  instances  in  which  cold-water  injections  seem  inadvisable  very  hot  water 
may  be  employed,  but  it  is  distinctly  disadvantageous  to  employ  tepid  water, 
which  has  a  relaxing  and  enervating  effect,  and  does  not  possess  the  healthy 
stimulant  effects  of  marked  cold  or  high  heat.  Often  it  is  best  to  employ 
normal  saline  solution,  since  by  this  means  maceration  of  the  intestinal 
mucous  membrane  is  avoided. 

Specific  treatment  for  bacillary  dysentery  promises  much  for  the  future. 


EPIDEMIC  GANGRENOUS  PROCTITIS  239 

Attempts  to  produce  a  protective  and  curative  serum  have  been  made,  and 
Shiga  maintains  that  he  reduced  the  mortahty  of  dysentery  one-third  by 
the  use  of  such  a  substance.  Up  to  November  1,  1899,  he  had  treated 
156  cases  with  his  serum,  with  a  mortahty  of  8.5  per  cent.  During  the  same 
period  166  cases  in  Tokio  and  Honjo  Hospitals  under  ordinary  treatment 
gave  a  mortahty  of  37.9,  and  398  at  Komogone  Hospital  gave  a  mortality 
of  34.6.  In  private  practice  also  mortality  was  high,  1119  cases  giving  a 
percentage  of  28.5.  Kitasato  likewise  obtained  a  low  mortality  rate  by  this 
plan  of  treatment.     (See  Cholera  Infantum.) 

Another  form  of  specific  treatment  is  that  which  is  directed  to  combating 
amoebic  dysentery  by  means  of  injecting  quinine  bisulphate,  in  the  strength 
of  1:5000,  sufficiently  high  in  the  rectum  for  it  to  exercise  its  fatal  effect 
upon  the  amoeba  coli.  Thymol  1:2500  may  also  be  used  in  this  way. 
(Thomas),  Harris  has  highly  recommended  hydrogen  peroxide  given  by 
injections  as  a  parasiticide. 

Stimulants  well  diluted  with  water  or  with  nutritive  broths  should  be  given 
if  needed,  and  strychnine  and  quinine  employed  in  convalescence  as  tonics. 

For  the  control  of  the  diarrhoea  when  excessive,  enemata  of  deodorized 
tincture  of  opium  and  starch-water  are  very  useful. 


EPIDEMIC  GANGRENOUS  PROCTITIS. 

Definition. — Epidemic  gangrenous  proctitis  is  an  acute  contagious  disease 
appearing  as  a  rapidly  spreading  ulceration  of  the  anus  and  rectum,  with 
prolapse  and  gangrene  of  the  ulcerated  rectum  and,  in  a  large  proportion 
of  cases,  death  in  coma  or  convulsions. 

This  disease,  originally  believed  to  be  limited  to  narrow  areas  in  Central 
and  South  America,  is  now  known  to  occur  much  more  widely  throughout 
the  tropical  zones.  It  is  generally  distributed  in  tropical  South  America 
and  in  Central  America.  It  has  been  observed  in  the  Philippines,  the 
Celebes,  and  New  Guinea. 

There  is  some  question  whether  this  affection  should  be  regarded  as  a 
distinct  disease  entity  or  not.  I  (Kieffer)  regard  it  as  a  localization  of  an 
intense  dysenteric  process  unusually  low  in  the  colon,  without  hazarding 
any  theory  as  to  the  cause  of  the  localization.  This  idea  is  strengthened  by 
the  well-known  liability  in  children  to  intussusception  above  the  sigmoid 
in  acute  dysentery.  It  is  quite  fair  to  assume  that  the  mechanism  of  the 
extrusion  of  the  rectum  in  these  cases  is  the  same. 

Etiology. — Nothing  is  known  of  the  direct  cause  of  this  curious  condition. 
Ackers,  of  Curacao,  states  that  it  is  the  common  belief  of  the  natives  in 
Venezuela  that  the  disease  is  caused  by  eating  unripe  maize,  of  which  the 
children  are  particularly  fond.  This  seems  hardly  probable,  although  the 
symptoms  of  pellagra,  which  are  assumed  to  be  due  to  fermented  maize, 
would  indicate  the  possibility  that  unripe  maize  may  account  for  the 
symptoms.  The  disease,  however,  has  been  observed  in  countries  in 
which  maize  is  practically  an  unknown  food  product.  I  (Kieffer)  have 
reported  one  case  in  which  the  Bacillus  pyocyaneus  was  undoubtedly  the 


240  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

active  organism.  A  high  degree  of  humidity  seems  an  essential  condition 
to  the  development  of  the  disease.  Ackers  observed  this  disease  in  fowls 
and  the  smaller  domestic  animals,  occasionally  in  calves.  In  Venezuela 
and  New  Guinea  the  disease  is  confined  to  children,  particularly  those  of 
the  poorer  classes,  and  in  the  rest  of  the  tropical  world  it  also  holds  true 
that  children  are  more  frequently  attacked  than  adults. 

Pathology. — The  rectum  and  anus  in  early  stages  are  affected  by  deep 
ulcers  overlaid  with  a  diphtheroid  pseudomembrane.  Two  forms  can  usually 
be  distinguished:  the  low  form  with  limitation  of  the  lesions  to  the  rectum 
between  the  sphincters  and  the  high  form  in  which  the  disease  extends  well 
up  to  the  sigmoid. 

Symptoms. — The  disease  begins  with  local  symptoms  referred  to  the  anus 
and  rectum.  There  is  burning  and  intolerable  itching  followed  by  severe 
dysenteric  symptoms.  After  twelve  to  twenty-four  hours  there  is  more  or 
less  constant  and  severe  tenesmus. 

The  evacuations,  at  first  feculent,  become  mucoid  and  finally  consist 
entirely  of  mucus  and  blood.  The  distress  grows  urgent,  effort  and  pain 
become  continuous,  and  there  is  a  constant  flow  or  bubbling  out  of  slimy 
mucus  stained  with  blood,  or  almost  pure  frothy  blood.  The  evacuations 
are  very  fetid.  As  the  disease  progresses  there  is  profound  collapse. 
Nervous  symptoms  appear  and  the  patients  become  either  delirious  or 
comatose.  In  children  there  may  be  convulsions.  Emaciation  is  rapid 
and  death  usually  occurs  in  convulsions  or  coma.  If  the  patient  sur- 
vives this  stage  the  rectum  is  extruded  and  undergoes  rapid  necrosis  and 
sloughing. 

In  the  early  stages  the  diagnosis  between  epidemic  gangrenous  rectitis 
and  dysenteric  lesions  in  the  descending  colon  can  only  be  made  by  exami- 
nation of  the  rectum.  In  advanced  cases  the  condition  is  self-evident.  The 
mortality  is  very  high,  but  even  comatose  patients  need  not  be  despaired 
of.  Recovery  occasionally  occurs  after  prolapse  and  sloughing  of  the 
rectum. 

Treatment. — ^The  Venezuelan  treats  this  disease  by  introducing  lemon- 
juice  or  diluted  aguardiente  into  the  rectum.  When  extrusion  of  the  rectum 
occurs  he  keeps  it  dry  by  dusting  with  wood-ashes.  Indications  are  for 
active  antisepsis  of  the  rectum  with  diluted  creolin  or  hydrogen  peroxide. 
Opium  will  be  necessary  for  the  control  of  pain,  and  is  best  applied  directly 
to  the  diseased  area.  If  prolapse  occurs  no  effort  should  be  made  at  first  to 
replace  it.  The  rectum  should  be  dusted  with  an  antiseptic  powder  or 
freshly  made  charcoal.    If  gangrene  occurs  the  rectum  must  be  extirpated. 


HILL  DIARRH(EA. 

Definition. — An  acute  morning  diarrhoea  with  white  stools  and  attended 
by  marked  flatulency.  It  is  a  disease  of  the  acclimatized  and  not  of  the 
new-comer  in  the  tropics. 

Etiology. — The  etiological  factors  in  the  production  of  hill  diarrhoea  are, 
first,  prolonged  residence  in  hot  countries  with  the  establishment  of  acclima- 


HILL  DIARRCEA  241 

tization,  then  an  unaccustomed  altitude,  five  to  six  thousand  feet,  with  a 
high  degree  of  humidity.  Under  these  conditions  the  dweller  in  the  low, 
hot  plains  who  goes  to  the  hills  is  very  prone  to  fall  a  victim  to  this  disease. 
It  is  consequently  observed  when  business  or  relaxation  takes  the  colonists 
into  mountainous  portions  of  the  tropics.  It  is  common  in  the  hill  sana- 
toria of  tropical  countries,  particularly  in  India,  where  it  was  named  Hill 
diarrhoea,  Simla  diarrhoea,  etc.  Hill  diarrhoea  bears  a  very  close  resemblance 
to  sprue.  The  cardinal  symptoms  differ  only  in  degree,  but  the  tendency 
of  hill  diarrhoea  is  so  constantly  to  recovery,  and  that  of  sprue  so  constantly 
downward,  that  they  must  be  considered  separately. 

Pathology. — Very  little  is  known  of  the  pathology  of  this  peculiar  con- 
dition. It  seems  to  be  clear  that  there  is  a  temporary  suspension  of  function 
of  the  liver  and  pancreas.  This  is  probably  the  expression  of  exhaustion 
resulting  from  the  extra  strain  on  already  overworked  digestive  organs 
seeking  to  adapt  themselves  to  a  further  change  of  climatic  conditions. 
Scheube  thinks  this  condition  depends  on  an  atonic  state  of  the  colon  which 
he  believes  to  be  a  common  sequel  to  long  residence  in  hot  countries,  and 
that  the  diarrhoea  is  due  to  chilling  of  the  abdomen  in  the  unaccustomed 
cold  and  dampness  of  the  early  morning  hours  of  the  mountainous  region 
of  the  tropics. 

The  tendency  in  the  vast  majority  of  cases  is  to  prompt  readjustment 
and  restoration  within  one  or  two  weeks.  A  small  proportion  of  cases 
persist  and  may  end  in  typical  sprue.  Crombie  reports  cases  in  which  cure 
has  taken  place  only  when  the  patients  returned  to  the  plains.  In  these 
cases  every  visit  to  the  hills  was  followed  by  this  diarrhoea. 

Symptoms. — Shortly  after  arrival  in  the  mountains  the  patient  is  troubled 
with  dyspeptic  symptoms  and  a  morning  diarrhoea.  On  the  succeeding 
days  the  diarrhoea  becomes  more  troublesome  until  it  reaches  eight  to  ten 
movements  daily.  It  comes  on  in  the  early  morning,  at  or  near  dawn,  with 
a  sudden  call  to  stool.  It  continues  during  the  forenoon  and  ceases  abruptly 
about  mid-day.  There  is  very  little  pain  and  that  only  as  a  vague,  inde- 
terminate discomfort  over  the  colon,  and  no  tormina  or  tenesmus.  The 
movements  are  large  and  frothy,  they  are  devoid  of  coloring  matter,  and 
look  like  stirred  mortar  or  whitewash.  They  have  an  unpleasant,  mawkish 
odor.  Dyspeptic  symptoms  are  pronounced.  There  is  distress  after  eating, 
particularly  in  the  morning,  and  there  may  be  marked  tympanitic  distention 
of  the  abdomen. 

Treatment. — Treatment  is  directed  to  the  restoration  of  intestinal  digestion 
and  the  maintenance  of  a  relative  degree  of  rest  to  the  gastrointestinal  tract 
by  putting  the  patient  on  liquid  or  milk  diet.  Small  doses  of  calomel  to 
stimulate  the  hepatic  function  are  of  value.  Similarly  pilocarpine  should  be 
tried  with  the  idea  of  increasing  the  flow  of  the  pancreatic  secretion.  Judicious 
use  of  the  digestive  ferments  should  be  made.  These  patients  should  be 
advised  to  keep  to  their  beds  during  the  morning  hours.  In  persistent  cases 
it  may  become  necessary  to  send  the  patients  down  to,  or  near,  the  sea  level. 


16 


242  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


SPRUE  (PSILOSIS). 

Definition. — Sprue  (Atrophic  Enteritis  of  the  Tropics)  is  not  a  distinct 
morbid  entity;  it  is  but  a  terminal  condition  of  many  devitalizing  and 
depressing  factors.  Sprue  may  be  defined  as  a  chronic  catarrhal  inflam- 
mation of  the  entire  alimentary  tract  tending  ultimately  to  most  extensive 
atrophy  of  the  gastrointestinal  glandular  structures,  characterized  clinically 
by  three  cardinal  symptoms — sore  mouth,  flatulency,  and  diarrhoea. 

Sprue  is  a  disease  of  the  entire  tropical  world.  The  Malayan  Archipelago, 
particularly  the  Phihppine  Islands,  South  China,  Amoy,  Ceylon,  Java,  and 
the  Malayan  Peninsula  are  the  regions  of  its  greatest  development. 

It  is  not  seen  in  subtropical  or  temperate  zones,  unless  in  imported  cases, 
with  the  exception  of  Japan  and  northern  China.  It  has  been  known  by 
many  names,  all  of  them  referring  to  one  or  another  of  the  peculiar  clinical 
manifestations  of  the  disease.  Thus,  it  has  been  called  "diarrhoea  alba," 
"  aphthae  tropicse,"  "  Ceylon  sour  mouth,"  and  "  white  flux."  The  name 
sprue  was  given  to  it  by  the  Dutch,  who  found  it  a  veritable  plague  in  their 
Javanese  possession.  Since  the  United  States  has  acquired  colonies  in  the 
sprue  region,  imported  cases  have  become  fairly  numerous  throughout  this 
country,  and  their  consideration  is  of  great  interest  to  the  general  practitioner. 

Etiology. — Extensive  studies  of  the  disease  have  failed  to  show  any  specific 
etiological  factor.  There  is  some  argument  whether  sprue  should  be  con- 
sidered a  specific  disease  or  whether  it  should  be  considered  as  a  terminal 
state  following  other  lesions.  Sambon  maintains  the  former.  Extensive 
studies  by  army  surgeons  in  Manila  show  that  the  latter  view  is  the  correct 
one.  The  disease  commonly  develops  in  the  tropics,  but  may  lie  dormant 
for  years  after  the  return  of  the  colonist  to  his  home  in  the  temperate  zone. 

The  conditions  that  predispose  to  the  development  of  sprue  are  the 
following:  The  large  majority  of  cases  follow  chronic  amoebic  dysentery  and 
its  sequelae,  chronic  ulceration  of  the  colon  and  abscess  of  the  liver,  with 
prolonged  suppuration.  Following  dysentery  the  intestinal  parasites,  and 
chief  of  these  the  uncinaria,  are  common  antecedents  of  sprue.  Next  is 
the  general  deterioration  in  chronic  malarial  poisoning,  and  lastly  syphilis 
is  a  cause.  To  these  must  be  added  the  physical  deterioration  incident  to 
prolonged  residence  in  hot  climates,  even  when  no  acute  illness  is  suffered, 
and  the  following  depressing  conditions :  childbirth  and  miscarriage,  chronic 
disease  of  the  kidneys,  suppurating  lesions  anywhere,  excessive  fatigue, 
long  marches,  and  prolonged  campaigns.  Some  writers  report  the  develop- 
ment of  sprue  as  following  the  prolonged  administration  of  iodides  and 
mercury.  Numerous  organisms  have  been  described  as  the  cause  of  sprue 
and  several  parasites,  particularly  the  strongyloides.  Amoebae  are  almost 
constantly  found  and  various  bacilli  of  the  typho -colon  group,  but  these 
must  all  be  considered  remnants  of  the  preceding  pathological  condition 
rather  than  direct  causes  of  the  disease  itself. 

Pathology. — Postmortem  examination  shows  complete  loss  of  subcutaneous 
and  mesenteric  fat.  The  tissues  and  cavities  are  extremely  dry;  the  small 
intestine  presents  extreme  thinning  of  its  walls  with  atrophy  of  the  mucosa 


SPRUE  243 

and,  in  some  cases,  entire  destruction  of  the  glandular  structures.  The 
serous  coat  is  normal.  Swelling  and  ulceration  of  Peyer's  patches  are  seen 
and  in  many  cases  the  colon  presents  the  usual  appearances  of  recent  or 
present  dysentery.  Parenchymatous  changes  occur  in  the  pancreas,  liver 
and  kidneys,  and  occasional  areas  of  fatty  degeneration  are  present. 

Symptoms. — Sprue  is  essentially  a  very  chronic  disease.  The  average 
duration  is  from  one  to  two  years,  although  cases  lasting  ten  years  or  more 
are  not  by  any  means  unusual.  The  patient  is  emaciated  and  anoBmic. 
The  complexion  is  muddy  and  sallow.  There  is  great  lassitude  and  weak- 
ness, and  mental  irritability  with  pronounced  disinclination  for  physical  and 
mental  labor.  The  disease  passes  through  numerous  stages  of  ameliora- 
tion and  numerous  recrudescences,  but  its  general  tendency  is  always  down- 
ward. The  principal  symptoms  of  sprue  are  sore  mouth,  diarrhoea,  and 
flatulence. 

The  mouth  lesions  of  sprue  are  constant  and  striking.  On  examination 
the  tongue  is  found  unusually  clean.  The  organ  is  small,  pointed,  and 
somewhat  yellowish.  Along  the  dorsum  of  the  tongue,  along  its  edges,  and 
on  the  under  side,  particularly  along  the  frsenum,  there  are  numerous,  fine, 
minute  ulcers,  with  a  thin,  aphthous  pellicle.  These  aphthous  spots  may  also 
be  present  on  the  uvula  and  palate.  Very  commonly  the  tongue  is  covered 
with  very  superficial  erosions  from  one-eighth  to  one-fourth  of  an  inch  in 
diameter,  frequently  coalescing  and  resulting  in  a  serpiginous  appearance. 
Where  these  marked  lesions  are  temporarily  absent,  the  tongue  still  has  an 
unusually  clean,  dry,  glazed  appearance,  and  looks  very  much  as  though 
it  had  been  recently  varnished.  The  condition  in  older  patients  may  be 
very  much  accentuated  and  extensive  fissures  may  develop.  The  patient 
complains  of  soreness  that  may  be  limited  only  to  the  tongue,  or  may 
involve  the  palate  or  uvula,  or  the  entire  mouth.  He  particularly  complains 
of  burning  or  a  stinging  pain  on  taking  salt  or  highly  seasoned  food. 
Occasionally  the  pain  is  also  present  on  deglutition,  and  the  progress  of 
the  food  bolus  on  its  way  to  the  stomach  is  indicated  by  a  burning  and 
stinging  pain  in  the  gullet,  showing  that  the  oesophagus  is  in  the  same 
condition  as  the  mouth.  Nausea  and  vomiting  are  sometimes  present  in 
advanced  cases,  the  vomiting  coming  on  without  reference  to  the  time  of 
taking  food.  Eructations  and  waterbrash  are  present;  the  appetite  is  very 
variable,  sometimes  being  entirely  absent,  at  other  times  ravenous. 

Flatulence  is  quite  marked.  The  patient  is  swollen  until  the  abdomen  is 
tense  and  drum-like.  In  this  condition  the  appearance  of  the  very  much 
emaciated  figure,  with  extremely  thin  arms  and  legs,  and  large,  inflated 
abdomen,  is  very  characteristic.  The  flatulence  is  always  aggravated  by 
taking  food  and  is  accompanied  by  a  constant  sense  of  oppression  and  a 
gnawing  and  burning  pain  in  the  stomach. 

Diarrhoea  is  the  most  distinctive  and  constant  symptom.  There  may  be 
only  one  or  two  movements  daily  or  there  may  be  as  many  as  ten  or  twelve. 
They  are  usually  passed  without  pain;  they  vary  very  much  in  their 
character,  but  are  nearly  always  liquid  or  semi-liquid.  They  are  frothy, 
white,  and  have  a  fetid,  mouse-like  odor.  Manson  describes  them  as 
looking  like  recently  stirred  whitewash.    They  are  usually  remarkably  large. 


244  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

Their  reaction  is  commonly  acid.  Microscopically  they  are  found  to  contain 
bowel  structure,  a  few  red  blood  cells,  and  intestinal  parasites,  of  which 
amoebae  are  the  most  frequent. 

As  the  disease  advances  emaciation  and  asthenia  become  extreme.  The 
skin  is  dry  and  scurfy,  the  patient  is  unable  to  assimilate  or  retain  food, 
and,  in  many  instances,  he  involuntarily  abstains  from  it  on  account  of  the 
severe  pain  in  the  mouth  and  throat.  In  all  marked  cases  there  is  secondary 
anaemia,  the  red  blood  corpuscles  being  reduced  as  low  as  1,000,000,  with 
some  degree  of  poikilocytosis  and  no  leukocytosis. 

Diagnosis. — Diagnosis  presents  no  difficulties,  when  the  existence  of  such 
a  disease  as  sprue  is  known  and  its  cardinal  symptoms  are  remembered. 
Incomplete  cases  in  which  one  or  the  other  symptom  may  predominate  or 
be  absent  may  give  rise  to  some  difficulties. 

Sprue  in  particular  must  not  be  confounded  with  chronic  dysentery, 
although  it  is  difficult,  in  cases  where  sprue  develops  from  dysentery,  to 
definitely  mark  the  period  where  the  one  disease  begins  and  the  other  ends. 

Prognosis. — If  treatment  is  instituted  before  the  atrophy  of  the  bowel  is 
too  far  advanced,  cure  is  the  rule.  If,  however,  so  much  of  the  secreting 
surface  of  the  bowel  is  destroyed  as  to  make  assimilation  impossible,  death 
is,  of  course,  inevitable. 

Treatment. — Treatment  consists  in  putting  the  patient  on  absolute  milk 
diet.  He  should  preferably  be  kept  in  bed  and  milk  administered  in  small 
feedings.  The  quantity  is  increased  as  rapidly  as  possible,  the  mouth 
symptoms  and  the  appearance  of  unchanged  milk  in  the  bowel  movements 
being  the  index  as  to  the  quantity  to  be  taken.  If  there  be  any  increase 
in  the  amount  of  soreness  of  the  mouth,  the  milk  must  be  reduced  for  a  time 
and  later  gradually  increased,  until  the  patient  is  taking  from  four  to  six 
quarts  daily.  This  regimen  must  be  persisted  in  from  four  to  six  weeks 
after  the  mouth  symptoms  disappear  and  the  bowel  movements  become 
solid.  Then  soft  diet  should  be  resumed  very  carefully.  Where  milk 
cannot  be  taken,  pure  meat  diet  may  be  used  or  an  exclusive  diet  of  meat- 
juice.  Success  has  also  attended  the  exclusive  use  of  a  fruit  diet.  Recent 
observations  have  shown  the  value  of  fruit,  particularly  of  berries,  in  the 
treatment  of  sprue  as  well  as  chronic  dysentery.  Manson  reports  the  case 
of  a  man  over  fifty  years  of  age,  at  which  time  of  life  the  prognosis  in  cases 
of  sprue  is  exceedingly  grave.  The  patient  was  first  treated,  with  little 
benefit,  with  milk  diet  and  other  special  diets;  finally  the  patient  was  put 
on  a  diet  of  strawberries.  The  stools  at  once  improved  and  the  patient  was 
soon  restored  to  health.  This  was  not  the  only  case  in  which  recovery 
followed  the  use  of  strawberries.  Manson  considers  this  a  decided  advance 
in  the  treatment  of  sprue.  Medicinally  salol  and  Dover's  powder  may  be 
given  for  control  of  the  diarrhoea.  For  their  tonic  and  reconstructive 
properties  iron  and  arsenic  should  be  used.  These  drugs  have  been  shown 
to  be  of  particular  advantage  in  this  disease  when  used  by  hypodermic 
injection. 


MALTA  FEVER  245 


NASHA  FEVER. 

Nasha,  nasa,  or  nakra  fever,  first  described  by  Fernandez  and  Mitra 
in  1894,  is  a  specific  fever  confined  to  certain  sections  of  India.  It  is  pre- 
ceded by  marked  congestion  of  the  nose  and  circumscribed  swelling  of  the 
nasal  septum.  The  disease  begins  with  malaise,  headache,  and  severe  pain 
in  the  muscles  of  the  neck,  back,  and  shoulders.  There  may  be  a  small, 
diffuse,  rosy  eruption.  The  fever  is  moderate  and  usually  lasts  from  three 
to  five  days,  gradually  subsiding  with  the  disappearance  of  the  nasal  symp- 
toms. In  rare  instances  sudden  diminution  of  the  local  symptoms  has  been 
followed  by  severe  cerebral  symptoms,  coma,  and  death. 

The  etiology  is  unknown.  It  occurs  principally  in  adults,  children  and 
the  aged  being  relatively  immune,  and  it  comes  on  usually  in  the  summer 
months.  Exposure,  unhygienic  surroundings,  and  poor  food  seem  to  be  the 
predisposing  factors.    One  attack  does  not  confer  immunity. 

There  are  some  reasons  for  believing  this  to  be  an  atypical  form  of  malaria. 
It  occurs  in  highly  malarious  localities,  where,  according  to  Bose,  swelling 
of  the  nasal  mucosa  is  a  common  symptom  with  fever.  As  against  this 
theory,  the  malarial  parasite  has  not  been  found  in  all  cases  and  quinine 
is  said  not  to  be  effective. 

Treatment  is  symptomatic.  Puncture  of  the  swollen  septum  is  said  to 
give  great  relief  to  the  local  and  general  symptoms. 


MALTA  FEVER. 

Definition. — Malta  fever,  or,  as  it  is  sometimes  called,  "undulant  fever," 
is  a  disease  which  is  comparatively  common  in  the  island  of  Malta.  The 
malady  occurs  not  only  in  Malta,  but  along  the  shores  of  the  Mediterranean 
Sea,  and  so  is  sometimes  called  "  Mediterranean  Fever."  When  it  occurs  at 
Gibraltar  it  is  called  "  Gibraltar  Fever  "  or  "  Rock  Fever,"  and  when  in 
Italy,  "  Neapolitan  Fever."  The  malady  is  due  to  an  infection  by  the  Micro- 
coccus melitensis.  Its  chief  clinical  characteristic  is  wave-like  or  undulant 
curves  of  febrile  movement.  There  are  also  recurring  exacerbations  of  fever 
with  profuse  sweats,  pains  in  the  limbs,  swelling  of  the  joints,  and  enlarge- 
ment of  the  spleen. 

History  and  Geographical  Distribution. — Although  the  first  accurate  account 
of  this  disease  was  published  in  1861  by  J.  A.  Marston,  who  described  it 
under  the  name  of  Mediterranean,  remittent,  or  gastric  remittent  fever,  it 
probably  has  been  endemic  in  the  islands  and  along  the  shores  of  the  Mediter- 
ranean Sea  for  centuries.  Hippocrates  described  cases  of  continued  remittent 
fever  which  in  their  entire  symptom-complex  correspond  with  certain 
manifestations  of  undulant  fever,  and  references  to  a  protracted  form  of 
fever  prevailing  in  Mediterranean  countries  were  made  by  writers  of  the 
eighteenth  century  and  by  Sir  William  Burnett  and  Dr.  Hennon  early  in  the 
nineteenth  century.  While  the  disease  is  most  common  at  Malta,  Gibraltar, 
in  the  Balearic  Islands,  in  Cyprus,  in  Crete,  and  along  the  southern  coast 


246  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

of  Italy,  evidence  is  constantly  being  produced  to  show  that  it  has  a  wide 
distribution  throughout  tropical  and  subtropical  regions.  Cases  of  un- 
doubted authenticity  have  been  reported  from  China,  India,  Porto  Rico,  and 
the  Philippine  Islands,  and  a  fever  occurring  in  Venezuela  closely  resembles 
it  clinically,  although  no  cases  in  which  the  specific  organism  has  been 
obtained  in  cases  in  that  country  are  on  record.  Recent  investigations 
have  revealed  its  presence  in  the  United  States,  but  all  of  the  patients 
seem  to  have  contracted  the  disease  in  some  one  of  its  endemic  foci.  The 
first  case  was  reported  in  1898  by  Musser  and  Sailer,  in  Philadelphia,  eight 
cases  have  been  treated  in  the  Army  and  Navy  Hospital  at  Hot  Springs, 
Arkansas,  and  another  has  recently  been  reported  from  Texas  by  Major  C. 
F.  Mason,  of  the  U.  S.  Army. 

Etiology. — The  pathogenic  organism  of  Malta  fever  is  the  Micrococcus 
melitensis,  which  was  discovered  in  1887  by  David  Bruce,  who  isolated  it  in 
pure  culture  from  the  spleens  of  nine  patients  who  died,  and  found  it  in 
two  instances  in  blood  drawn  from  the  spleen  during  life.  This  microbe  is 
a  minute,  round  or  oval  coccus,  staining  readily  with  the  aniline  dyes,  but 
not  by  Gram's  method.  It  grows  very  slowly  in  bouillon,  agar-agar,  and 
gelatin,  and  agglutinates  when  placed  in  blood  serum  drawn  from  indi- 
viduals affected  with  the  disease.  A  joint  commission,  appointed  by  the 
British  Government,  has  proved  it  possesses  great  vitality,  for  the  organism 
was  found  alive  after  sixty-nine  days  in  dried,  sterilized  manured  soil, 
after  eighty  days  on  dried  fabrics,  after  seventy-two  days  in  damp  soil,  and 
after  thirty-seven  days  in  sterilized  water.  When  injected  into  monkeys  it 
produces  a  malady  similar  to  Malta  fever,  and  its  specific  action  in  the 
human  subject  has  been  demonstrated  by  several  cases  of  accidental  inoc- 
ulation. Some  investigators  believe  that  this  organism  gains  entrance  to 
the  body  through  the  alimentary  organs,  others  think  that  it  enters  through 
the  respiratory  tract,  while  still  others  are  of  the  opinion  that  mosquitoes 
are  the  agents  of  its  dissemination.  Monkeys  have  been  infected  at  the 
will  of  an  experimenter,  when  forced  to  breathe  an  atmosphere  laden  with 
dust  containing  the  specific  organism.  Horrocks  has  shown  that  in  regions 
in  which  the  disease  is  prevalent,  milch  goats  are  often  infected  and  that 
they  may  excrete  the  micro-organism  in  their  milk,  so  infecting  human 
beings  who  partake  of  it.  Malta  fever  is  a  disease  of  summer,  being  most 
prevalent  in  June  and  July.  Persons  of  all  ages  are  subject  to  it,  although 
the  period  of  its  greatest  incidence  is  said  by  Maltese  physicians  to  be 
between  the  sixth  and  the  thirtieth  years.  Sex  appears  to  be  without 
influence  in  its  causation.  One  attack  appears  to  confer  immunity,  at 
least  for  a  number  of  years. 

Pathology. — ^The  gross  morbid  changes  observed  after  death  vary  some- 
what according  to  the  stage  of  the  disease  in  which  death  occurs.  In  those 
cases  which  die  during  the  first  four  weeks  of  the  attack,  the  spleen  is  invari- 
ably congested  and  enlarged  and  often  is  so  soft  that  it  resembles  a  large 
mass  of  clotted  blood.  The  meninges,  the  liver,  the  stomach  and  intestines, 
and  the  kidneys  are  also  frequently  congested,  and  the  lungs  are  always 
congested  at  their  bases,  while  in  some  cases  lobular  consolidation  takes 
place.     The  heart  occasionally  shows  granular  or  fatty  degeneration  and 


MALTA  FEVER  247 

in  a  few  instances  pericardial  effusion  occurs.  In  cases  which  die  late  in 
the  disease  there  is  evidence  of  a  prolonged  toxic  action  upon  the  tissues. 
The  liver  and  spleen  are  larger  than  normal  and  of  firm  consistency,  due  to 
the  formation  of  fibrous  tissue,  and  the  heart  is  usually  pale,  its  walls  are  thin 
and  its  cavities  dilated.  The  spleen  is  the  only  organ  which  shows  charac- 
teristic microscopic  changes,  namely,  an  increase  in  lymphoid  tissue  and  the 
presence  of  large  numbers  of  the  specific  micro-organism.  Sections  of  the 
liver  and  kidneys  show  granular  or  fatty  degeneration.  As  to  blood  changes 
there  is  a  reduction  in  the  number  of  red  cells,  alterations  in  their  size  and 
shape,  and  a  deficiency  of  haemoglobin.  The  white  cells  are  often  relatively 
increased,  the  basophiles  being  in  excess. 

The  incubation  period  is  from  three  to  twenty  days,  most  commonly 
fifteen. 

Symptoms. — The  onset  of  the  typical  or  undulant  form  of  the  disease  is 
gradual,  and  is  attended  by  lassitude,  anorexia,  nausea,  headache,  insoTnnia, 
and  slight  evening  elevation  of  temperature.  As  the  morbific  process  advances 
the  digestive  and  nervous  symptoms  become  intensified,  and  the  temperature 
rises  slowly  day  by  day,  remitting  somewhat  each  morning,  until  it  reaches 
a  level  varying  from  103°  to  105°.  Here  it  is  maintained  for  a  varying 
period  of  time,  and  then  falls  slowly  with  profuse  sweating.  The  other 
symptoms  abate  simultaneously.  Soon,  however,  the  temperature  rises 
again  and  a  condition  similar  to  the  one  just  described  supervenes,  consti- 
tuting a  relapse,  of  which  several  occur.  The  most  noteworthy  symptom  of 
Malta  fever  is  therefore  the  persistent  recurrence  of  febrile  movements  which 
are  wave-like  in  character,  and  which  last  from  seven  to  twenty-one  days. 
They  are  followed  by  a  period  of  apyrexia  or  of  very  moderate  fever,  which 
lasts  for  a  few  days,  when  the  febrile  movement  returns  as  before.  In  this 
manner  the  disease  may  persist  for  months,  not  being  self-limited,  as  is  the 
course  of  typhoid  fever.  The  active  fever,  the  profuse  sweats,  and  the 
pain  continuing  for  so  long  a  period  produce  great  exhaustion  and  emaciation. 
Sometimes  cardiac  or  pulmonary  complications  arise  which  determine  a 
fatal  issue  of  the  malady. 

In  the  majority  of  cases  of  this  type,  however,  convalescence  ensues,  but 
it  is  slow  and  often  attended  by  neuralgic  and  rheumatoid  symptoms,  and 
occasionally  by  orchitis. 

Variations  from  the  typical  form  of  the  disease  are  not  at  all  uncommon 
Some  cases  are  characterized  by  rapid  onset  and  the  early  development  of 
severe  constitutional  symptoms,  which  usually  end  in  death,  while  other 
cases  run  an  extremely  mild  course  with  little  constitutional  disturbance 
other  than  general  malaise  and  slow  but  progressive  anaemia  and  emacia- 
tion. In  this  form  the  temperature  is  often  intermittent,  rising  several 
degrees  each  afternoon  and  falling  to  normal  or  nearly  normal  the  next 
morning. 

Diagnosis.  —  Accurate  diagnosis  of  Malta  fever  depends  upon  the  agglu- 
tinative serum  test  between  the  blood  and  the  micrococcus,  which  should 
be  made  whenever  possible.  This  reaction  is  almost  always  obtainable  by 
the  sixth  day  after  the  development  of  pyrexia  and  often  as  early  as  the 
fourth.      F.  J.  A.  Dalton,  of  the  British  navy,  finds  that  trustworthy  re- 


248 


DISEASES  DiJE   TO  A  SPECIFIC  INFECTION 


W- 


(•HHVJ)  aanivaadwai. 


suits  are  obtained  by  tlie  use  of  a  dilution  of 
1  :  50,  with  a  time  limit  of  half  an  hour. 

Clinically,  diagnosis  presents  many  difficul- 
ties, for  the  different  manifestations  of  the 
disease  make  it  particularly  liable  to  be  con- 
founded with  a  variety  of  affections,  such  as 
typhoid  fever,  tuberculosis,  chronic  rheuma- 
tism, malaria,  and  malarial  cachexia.  Suspi- 
cion as  to  the  nature  of  typical  cases  should 
be  aroused  by  the  presence  of  an  undulating 
temperature  curve  and  the  characteristic  fre- 
quent relapses.  Additional  aids  to  the  differ- 
ential diagnosis  may  be  named  as  follows: 

From  malarial  fever  we  can  separate  Malta 
fever  by  several  factors  which  make  differen- 
tiation possible.  In  the  first  place  the  absence 
of  the  Plasmodium  of  malaria  in  the  blood, 
and  the  presence  of  the  Micrococcus  melitensis 
in  the  spleen  on  puncture  is  of  course  a  defi- 
nite means  of  separation.  Again,  the  fever 
does  not  yield  to  quinine  as  does  that  of  ma- 
laria, and  the  pyrexia  is  too  persistent  for  the 
intermittent  type  of  that  disease,  although  at 
times  the  waves  of  fever  may  be  abrupt  enough 
to  resemble  it.  Again,  the  marked  arthritic 
symptoms  and  the  neuralgic  pains  are  not  met 
with  in  malarial  infection. 

The  possibility  of  tuberculosis  must  be  also 
considered.  Careful  physical  examination  of 
the  thorax  and  abdomen  will  usually  reveal 
signs  of  tuberculosis  if  it  be  present,  and  if 
need  be  the  tuberculin  test  can  be  applied. 
Typhoid  fever  presents  a  temperature  range 
after  the  first  few  days  which  does  not  re- 
semble that  of  Malta  fever,  and  the  absence 
of  rose  spots  in  Malta  fever  is  also  an  impor- 
tant differential  point.  The  presence  of  the 
Widal  test  will  also  aid  in  the  differentiation. 

Duration  and  Prognosis. — The  average  dura- 
tion is  from  seventy  to  ninety  days,  although 
some  cases  last  as  long  as  six  months.  Prog- 
nosis as  regards  life  is  favorable,  the  mortality 
being  about  2  per  cent.  From  the  evidence 
thus  far  accumulated  it  seems  that  the  serum 
test  may  afford  prognostic  as  well  as  diagnostic 
information,  for  it  has  been  observed  that  those 
cases  in  which  the  agglutinating  power  of  the 
blood  serum  is  high  during  the  early  stages  of 
the  fever  run  a  favorable  course,  while  those  in 
which  the  agglutinins  remain  low  during  the 


BERIBERI 


249 


entire  course  of  the  fever  are  subject  to  many  relapses  and  a  protracted  con- 
valescence. A  continuous  rise  with  improving  clinical  symptoms  indicates 
approaching  convalescence  (Bassett-Smith). 

Complications. — The  principal  complications  are  hyperpyrexia,  cardiac 
failure,  and  pulmonary  congestion.  Pleural  and  pericardial  effusions  some- 
times occur,  and  persistent  vomiting  has  been  observed  by  Hughes,  who 
regards  it  as  a  very  dangerous  complication. 


Fig.  42 


Temperature  chart  in  the  intermittent  form  of  Malta  fever.    (Hughes.) 

Treatment. — Malta  fever  has  to  be  treated  solely  on  the  expectant  method, 
for  there  are  no  specific  remedies.  The  diet  should  be  nutritious  and  support- 
ing. Dalton,  of  the  English  navy,  deprecates  the  practice  of  keeping  Malta 
fever  patients  on  liquid  food.  All  his  patients  who  do  not  have  an  evening 
temperature  higher  than  103°  are  put  on  solid  food,  such  as  eggs,  bread, 
and  rice,  and  in  addition  receive  two  or  three  pints  of  milk  a  day.  If  this 
diet  is  well  borne,  it  is  supplemented  in  the  course  of  a  few  days  by  fish  or 
meat.  In  severe  cases  with  high  temperature,  foul  tongue,  and  diarrhoea, 
nothing  but  liquid  diet  is  given.  Dalton  also  believes  that  patients  whose 
temperature  keeps  below  102°  are  benefited  by  being  allowed  to  sit  up  part 
of  the  time,  it  being  necessary,  of  course,  to  have  them  avoid  exertion  and 
not  remain  up  too  long.  The  bowels  should  be  carefully  regulated.  Cold 
spongings  with  friction  should  be  used  to  reduce  fever  and  the  kidneys  be 
kept  active  by  mild  diuretics.  When  the  patient  is  strong  enough  to  travel, 
he  is  greatly  benefited  by  change  of  climate.  During  the  early  stages  of 
convalescence  he  should  receive  inunctions  of  oils  and  cocoa-butter,  get 
plenty  of  fresh  air  and  sunshine,  and  receive  aids  to  digestion,  with  iron  to 
overcome  his  anaemia,  which  is  always  marked. 


BERIBERI. 

Definition. — Beriberi  is  sometimes  called  Endemic  Multiple  Neuritis, 
and  is  a  specific  infectious  disease  occurring  in  nearly  all  tropical  and 
subtropical  countries.  The  disease  is  endemic,  is  associated  with  marked 
evidences  of  peripheral  neuritis,  with  sensory  and  motor  palsies,  and  pro- 
found alteration  of  the  motor  mechanism  of  the  heart. 

History. — The  recognition  of  beriberi  as  a  distinct  morbid  entity  is  almost 
as  old  as  recorded  medicine.    The  first  mention  of  it  was  made  by  Strabo, 


250  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

who  describes  the  development  of  this  disease  in  the  Roman  armies  operating 
in  Arabia  (24  B.C.).  It  is  also  described  in  the  medical  writings  of  the 
Chinese  of  the  second  and  seventh  centuries.  It  has  occupied  an  important 
place  in  the  histories  of  all  colonizing  powers.  Dutch  and,  later,  British 
observers  recognized  its  specific  nature  in  the  beginning  of  the  nineteenth 
century.  Our  later  knowledge  of  the  disease,  particularly  the  recognition 
of  the  specific  pathological  lesions,  is  due  to  the  labors  of  the  German 
teachers,  Scheube  and  Baelz,  in  Japanese  universities. 

Distribution. — Speaking  generally,  the  centres  of  greatest  intensity  of 
beriberi  are  the  Malayan  countries.  It  devastates  the  coolie  mining  camps 
and  the  plantations  of  the  Malayan  peninsula.  It  has  been  a  veritable 
scourge  to  the  armies  of  England  in  India,  and  of  Holland  in  Sumatra.  It 
is  always  present  in  Japan,  and  in  portions  of  the  Philippine  Islands  it  is 
very  common  and  was  the  scourge  of  Aguinaldo's  armies.  It  has  occurred 
in  widespread  epidemics  throughout  the  whole  tropical  and  subtropical 
zones.  It  is  found  in  the  principal  parts  of  the  world  and  has  appeared 
as  an  asylum  disease  in  many  temperate  regions.  In  the  United  States 
beriberi  has  been  encountered  with  considerable  frequency  in  the  principal 
ports.  It  has  been  observed  in  asylums  for  the  insane  in  Alabama  and 
Arkansas.  Birge  and  Putnam  have  encountered  it  among  the  fishermen  on 
the  Grand  Banks.  It  seems  very  likely  that  beriberi  occurs  quite  frequently 
in  Louisiana.  Within  recent  years  it  has  been  observed  among  Chinese 
fishermen  from  the  Alaskan  coast;  by  Currie  and  by  Bailey  in  a  settlement 
of  Japanese  at  Cumberlands,  British  Columbia;  in  New  Bedford  whalers, 
and  in  several  Dutch  ships  entering  our  ports. 

Etiology. — In  studying  the  etiology  of  beriberi,  the  most  striking  fact  is 
the  part  that  the  general  hygienic  surroundings  play  in  the  development  of 
the  disease.  The  chief  factor  is  overcrowding.  Where  natives  are  crowded 
together,  as  in  jails,  ships,  and  barracks,  particularly  under  poor  hygienic 
surroundings,  with  an  insufficient  or  poorly  selected  dietary,  in  the  presence 
of  considerable  heat  and  moisture,  the  conditions  are  very  favorable  to  the 
development  of  beriberi. 

The  climatic  conditions  favoring  the  spread  of  beriberi  are  increased 
heat  and  increased  humidity.  Consequently,  in  tropical  countries  the 
greater  number  of  cases  are  observed  during  the  seasonal  rains.  In  the 
Malayan  peninsula  Wright  has  observed  the  greatest  number  of  cases  during 
the  prevalence  of  the  southeast  monsoon,  during  which  season  the  relative 
humidity  is  at  its  highest.  The  disease  is  also  observed  with  great  frequency 
when  these  conditions  are  artificially  maintained,  as  in  the  crowded,  exces- 
sively heated  and  poorly  ventilated  forecastles  of  ships  carrying  Lascar  or 
Coolie  crews.  Beriberi,  as  a  rule,  is  a  disease  of  lower  levels  and  ceases 
abruptly  at  3000  feet  above  the  sea,  although  even  in  this  important  point 
exceptions  have  been  noted. 

With  regard  to  the  specific  etiology  of  beriberi  much  confusion  has  existed. 
Two  principal  views  are  held :  The  first,  and  the  one  to  which  all  the  later 
evidence  points  as  the  correct  one,  is  that  the  disease  is  due  to  a  specific 
germ  infection,  and,  second,  that  the  disease  is  a  nutritional  disorder  con- 
sequent on  either  deteriorated  or  deficient  food,  or  a  nitrogen  starvation. 


BERIBERI  251 

Gelpke,  Miura,  and  Grimm  have  advanced  the  theory  that  in  various  ways 
fish  were  the  infecting  agents  or  carriers  of  the  infection  of  beriberi,  the 
various  theories  ranging  from  the  latency  of  infected  or  spoiled  fish  to  the 
specific  statement  that  beriberi  is  due  to  eating  raw  fish,  particularly  a 
number  of  varieties  of  the  scomboidse  (Miura)  or  the  infection  of  dried  fish 
by  a  species  of  trichina  (Gelpke). 

The  recent  exceedingly  valuable  studies  by  Wright  have  definitely  excluded 
the  fish  theory,  since  his  observations  were  made  among  a  number  of  prisoners 
from  whose  dietary  fish  was  totally  excluded.  Ross  has  recently  suggested 
the  idea  that  beriberi  may  be  due  to  arsenical  poisoning.  In  pursuing 
these  studies  he  found  arsenic  in  appreciable  quantities  in  the  hair  of  a 
number  of  cases  from  Penang.  Manson  has  called  attention  to  the  very 
common  adulteration  of  Chinese  tobacco  with  arsenic  in  order  to  give  a 
particularly  desired  garlic  flavor.  These  cases  must,  however,  be  consid- 
ered accidental  or  coincidences  in  which  laborers  in  arsenical  ores,  canned 
provisions,  adulterated  tobacco,  etc.,  have  added  to  the  symptoms  of  beri- 
beri a  chronic  arsenical  poisoning  closely  resembling  beriberi.  Competent 
observers  have  failed  to  find  arsenic  in  the  great  majority  of  cases. 

The  greatest  conflict  has  always  been  waged  over  the  theories  connecting 
beriberi  with  rice  and  rice-eating.  The  disputants  are  divided  into  two 
classes,  one  of  which  considers  the  disease  as  a  toxaemia  due  to  a  fungus 
poisoning  of  the  rice,  placing  it  in  the  category  of  diseases  like  chronic 
maize  intoxication,  or  pellagra.  The  second  class  assumes  that  with  rice 
as  the  bulk  of  an  inadequate  dietary  the  disease  develops  as  the  expression 
of  nitrogen  starvation.  It  is  indeed  curious  to  see  how  universal  is  the  belief, 
in  countries  and  among  peoples  where  beriberi  is  endemic,  that  the  disease 
is  due  to  bad  rice.  In  the  Philippines  the  sailor  or  convict  suffering  from 
beriberi  not  only  ascribes  his  condition  to  rice,  but  will  confidently  point 
out  the  particular  rice  which  has  brought  him  to  his  evil  state.  There  is 
very  much  that  is  significant  in  the  facts  adduced  in  support  of  this  theory. 
The  disease  is  known  to  affect  almost  entirely  the  rice-eating  peoples,  and 
it  is  carried  by  these  people  into  new  regions.  Perhaps  the  most  suggestive 
of  all  facts  in  the  etiology  of  beriberi  is  the  extraordinary  decrease  in  the 
cases  occurring  in  the  Japanese  navy  and  army  coincident  with  an  improved 
dietary,  in  which  a  large  part  of  the  rice  component  of  the  nation  was  substi- 
tuted by  bread  and  meat.  But  it  must  also  be  remembered  that  at  the  same 
time  the  most  pronounced  advances  were  made  in  Japan  in  general  hygienic 
and  sanitary  reforms,  and  a  large  part  of  the  good  results  must  be  ascribed 
to  these. 

As  against  the  theory  that  rice  diet  involving  nitrogen  deficiency  is  the 
cause  of  the  disease  we  have  a  host  of  valuable  observations.  In  the  Dutch 
armies  dietary  changes  produced  no  mitigation  of  the  disease.  Wright  in  his 
observations  in  Kwala  Lumpor  Jail,  in  the  Federated  Malay  States,  kept 
the  prisoners  on  a  dietary  in  which  there  was  a  decided  preponderance  of 
nitrogenous  elements  with  the  same  incidence  rate  of  the  disease.  Finally, 
in  this  country  Ashmead  in  New  York  and  Daland  in  Philadelphia  have 
observed  the  disease  in  sugar  ships  that  had  no  rice  aboard.  Nevertheless 
it  must  be  conceded  that  nutritional  disturbances  which  are  very  commonly 


252  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

present  in  rice-eating  peoples  have  a  distinct  predisposing  influence  to  the 
development  of  the  disease.  With  regard  to  the  theory  that  smutted  or 
infected  rice  is  the  cause  of  the  disease,  exhaustive  examination  of  raw  rice 
has  revealed  nothing  but  Aspergillus  niger  and  Bacillus  subtilis.  In  order  to 
exclude  this  factor  the  rice  has  been  boiled  and  prepared  under  two  or  three 
atmospheres  of  steam  pressure,  thus  ensuring  the  destruction  of  any  germ 
or  toxin  with  entirely  negative  results  as  to  the  prevention  or  diminution  of 
the  disease. 

Other  observers  have  connected  the  disease  with  various  intestinal  para- 
sites, uncinaria  and  strongyloides  intestinalis,  or  with  hsemic  plasmodia 
(Glogner),  but  these  have  all  been  shown  to  be  accidental  complications, 
not  causes,  and  due  to  the  prevalence  in  given  sections  of  either  intestinal 
parasites  or  the  malarial  plasmodium  along  with  the  beriberi. 

There  remains,  then,  the  theory  that  the  disease  is  due  to  a  specific  germ 
infection.  The  studies  of  Wright  have  given  a  very  strong  evidence  in  this 
direction.  The  statement  of  Wright's  vie,ws  is  best  given  in  his  own  words: 
"The  theory  of  the  causation  of  beriberi  that  fits  the  facts  is  that  beriberi 
is  due  to  a  specific  organism  which  gains  entrance  to  the  body  via  the  mouth, 
that  it  develops  and  produces  a  toxin  chiefly  in  the  pyloric  end  of  the  stomach 
and  duodenum,  and  that  the  toxin,  being  absorbed,  acts  atrophically  in  the 
peripheral  terminations  of  the  afferent  and  efferent  neurons.  Further,  that 
the  specific  organism  escapes  in  the  feces  and  lodges  in  confined  places 
through  accident  or  careless  personal  habits  of  those  affected  by  this  dis- 
order, and  that  in  the  presence  of  congenial  meteorological,  chmatic,  and 
artificial  conditions  of  close  association  from  overcrowding,  the  organism 
becomes  virulent  and,  gaining  entrance  to  the  healthy  body  in  food,  etc., 
contaminated  by  it,  gives  rise  to  an  attack  of  the  disease." 

This  theory  of  the  disease  is  also  borne  out  by  the  peculiar  epidemic 
extensions  of  beriberi  and  by  the  well-known  infection  of  places,  separate 
dwellings,  particular  ships,  and  certain  wards  or  barracks  in  jails  or  camps. 
W^right  has  clinched  his  arguments  by  infecting  monkeys,  and  also  by  pro- 
ducing typical  beriberi  in  them  by  placing  them  in  the  cells  with  beriberi 
cases.  I  (Kieffer)  have  seen  a  typical  case  of  beriberi  in  a  monkey  which 
was  fed  by  a  Filipino  convalescent  from  beriberi,  and  have  produced 
unmistakable  beriberi  in  other  monkeys  in  the  same  way.  In  support  of 
the  idea  that  the  contamination  is  carried  by  the  feces,  the  universal  lack 
of  any  hygienic  precautions  in  defecation  or  disposal  of  the  fecal  matters  of 
the  sick  in  tropical  countries  must  be  remembered.  Also,  that  cleanliness 
of  the  anal  region  is  very  much  neglected..  ^^Taen  we  finally  remember 
that  these  peoples  almost  universally  eat  with  their  fingers,  that  the  fingers 
are  almost  certainly  contaminated  with  fecal  matter,  and  that  the  custom 
is  to  eat  out  of  a  common  bowl,  these  theories  gain  very  much  more  weight. 
To  complete  the  observations  on  the  etiology  of  beriberi  it  must  also  be 
remembered  how  often  beriberi  has  spread  to  the  proportions  of  an 
epidemic  in  tropical  countries  following  an  epidemic  of  cholera. 

Frequency. — Beriberi  is  observed  much  more  frequently  in  males  than  in 
females;  not  because  there  is  any  greater  susceptibility  in  the  male,  but 
because  women  form  a  comparatively  small  number  in  Coolie  camps,  jails, 


BERIBERI  253 

prisons,  and  ships.  Given  an  equal  degree  of  exposure,  there  is  no  reason  to 
believe  one  sex  more  resistant  than  the  other.  With  respect  to  age,  beriberi 
may  be  said  to  be  a  disease  of  early  adolescence  and  adult  life.  Although 
it  is  true  that  cases  have  been  observed  in  infants  in  the  endemic  areas,  yet 
the  occurrence  of  beriberi  in  children  under  ten  years  is  very  rare.  The  great 
majority  of  cases  occur  between  the  tv^entieth  and  fortieth  year,  although 
it  must  also  be  remembered  that  a  large  proportion  of  those  exposed  to  the 
disease  are  young  adults. 

Beriberi  is  chiefly  a  disease  of  the  yellow  races,  occurring  principally  in 
emigrants.  At  the  present  day  beriberi  is  very  rarely  observed  in  Europeans 
and  North  Americans.  The  white  races  enjoy  a  nearly  complete  immunity, 
due  in  part  to  the  better  hygienic  conditions  under  which  they  live. 

The  Prophylaxis  of  Beriberi. — When  the  disease  breaks  out  in  ships,  jails, 
asylums,  or  barracks,  these  had,  whenever  possible,  better  be  temporarily 
abandoned.  They  should  then  be  thoroughly  disinfected  and  whitewashed 
or  repainted.  Old  woodwork  should  be  scraped  and  painted  or  torn  out. 
In  ships  the  bilges  should  be  cleaned.  If  dampness  exists  from  deficient 
drainage  it  should  be  remedied.  Ample  ventilation  must  be  provided.  The 
dietary  should  be  revised,  and  wherever  possible  beans  or  meal  substituted  for 
rice,  and  a  sufficient  amount  of  fresh  animal  food  allowed. 

Pathology  and  Morbid  Anatomy. — When  death  occurs  rigor  mortis  is 
slight  and  of  short  duration.  If  the  case  be  recent  and  acute,  or  if  death 
be  due  to  cardiac  paralysis,  the  cadaver  bears  all  the  evidence  of  intense 
dyspnoea  and  cyanosis.  The  eyes  are  staring,  the  conjunctiva  suffused 
with  blood,  the  cervical  veins  tumid  and  full,  the  lips  covered  with  bloody 
froth.  In  the  atrophic  cases  there  is  very  considerable  wasting.  In  the 
dropsical  cases  the  effusion  is  commonly  associated  with  huge  thoracic, 
pericardial,  and  abdominal  dropsies  and  oedema  of  the  lungs.  In  acute 
cases  marked  congestion  of  the  pyloric  end  of  the  stomach  and  of  the  duo- 
denum with  punctiform  hemorrhages  is  found.  The  duodenal  glands  are 
swollen  and  congested.  Wright  considers  this  to  be  the  specific  lesion  of 
the  disease,  and  states  that  it  is  always  found  when  the  case  ends  fatally 
within  three  weeks  of  the  beginning  of  the  disease. 

The  liver  and  kidneys  are  enlarged,  hypersemic,  and  show  cloudy  swell- 
ing. The  spleen  is  enlarged,  but  otherwise  shows  no  characteristic  changes. 
The  heart  is  enlarged,  the  principal  changes  being  found  in  the  right 
side.  The  ventricle  is  both  hypertrophied  and  dilated.  Microscopically 
there  is  usually  marked  fatty  degeneration  of  the  myocardium.  The 
intrinsic  nerve  cells  of  the  heart  show  marked  atrophic  changes.  The 
terminations  of  the  vagus  are  also  atrophied.  The  trunk  of  the  vagus  is 
not  involved  in  early  cases,  but  in  later  cases  the  trunk  of  this  nerve  as 
well  as  the  splanchnics  and  phrenics  are  profoundly  degenerated.  The 
peripheral  nerves  show  striking  and  constant  changes.  These  begin  with 
degeneration  of  the  terminal  branches  of  the  nerves.  Not  only  the  mus- 
cular but  also  the  cutaneous  twigs,  and  in  advanced  cases  the  main 
nerve  trunks,  may  be  involved.  The  nerve  changes  are  present  in 
proportion  to  the  extent  and  intensity  of  the  paralysis  during  life. 

The  voluntary  muscles  show  similar  changes  in  the  distribution  of  the 


254  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

degenerated  nerves.  The  muscle  fibres  undergo  fatty  degeneration,  the 
striations  disappear,  the  nuclei  are  enlarged,  and  the  interstitial  connective 
tissue  may  be  increased.  The  central  nervous  system  shows  in  the  brain 
and  cord  congestion  of  the  meninges  and  brain  substance,  with  increase 
in  the  cerebrospinal  fluid.  Degenerative  changes  can  be  found  in  the 
posterior  ganglia,  and  sometimes  atrophy  of  the  posterior  columns  is  present. 

Incubation. — The  incubation  period  of  beriberi  has  not  been  definitely 
determined.  Pekelharing  and  Winkler  have  placed  it  as  being  a  long  one, 
possibly  extending  over  months.  In  Wright's  study  of  newly  arrived  emi- 
grants into  infected  regions,  78  cases  developed  within  thirty  days  after 
arrival  and  no  less  than  12  of  them  within  ten  days;  so  that  he  has  no 
hesitation  in  saying  that  the  incubation  of  beriberi  is  between  ten  and 
twenty  days.    These  observations  need  confirmation. 

Symptoms. — Clinically,  several  types  of  the  disease  are  recognized.  There 
are  atrophic  cases  (paraplegic  or  dry  beriberi),  dropsical  cases  (wet  beriberi), 
acute  pernicious  cases,  and  mild  or  rudimentary  cases.  These  classes  repre- 
sent not  only  variations  of  type,  but  variations  of  intensity. 

The  disease  is  usually  ushered  in  by  marked  prodromata.  There  is  loss 
of  appetite,  with  severe  pain  in  the  epigastrium  and  oppression  in  the  chest. 
With  these  symptoms  there  is  a  slight  febrile  rise.  In  a  few  cases  rigors, 
lassitude,  mental  disturbances,  and  head  pains  are  observed. 

Atrophic  Cases. — After  a  few  days  or  weeks  the  patient  notices  a  slowly 
increasing  weakness  of  the  legs,  with  pain  and  tension  in  the  calf  muscles. 
There  is  next  a  loss  of  sensation  in  the  soles  of  the  feet.  The  patient  does 
not  "feel"  the  floor,  or  feels  as  though  a  soft  insole  had  been  placed  between 
the  foot  and  the  shoe  or  sandal.  This  increases  until  the  patient  becomes 
bedridden.  As  a  rule,  the  palsies  are  confined  to  the  legs  and  trunk,  some- 
times invading  the  arms,  and  very  rarely  affecting  the  head  and  neck.  The 
paralyzed  limbs  rapidly  atrophy  and  areas  of  anaesthesia  and  hypersesthesia 
develop.  Examination  shows  the  superficial  reflexes  preserved;  the  deep 
reflexes  lost.  The  calf  muscles  and  extensors  of  the  legs  are  extensively 
wasted.  The  palsy  is  nearly  always  flaccid,  may  be  quite  profound,  and  is 
more  marked  in  the  extensors  than  in  the  flexors,  resulting  in  drop-wrist 
and  paralytic  equinovarus.  The  electric  muscle  reactions  are  markedly 
altered.  From  the  beginning  there  is  marked  diminution,  going  on  to  total, 
loss  of  reaction  to  both  galvanic  and  faradic  stimulation. 

The  sensory  symptoms  closely  parallel  the  distribution  of  the  motor 
symptoms,  and  are  even  more  constant.  Spots  of  ancesthesia  and  parcesthesia 
are  formed  on  the  feet,  calves,  legs,  trunk,  and  arms.  Recovery  from 
the  condition  is  extremely  tedious.  Gradually  the  areas  of  hypersesthesia 
disappear,  sensation  and  motion  return,  and  in  the  course  of  ten  to  twelve 
months  the  atrophied  muscles  regain  their  contour. 

Dropsical  cases  resemble  the  atrophic  cases  plus  marked  cardiac  phe- 
nomena with  dropsy.  Sometimes  the  dropsical  cases  develop  from  the 
atrophic.  The  dropsy  begins  in  the  feet  and  legs  and  spreads  until  the  whole 
body  is  affected.  The  face  and  lips  are  puffy  and  heavy.  The  arms,  legs,  and 
trunk  are  pudgy.  With  this  there  are  marked  evidences  of  cardiac  distress. 
There  are  cyanosis  of  the  lips  and  fingers,  dyspnoea,  and  a  marked  sense  of 


BERIBERI  255 

oppression  in  the  prsecordium.  Usually  the  patient  is  quite  helpless,  or,  if 
he  can  walk,  the  slight  exertion  is  attended  by  breathlessness  and  palpita- 
tion, these  symptoms  being  very  much  increased  by  effusion  into  the 
serous  cavities.  The  urine  is  greatly  diminished,  but  contains  no  albumin. 
After  persisting  for  weeks  or  months  the  dropsy  may  rapidly  disappear, 
with  an  enormous  increase  in  the  urine.  As  a  rule,  these  cases  do  not  present 
the  extreme  grades  of  paralysis  and  atrophy  that  are  found  in  the  first  type. 
Yet  the  absorption  of  the  dropsical  fluid  will  reveal  marked  wasting  that  may 
have  been  completely  masked  by  the  semi-solid  appearance  of  the  effusion. 

In  both  types  of  cases  the  cardiac  changes  are  marked.  The  pulse  rate  is 
usually  increased  and  slight  exertion  serves  to  further  increase  the  rapidity 
to  120  to  140  beats  per  minute.  The  heart  is  enlarged,  particularly  on  its 
right  side.  The  carotids  pulsate  violently  and  in  the  severe  cases  pulsation 
is  seen  in  the  jugular  veins.  Systolic  and  diastolic  murmurs  are  heard,  the 
murmurs  being  propagated  very  widely,  sometimes  even  into  the  bronchial 
and  femoral  arteries.  Reduplication  of  the  sounds  is  frequently  heard,  and 
there  is  equal  spacing  between  the  sounds.  Despite  the  forcible  cardiac  beat 
and  the  violent  pulsation  in  the  vessels  of  the  neck,  the  peripheral  pulse  is 
remarkably  small  and  weak.  All  these  cardiac  phenomena  are  exceedingly 
fugitive.  Even  the  most  pronounced  murmurs  and  evidences  of  dilatation 
come  and  go  with  rapidity. 

Acute  Pernicious  Beriberi. — This  form  attacks,  as  a  rule,  the  more 
vigorous  adults.  It  may  appear  as  an  acute  type  from  the  very  beginning, 
or  it  may  represent  a  sudden,  fatal  episode  in  mild  or  convalescent  cases. 
Beginning  in  the  ordinary  way,  the  disease  advances  with  great  rapidity, 
so  that  the  man  becomes  bedridden  in  a  few  days.  The  symptoms  of  car- 
diac involvement  begin  early  and  are  marked.  When  this  type  develops 
from  the  milder  forms  the  change  is  very  sudden.  Palpitation  and  dyspnoea 
become  more  and  more  severe.  The  patient  gasps  and  struggles  for  breath. 
He  complains  of  extreme  pain  in  the  prsecordium.  He  breathes  with  tremen- 
dous, laboring,  gasps.  The  vessels  of  the  neck  pulsate  violently.  The  eyes 
are  suffused  and  staring.  A  blood-flecked  foam  collects  on  the  lips;  unless 
speedily  relieved  the  patient  dies  a  most  dreadful  death.  In  these  cases  the 
urine  is  notably  diminished  or  even  suppressed.  Nausea  and  vomiting  are 
common  toward  the  end. 

Mild  and  rudimentary  beriberi  of  all  degrees  are  observed.  These 
cases  usually  complain  of  pain  and  tension  in  the  legs,  with  weakness  and 
numbness.  The  anaesthetic  areas  may  be  very  small  and  sharply  marked. 
The  patient  usually  develops  some  degree  of  cardiac  irritability  and  palpita- 
tion. There  may  or  may  not  be  oedema  of  the  legs.  These  cases  are  im- 
portant because  here  and  there  a  very  mild  case  may  suddenly  develop  an 
acute  pernicious  cardiac  attack.  As  a  rule,  however,  they  clear  up  com- 
pletely, rarely  lasting  over  the  cool  season. 

Special  mention  should  be  made  of  the  skin  s}Tnptoms.  Petechice  and 
herpes  of  the  lips  are  very  common  in  beriberi,  as  is  also  a  diffuse  or  blotchy 
redness  in  the  arms  and  legs.  After  the  very  beginning  of  the  disease  there 
is  no  fever.  A  marked  rise  of  temperature  means  a  reinfection  or  the 
development  of  some  complication. 


256  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

The  blood  shows  no  characteristic  nor,  indeed,  any  marked  changes  in 
beriberi.  As  a  rule,  there  is  a  very  moderate  diminution  of  the  red  cells. 
In  severe  and  long-continued  cases  the  ansemia  may  become  more  marked, 
with  some  considerable  loss  of  hemoglobin,  the  color  index  being  minus. 
In  the  average  cases  there  is  no  change  in  the  white  corpuscles.  In  severe 
cases  a  moderate  leukocytosis  is  found.  The  bacteriological  findings  are 
negative. 

The  urine  shows  very  little  change.  The  urea  is  diminished,  and,  as  a  rule, 
the  specific  gravity  is  also  decreased.  Sugar  and  albumin  are  not  found. 
Indican  is  present  in  large  amounts  (Baelz).  The  urine  is  diminished  in 
quantity  in  the  pernicious  cases,  even  to  comjplete  suppression.  In  the  cases 
of  wet  beriberi  the  urine  is  greatly  diminished.  The  secretion  is  re-established 
when  the  exudations  begin  to  be  absorbed.  Under  these  circumstances 
an  unusually  large  amount  of  urine  may  be  passed,  and  this  re-establish- 
ment of  the  renal  function  is  a  very  favorable  prognostic  symptom. 

Diagnosis. — The  occurrence  of  beriberi  in  its  usual  form  in  the  endemic 
area,  or  in  persons  hailing  from  infected  regions,  offers  no  diagnostic  diffi- 
culty. When  the  cases  occur  in  groups,  the  symptoms  of  peripheral  neuritis 
point  to  nothing  else.  In  isolated  cases,  however,  the  diagnosis  is  not  by 
any  means  easy,  and  the  distinction  between  arsenical  or  alcoholic  neuritis 
and  beriberi  may  be  difficult.  The  presence  of  oedema  is  significant  of 
beriberi.  The  earlier  and  more  decided  alterations  in  the  deep  reflexes 
and  the  palpitating  and  irritable  heart  also  point  to  beriberi. 

Prognosis. — The  percentage  mortality  of  beriberi  depends  on  the  per- 
nicious cases.  The  latter  are  almost  always  fatal  and  furnish  certainly  90 
per  cent,  of  the  total  mortality.  In  the  remaining  cases  the  mortality  varies 
widely  in  different  epidemics.  Ten  per  cent,  would  be  a  very  fair  average 
mortality,  although  it  may  run  as  high  as  40  per  cent.  There  is  no  disease  in 
which  prognosis  is  so  uncertain  and  hazardous.  Again  and  again  I  (Kieffer) 
have  seen  cases  I  considered  practically  well,  certainly  out  of  all  danger,  die 
with  rapidity  in  the  appalling  cardiac  crisis  of  this  disease.  The  prognosis 
is  favorable,  without  regard  to  the  extent  of  the  paralytic  lesions,  in  propor- 
tion to  the  integrity  of  the-  innervation  of  the  heart.  Increase  of  the  urine 
is  a  favorable  sign.  So,  too,  are  return  of  appetite  and  sexual  desire.  On 
the  other  hand,  increasing  irregularity  of  the  heart;  equal  spacing  of  the 
cardiac  intervals,  the  short  and  long  pause  becoming  equal  or  nearly  so; 
increasing  cyanosis,  paralysis  of  the  diaphragm,  and  diminishing  urine  are 
very  unfavorable  signs.  The  presence  of  bronchitis,  pneumonia,  dysentery, 
alcoholism,  and  icterus  are  unfavorable.  Vomiting  is  as  sinister  a  symptom 
in  beriberi  as  is  black  vomit  in  yellow  fever. 

Treatment. — Baelz  has  recommended  the  use  of  salicylic  acid  or  the  salicy- 
late of  sodium  in  15  grain  doses  four  times  a  day.  Their  value  is  prob- 
lematical. As  much  may  be  said  for  the  plan  of  freely  purging  these  patients. 
When  constipation  exists  in  beriberi  a  mild  saline  is  indicated,  otherwise  it 
is  not  useful.  In  acute  cases  the  dyspnoea,  cardiac  distress,  and  girdle  pain 
are  best  controlled  by  morphine  hypodermically.  This  remedy  may  allay 
the  vomiting. 

For  cardiac  cases,  particularly  those  with  dropsy,  digitalis  is  the  best 


ANTHRAX  257 

remedy.  It  must  be  given  freely  in  large  doses.  The  cardiac  attacks  are 
best  controlled  by  nitroglycerin  or  inhalations  of  the  nitrite  of  amyl.  These 
remedies  should  always  be  readily  accessible  in  beriberi  wards.  If  the 
symptoms  of  cardiac  failure  become  severe,  the  patient  should  be  bled. 
It  will  frequently  be  found  impossible  to  bleed  at  the  elbow,  under  which 
circumstances  the  patient  should  be  bled  from  the  jugulars.  About  400  c.c. 
should  be  drawn.  The  relief  from  this  measure  is  prompt  but  evanescent, 
but,  as  Manson  says,  "the  patient  is  for  the  time  being  tided  over  an  acute 
danger  and  given  another  chance." 

The  patient  should  be  put  on  a  liberal  diet  scale  in  which  nitrogenous 
foods  and  fats  form  a  conspicuous  part.  He  should  be  kept  in  a  dry,  sunny 
room,  and  whenever  possible  should  be  out  of  bed  in  the  open  air.  The 
best  remedy  we  have  is  removal  of  the  sufferer  from  the  endemic  area.  The 
extreme  value  of  this  measure  is  common  knowledge  to  all  tropical  prac- 
titioners. If  the  patient  cannot  be  removed  from  the  town  or  province, 
removal  to  another  house  does  a  great  deal  of  good,  particularly  if  one  on 
high  and  dry  ground  is  chosen. 

The  treatment  of  the  residual  palsies  is  the  same  as  that  of  any  other 
form  of  severe  polyneuritis. 


ANTHRAX. 

Definition. — Anthrax  is  an  infectious  disease  due  to  the  presence  of  the 
Bacillus  anthracis.  It  is  much  more  common  in  Europe  and  in  South  America 
than  in  the  United  States  and  England,  and  affects  animals  far  more  fre- 
quently than  man.  While  it  is  possible  for  one  man  to  convey  it  to  another 
by  contact,  the  infection  in  the  great  majority  of  instances  takes  place  directly 
from  one  of  the  lower  animals.  Among  animals  it  is  met  with  most  fre- 
quently among  herbivora,  next  among  omnivora,  and  least  frequently 
among  carnivora.  Anthrax  is  sometimes  called  malignant  pustule,  splenic 
fever,  charbon,  and  carbuncle.  The  first  synonym  is  unfortunate,  for  in  many 
cases  no  pustule  is  found;  the  second  synonym  is  incorrect,  as  in  man  the 
spleen  is  not  particularly  affected,  and  the  last  is  equally  erroneous,  as  it  is 
an  entirely  different  state  from  ordinary  carbuncle  due  to  the  staphylococcus. 

History. — Anthrax  as  it  occurs  in  man  has  been  recognized  for  over  2000 
years,  and  as  long  ago  as  the  time  of  the  Romans  it  was  treated  by  the 
cautery.  During  the  seventeenth  and  eighteenth  centuries  it  was  very 
prevalent.  Barth^lemy  proved  in  1823  that  animals  could  be  inoculated 
with  it.  In  1850  Heusinger  published  an  accurate  and  exhaustive  account 
of  the  disease.  The  bacillus  was  observed  in  the  blood  by  Pollender  in  1849 
and  its  relation  to  the  disease  was  more  fully  worked  out  by  Davaine  in 
1863.  Since  then  this  discovery  has  been  confirmed  by  many  observers, 
the  chief  of  whom  are  Pasteur  and  Koch. 

Etiology. — As  already  stated,  anthrax  is  due  to  the  entrance  into  the  body 

of  the  anthrax  bacillus.    It  usually  occurs  as  a  result  of  handling  some  part 

of  an  animal  which  has  suffered  from  this  malady.     Of  Legge's  211  cases 

72  were  in  workers  in  wool  and  65  were  handlers  of  hides.    The  infection 

17 


258  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

takes  place  through  some  break  in  the  skin,  as  a  rule,  and  in  the  great 
majority  of  cases  the  site  of  inoculation  is  the  hand  or  forearm,  but  it  may 
appear  on  the  face  and  chest.  In  Legge's  series  infection  occurred  in  the 
neck  in  84  cases,  in  the  face  and  head  in  77,  forearm  16,  and  in  but  one 
case  was  the  finger  thought  to  be  the  point  of  infection.  Sometimes  more 
than  one  point  of  infection  is  present;  but  it  occasionally  happens  that  no 
external  lesion  is  to  be  found,  although  general  systemic  infection  is  mani- 
fest. In  such  instances  the  bacillus  gains  access  to  the  body  by  being  inhaled 
in  dust,  or  by  being  swallowed  in  milk  or  other  food.  Rarely  infection 
of  an  external  wound  takes  place  by  the  transference  of  the  bacillus  by  flies 
from  an  infected  animal  to  the  break  in  the  skin  of  man  or  animal. 

Prevention. — The  disease  can  be  prevented  in  man  by  forbidding  work- 
men to  handle  raw  hides  or  infected  animals  if  they  have  any  superficial 
wounds,  by  the  use  of  respirators  designed  to  prevent  the  inhalation  of  dust 
laden  with  the  bacillus  of  the  disease,  and  by  the  disinfection  of  wool,  hair, 
rags,  and  other  articles  of  commerce  which  may  convey  the  infection 

All  animals  suffering  from  anthrax  should  be  killed  and  then  destroyed 
by  burning.  Mere  burial  is  insufficient,  for  it  is  claimed  that  earth-worms 
are  capable  of  carrying  the  bacilli  to  the  surface  and  so  causing  the  reinfec- 
tion of  healthy  animals.  When  incineration  is  impossible  burial  in  quick- 
lime may  be  resorted  to.  It  is  needless  to  add  that  the  utmost  care  must 
be  exercised  by  physicians  and  nurses  in  dressing  cases  of  this  disease  when 
it  occurs  in  man. 

Frequency. — In  the  United  States  anthrax  is  not  a  very  common  disease 
even  among  sheep  and  cattle,  and  is  rarely  met  with  in  man.  Inquiry 
among  employers  of  men  who  handle  raw  hides  in  Philadelphia  develops 
the  fact  that  it  is  very  seldom  met  with,  and  when  it  occurs  is  nearly  always 
the  result  of  handling  imported  hides. 

Pathology  and  Morbid  Anatomy. — The  changes  in  the  skin  produced  by 
primary  external  anthrax  will  be  described  later  under  the  head  of  Symp- 
toms. When  systemic  infection  occurs  as  the  result  of  either  external  or 
internal  primary  inoculations,  very  marked  lesions  of  the  viscera  become 
apparent.  The  bronchial  glands  are  generally  swollen,  and  their  increase 
in  size  may  be  quite  remarkable.  The  pericardium  may  be  dotted  by 
petechial  spots,  and  its  cavity  may  contain  a  considerable  quantity  of  gela- 
tinous material.  The  muscles,  including  the  heart,  are  dark  colored,  soft, 
and  flabby.  The  blood  is  fluid  and  dark  in  hue — sometimes  almost  black. 
Clots  may  be  found  in  the  pericardial  space.  Clear,  straw-colored  fluid 
may  be  present  in  the  pleural  cavity,  and  if  the  lungs  are  affected  they  are 
found  engorged  with  dark-colored  blood,  the  right  lung  being  more  affected 
than  the  left  as  a  rule;  the  posterior  portion  is  most  congested  and 
oedematous,  particularly  at  the  bases.  Sometimes  pulmonary  infarctions 
are  present. 

In  the  abdominal  cavity  numerous  extravasations  of  the  blood  may  be 
found  in  the  mesentery.  Petechial  hemorrhages  may  be  present  in  the 
stomach  and  intestines.  The  spleen  is  usually  enlarged  and  contains  a 
large  amount  of  grumous  blood.  Microscopic  examination  of  the  tissues 
of  the  body,  when  general  infection  is  present,  discloses  the  bacillus  usually 


ANTHRAX  259 

in  large  numbers.  They  are  particularly  numerous  in  the  small  blood- 
vessels and  lymph  glands  which  are  near  the  site  of  the  primary  lesion. 

Symptoms. — Anthrax  occurs  in  two  forms,  the  external  and  internal. 
The  external  form  manifests  itself  by  the  development  at  the  point  of  infec- 
tion, about  three  to  six  days  after  contact  with  the  source  of  the  disease,  of 
a  small,  itching  papule,  which  is  soon  surrounded  by  an  inflamed  area. 
Usually  this  lesion  is  so  insignificant  that  no  attention  is  paid  to  it  save  the 
scratching  or  rubbing  of  it.  There  may  be  a  history  of  an  abrasion,  scratch, 
or  pimple  through  which  infection  has  occurred.  The  papule  speedily 
becomes  red  and  angry-looking,  and  at  its  summit  a  vesicle  develops  which 
is  filled  with  bloody  serum.  Around  this  centre  of  infection,  on  the  reddened 
and  oedematous  zone  or  base,  additional  papules  and  vesicles  appear  and 
the  inflammatory  process  spreads  rapidly  in  all  directions.  The  vesicles 
may  become  dry  and  crusty,  and  as  they  do  so  the  tissues  underneath  undergo 
softening,  the  central  part  becoming  black  and  necrotic.  Curiously  enough, 
this  rapid  process  rarely  causes  much  pain,  but  the  neighboring  lymphatic 
vessels  become  reddened  and  the  nodes  enlarged.  By  the  end  of  forty- 
eight  hours  after  the  papule  first  appears  the  anthrax  bacilli  may  be  found 
in  the  blood,  and  in  such  a  case  the  symptoms  of  systemic  disturbance 
rapidly  become  very  marked. 

The  local  lesion  rapidly  spreads  up  the  arm  if  the  hand  be  the  part  first 
attacked,  and  the  part  becomes  intensely  swollen  and  livid,  the  skin  being 
dotted  by  blebs,  but  it  is  a  noteworthy  fact  that  the  rapid  spread  of  the 
surrounding  inflammation  is  due  largely  to  secondary  infection  by  other 
organisms.  In  cases  of  pure  anthrax  infection  the  central  papule  is  often 
surrounded  by  an  area  of  induration,  but  no  red  areola  even  after  the  slough 
has  formed.  There  is  general  wretchedness  and  rapidly  increasing  debility, 
followed  by  rigors,  high  fever,  sweats,  and  diarrhoea,  but  after  the  early  stages 
the  fever  falls  and  the  temperature  may  be  normal.  Delirium  rapidly  ensues, 
and  dyspnoea  and  cyanosis,  with  profound  evidences  of  septic  infection,  close 
the  scene  in  death.  In  some  cases,  however,  the  mind  remains  perfectly 
clear. 

When  recovery  takes  place  the  local  area  is  walled  off  by  protective  efforts 
on  the  part  of  the  body,  so  that  severe  constitutional  symptoms  do  not 
appear.  The  diseased  tissues  at  the  focus  of  infection  undergo  necrosis,  are 
thrown  off,  and  healing  is  finally  accomplished. 

A  second  form  of  external  anthrax  infection  is  that  which,  because  of  its 
course,  is  called  malignant  anthrax  cedema.  This  usually  develops  on  the 
face  or  head  and  differs  from  the  type  just  described  in  that  no  papule  or 
similar  local  lesion  is  present,  but  in  its  stead  an  intense  oedema  of  the  tissues 
is  produced.  So  active  may  be  the  local  process  that  the  parts  may  speedily 
slough  or  become  gangrenous.    Death  usually  comes  rapidly  to  such  cases. 

The  internal  form  of  anthrax  manifests  itself  in  the  lungs  or  alimentary 
tract.  In  the  first  instance  the  anthrax  bacilli  enter  the  respiratory  passages 
by  inhalation  in  the  dust  arising  from  the  handling  of  dried  hides  or  wool. 
Hence  it  is  called  "wool-sorters'  disease."  The  symptoms  in  these  cases 
vary  to  an  extraordinary  degree  in  their  severity.  In  some  instances  the 
patient  feels  wretched  and  miserable,  and  soon  has  a  chill  which  is  followed 


260  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

by  fever  and  very  marked  thoracic  distress.  There  may  be  pain  in  the 
side  and  labored,  difficult  breathing.  Cough  may  or  may  not  be  present. 
The  face  becomes  livid,  marked  cyanosis  develops,  and  the  patient  dies  in  a 
few  hours  or  days  in  asthenia  and  collapse.  Pneumonia  is  rare,  but  areas 
of  impaired  resonance  on  percussion  and  bronchial  breathing  may  be  found 
as  the  result  of  enlargement  of,  and  pressure  by,  the  bronchial  and  mediastinal 
glands.  In  other  cases  the  symptoms  are  so  mild  and  indefinite  as  to  possess 
no  diagnostic  value.  A  workman  may  feel  only  weak  and  feeble,  his  hands 
may  be  cold,  and  his  breathing  oppressed,  yet  he  may  die  within  twenty- 
four  hours  in  collapse.  Bell  records  several  cases  in  which  death  came 
within  twenty-four  hours  of  what  seemed  to  be  perfect  health. 

When  the  intestinal  tract  is  infected,  there  are  present  diarrhoea,  vomiting, 
great  weakness,  and  failure  of  the  circulation  followed  by  collapse  and  death 
in  from  two  to  five  days. 

Diagnosis. — In  the  external  form  of  the  disease  the  occupation  of  the 
patient  and  the  presence  of  an  itching  papule  should  at  once  arouse  the 
suspicion  of  anthrax  infection,  which  will  be  strengthened  by  the  rapid  for- 
mation of  the  vesicle  already  described.  The  diagnosis  can  be  confirmed  by 
a  microscopic  examination  of  the  fluid  for  the  bacillus,  or  by  inoculating  a 
mouse  with  one  drop  of  the  fluid  from  a  vesicle.  This  wifl  cause  the  death 
of  the  mouse  in  about  forty-eight  hours,  and  in  its  organs  the  bacillus  will 
be  found  in  immense  numbers,  and  from  these  cultures  may  be  made. 

This  condition  is  separated  from  carbuncle  by  the  lack  of  pus  and  by 
the  absence  of  its  sloughing  core.  From  erysipelas  of  the  phlegmonous  type, 
or  from  diffuse  cellulitis,  it  is  separated  in  the  later  stages  by  the  absence  of 
pain  and  fever.  From  malignant  oedema  it  is  distinguished  by  the  absence 
of  crepitation  due  to  gas  in  the  tissues.  Agglutination  tests  based  on  the  same 
principle  as  the  Widal  test  in  typhoid  fever  have  not  been  generally 
adopted. 

Prognosis. — The  prognosis  of  the  external  form  depends  upon  the  degree 
of  general  systemic  infection,  and  therefore  the  size  of  the  local  lesion  has 
not  any  great  importance  in  determining  the  outlook  It  not  rarely  hap- 
pens that  a  small  papule  may  be  followed  by  the  death  of  the  patient  in  a 
few  days,  whereas  a  larger  lesion  may  be  recovered  from.  Thus,  Bell  states 
that  a  patient  with  so  severe  a  lesion  on  the  face  as  to  have  large  bullae  and  a 
free  discharge  of  straw-colored  fluid,  with  swelling  of  the  entire  head  and  the 
submaxillary  glands,  may  recover.  In  other  words,  everything  depends 
upon  the  degree  of  systemic  infection.  A  rapid-running  pulse  is  always  an 
evil  omen. 

Death  may  come  as  early  as  the  first  day  of  illness,  but  the  majority  of 
deaths  occur  on  the  fourth  to  seventh  day.  So  far  as  mortality  is  concerned 
statistics  vary  very  greatly,  probably  because  of  variations  in  the  virulence  of 
the  infection.  Thus,  Woolmer  states  that  out  of  50  cases  he  lost  only  2,  and 
Muskett  treated  50  cases  with  one  death;  whereas  in  England,  even  when 
the  workmen  have  been  taught  to  present  themselves  for  treatment  at  once, 
the  mortality  has  been  21  per  cent.,  and  in  some  collections  of  statistics  it 
has  reached  50  per  cent.  In  Eppinger's  epidemic  among  rag-pickers  78 
out  of  88  cases  were  fatal. 


HYDROPHOBIA  261 

In  the  internal  form  the  prognosis  is  bad  and  death  often  comes,  as  already 
stated,  as  early  as  twenty-four  hours  after  the  primary  symptoms.  Cases 
in  which  recovery  has  taken  place  are,  however,  on  record. 

Treatment. — The  treatment  of  the  external  form  consists  in  the  destruction 
by  actual  cautery  of  the  primary  focus  of  the  disease  at  the  earliest  possible 
moment.  If  this  is  not  done  it  should  be  excised.  Not  only  should  the 
infected  tissues  be  removed,  but  the  surrounding  tissues  for  at  least  an  inch 
as  well.  As  soon  as  this  is  done  the  part  is  to  be  swabbed  with  pure  carbolic 
acid  and  then  dressed,  so  that  drainage  into  the  dressings  may  occur.  The 
patient's  vitality  should  be  maintained  by  good  food  and  stimulants,  and 
anthrax   antitoxin    should  be  given. 

Within  the  last  few  years  an  anti-anthrax  serum  has  been  employed  with 
success.  Legge  states  the  following  facts  as  to  its  use:  (1)  In  very  large 
doses  it  is  innocuous;  (2)  it  can  be  well  borne  even  when  introduced  into 
the  veins;  (3)  no  case  taken  in  an  early  stage,  or  of  moderate  severity,  is 
fatal  if  treated  with  serum;  (4)  with  the  serum  some  cases  are  saved  when 
the  condition  is  most  critical  and  prognosis  almost  hopeless;  (5)  when  in- 
jected into  the  veins  the  serum  quickly  arrests  the  extension  of  the  oede- 
matous  process  so  as  to  reduce  notably  the  danger  from  suffocation  which 
exists  in  many  of  the  cases  where  the  pustule  is  situated  on  the  face  or 
neck;  (6)  the  serum,  if  used  early  enough,  reduces  to  a  minimum  the  de- 
struction of  tissue;  (7)  in  some  situations  of  the  pustule,  as  the  eyelid, 
serum  must  be  used  in  preference  to  any  other  treatment;  (8)  persons 
attacked,  when  treated  with  the  serum,  appear  to  become  convalescent  in 
the  course  of  a  few  hours;  to  these  I  may  add  (9)  that  in  internal  anthrax 
if  it  is  administered  intravenously  it  is  the  only  treatment  which  can  hold  out 
any  hope. 

In  almost  all  cases  injection  of  the  serum  is  followed  by  a  rise  in 
temperature  often  to  over  105°,  and  with  this  there  is  an  improvement 
in  the  general  condition  of  the  patient.  The  prognosis  where  there  is  this 
rise  Sclavo  regards  as  favorable.  In  the  same  way  the  necrotic  process 
itself  is  to  be  regarded  as  a  sign  that  the  organism  is  making  effort  to  re- 
sist the  anthrax  infection. 


HYDROPHOBIA. 

Definition. — Hydrophobia  is  an  acute  infectious  disease  of  animals  com- 
municable to  man,  the  specific  cause  of  which  has  not  as  yet  been  isolated. 
It  is  characterized  by  great  restlessness  and  delirium,  by  an  apparent  dread 
of  water  in  some  instances,  and  by  delirium  and  paralysis  in  its  later  stages. 
It  is  often  called  "  rabies  "  or  "  lyssa." 

History. — Hydrophobia  was  well  described  as  long  ago  as  nearly  500 
B.C.  by  Democritus,  but  not  until  about  200  years  B.C.  was  it  described 
in  man.  Since  then  it  has  been  discussed  by  many  ancient  and  modern 
writers,  of  whom  Griiner,  in  1813,  found  that  the  saliva  was  the  vehicle  of 
infection. 

Trousseau  wrote  its  best  description  in  modern  times  in  1850,     In  1882 


262  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

Pasteur  first  clearly  discussed  the  cause  of  the  disease  and  devised  a  plan 
of  rational  treatment. 

Distribution. — No  less  an  authority  than  Virchow  beheved  that  hydrophobia 
was  not  to  be  met  with  in  Greenland,  Denmark,  Africa,  and  parts  of  Asia 
and  South  America,  and  with  others  claimed  that  it  is  peculiar  to  temperate 
zones;  but  in  1860  an  epidemic  occurred  in  Greenland  among  animals  when 
the  temperature  was  25°  below  zero.  Boulanger  is  probably  correct  in  stating 
that  no  part  of  the  world  is  free  from  it.  The  idea  that  it  is  more  prevalent 
in  summer  than  in  winter  is  erroneous.  Suzor  has  reported  twice  as  many 
cases  in  animals  in  March,  April,  and  May  as  in  the  summer  months.  Two- 
fifths  of  all  cases  in  human  beings  are  under  fifteen  years  of  age.  The 
disease  affects  dogs,  skunks,  foxes,  and  wolves  more  commonly  than  other 
animals,  but  all  animals  are  apparently  susceptible  to  it.  Cows  may  develop 
it  from  dog-bites  or  from  bites  of  other  infected  cows,  and  in  1888  I  saw 
a  number  of  deer  from  the  royal  herd  in  Richmond  Park,  near  London, 
which  suffered  from  this  disease  and  which  were  studied  at  the  Brown 
Institution. 

Etiology. — As  already  stated,  the  cause  of  this  disease  has  not  been  deter- 
mined with  certainty,  although  recently  Negri  claims  to  have  established 
that  it  is  due  to  a  protozoal  organism.  It  is  known  that  its  cause  has  a 
special  affinity  for  the  nervous  system,  and  is  found  in  the  saliva,  but  not  in 
the  urine  or  the  blood.  The  disease  can  be  passed  from  animal  to  animal, 
from  an  animal  to  man,  and  from  man  to  an  animal,  and  it  can  be  passed 
on  from  one  to  another  without  rapidly  losing  its  virulence.  The  transfer 
is  always  made  through  some  solution  of  continuity,  usually  a  bite,  but  it 
has  occurred  through  a  pimple,  and  it  is  said  to  have  been  transferred  by 
the  milk  of  a  nursing  mother. 

In  the  dog  it  has  been  proved  that  the  saliva  may  be  virulent  as  long  as 
three  days  before  any  symptoms  of  the  disease  appears. 

Prevention.— The  only  efficient  measures  of  prevention  are  the  universal 
muzzling  of  dogs,  particularly  when  a  mad  dog  is  known  to  have  been  in  the 
neighborhood,  and  the  killing  of  all  animals  found  suffering  from  the  disease. 
In  London  the  muzzling  of  dogs  decreased  the  disease  from  176  cases  in 
dogs  in  1889  to  3  in  1892,  but  on  relaxation  in  enforcing  the  law  the  number 
of  cases  in  dogs  and  man  rose  again  to  about  the  original  number.  (For 
preventive  inoculation  see  Treatment.) 

Frequency. — Hydrophobia  is  not  a  common  malady  in  animals,  and  is  rare, 
comparatively  speaking,  in  man.  Sporadic  cases  are  met  with  in  animals 
in  every  large  city  during  the  year.  (For  statistics  see  Salmon's  article  in 
the  Year  Book  of  the  U.  S.  Department  of  Agriculture,  1901.)  Woodhead 
states  that  only  about  16  per  cent,  of  those  bitten  by  rabid  animals  become 
victims  of  the  disease. 

Pathology  and  Morbid  Anatomy. — It  has  been  generally  stated  that  there  is 
nothing  pathognomonic  in  the  morbid  anatomy  of  rabies,  but  recent  studies 
controvert  this  view.  Examined  microscopically  the  medulla  and  spinal  cord 
show  small  hemorrhages  and  large  numbers  of  small  round  cells  in  the  peri- 
vascular Ivmph  spaces  and  around  the  motor  ganglia  cells,  and  progressive 
degenerative  changes  in  the  spinal  nerve  cells  appear,  consisting  in  chroma- 


.    HYDROPHOBIA  263 

tolysis  and  overgrowth  of  the  nucleolus.  These  changes  are,  however,  by  no 
means  pathognomonic,  as  they  may  be  found  in  other  diseases. 

Van  Gehuchten  and  Nelis  have,  however,  discovered  changes  in  the 
peripheral,  cerebral,  and  sympathetic  ganglia,  in  the  intervertebral  ganglia, 
and  in  the  plexiform  ganglia  of  the  pneumogastric  nerve,  which  they  consider 
to  be  diagnostic  of  rabies.  These  changes  consist  in  the  destruction  of  the 
nerve  cells  by  newly  formed  cells  from  the  capsule.  Ravenel  and  McCarthy 
have  studied  (1901)  28  cases  of  rabies  occurring  in  dogs,  rabbits,  and  other 
animals,  and  found  these  changes  in  all  but  one  case.  The  plexiform  ganglia 
were  affected  in  all  in  which  positive  results  as  to  the  presence  of  the  rabies 
were  obtained.  In  21  cases  the  bulb  was  examined  for  the  rabic  tubercle 
of  Babes,  and  positive  results  were  obtained  in  19,  although  in  2  no  distinct 
tubercle  formation  was  observed,  chromatolysis  only  being  present.  The 
rabic  tubercle  of  Babds  is  an  accumulation  of  embryonal  cells  around  the 
nerve  cells.  The  cells  of  the  bulbar  nuclei  undergo  degeneration  and  mani- 
fest various  stages  of  chromatolysis. 

As  a  result  of  their  studies  Ravenel  and  McCarthy  conclude  that  these 
changes,  taken  in  connection  with  the  clinical  symptoms,  afford  a  rapid  and 
trustworthy  means  of  diagnosis  of  hydrophobia,  but  that  their  absence  does 
not  imply  that  the  disease  is  not  present.  They  also  believe  that  the  rabic 
tubercle  of  Babds  is  present  often  enough  to  afford  diagnostic  evidence  in 
cases  where  the  central  nervous  system  only  is  obtainable  without  any 
ganglia. 

Symptoms  in  Animals . — The  symptoms  of  rabies  in  animals  vary  greatly.  In 
the  dog  we  find  that  he  is  at  first  stupid  and  heavy  and  often  cross  and  rest- 
less. When  he  stands  up  he  may  sway  slightly  and  stagger  when  he  runs. 
At  this  time  he  is  easily  frightened  and  his  reflexes  are  acutely  increased.  He 
usually  refuses  food  and  drink,  but  will  often  gulp  down  all  sorts  of  substances 
not  food,  such  as  rags,  manure,  and  pieces  of  wood.  Even  at  this  time  he 
may  be  obedient,  and  may  not  bite  his  master,  although  he  will  snap  at  a 
stranger.  The  bark  is  muflfled  and  peculiar,  and  may  be  a  series  of  yelps 
or  howls,  the  lower  jaw  never  completely  closing  as  in  health.  Thirst  may 
be  manifest,  but  though  the  animal  may  lap  the  water,  spasm  of  the  throat 
prevents  swallowing.  The  idea  that  a  mad  dog  has  a  peculiar  dread  of 
water  is  erroneous.  Any  repulsion  he  may  have  to  it  is  due  to  the  spasm  of 
the  gullet. 

He  next  becomes  dehrious  and  maniacal,  galloping  or  swiftly  trotting,  with 
a  slouching  demeanor,  as  if  shrinking  from  some  enemy.  The  jaws  are 
usually  open,  and  the  saliva  may  flow  freely  from  the  mouth.  Some 
amblyopia  may  develop  so  that  he  is  prone  to  run  into  objects  which  should 
be  easily  avoided.  This  may,  however,  be  due  to  stupidity  or  muscular 
inco-ordination.  Sometimes  he  seems  to  see  imaginary  objects  and  snaps  at 
them.  Rapid  emaciation  is  a  noteworthy  symptom.  Finally,  the  animal 
becomes  more  feeble  and  paralyzed.  The  paralysis  is  gradual  in  onset. 
The  hind  legs  are  at  first  moved  with  difficulty  and  finally  the  animal  sinks 
on  his  haunches,  there  being  a  simultaneous  loss  of  power  in  the  fore- 
legs, upon  which,  however,  he  can  occasionally  raise  himself.  During  this 
period  convulsions  may  ensue.    Death  occurs  on  the  fifth  or  sixth  day  as  a 


264  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

rule,  but  life  may  be  prolonged  until  the  eighth  day,  but  never  longer  than 
the  tenth  day. 

In  some  cases,  probably  in  those  which  are  very  severe,  the  paralysis  may 
develop  almost  at  once. 

Animals  sometimes  manifest  symptoms  of  what  is  known  as  "dumb 
rabies,"  which  is  to  be  distinguished  from  the  maniacal  form.  In  this  con- 
dition the  lower  jaw  is  dropped  and  the  animal  is  unable  to  close  the  mouth. 
The  tongue  hangs  out  and  the  saliva  dribbles.  As  the  jaw  is  paralyzed  the 
dog  is  unable  to  bite,  and  does  not  attempt  to  do  so.  This  form  usually 
causes  death  in  about  two  to  four  days.  It  is  important  that  these  mani- 
festations of  dumb  rabies  be  remembered.  Dr.  Gill,  a  veterinary  surgeon  of 
New  York,  asserts  that  this  is  a  very  common  form  of  the  disease,  which 
frequently  misleads  persons  into  thinking  that  the  dog  has  a  bone  in  its 
throat.  They  are  still  further  deceived  by  the  fact  that  the  animal  has  no 
hydrophobia  and  not  infrequently  actually  plunges  his  head  into  water,  or 
will  even  swim  a  river.  He  adds  as  additional  advice:  "Beware  of  a  dog 
when  it  becomes  dull  and  hides  away,  appears  restless,  is  always  on  the 
move  and  prowling,  whose  countenance  is  sombre  and  sullen,  and  which 
walks  with  his  head  down  like  a  bear.  Beware  of  one  which  barks  at  nothing 
when  all  is  still.  Beware  of  the  dog  that  barks  incessantly  and  tears  up 
things.  Look  out  for  the  dog  which  has  become  too  fond  of  you  and  is  con- 
tinually licking  your  hand  and  face;  and  beware,  above  all,  of  the  dog  which 
has  difficulty  in  swallowing,  which  appears  to  have  a  bone  in  its  throat, 
and  of  one  which  has  wandered  away  from  home  and  returns  covered  with 
dirt,  exhausted  and  miserable." 

These  symptoms  in  the  dog  have  been  described  in  detail  because  a  correct 
diagnosis  of  the  malady  in  the  dog  is  of  vital  importance  in  determining 
whether  a  patient  is  to  be  a  victim  of  rabies  and  if  he  should  be  given 
Pasteur's  treatment. 

Symptoms  in  Man. — When  a  human  being  is  infected  by  rabies  the  stage 
of  incubation  may  last  from  fourteen  days  to  eighteen  months,  although 
if  the  animal  produces  a  punctured  wound  and  is  in  the  active  stage  of  the 
disease  the  shorter  period  is  more  common.  It  is  usually  shorter  in  young 
children  than  in  adults.  At  the  end  of  the  period  of  incubation  the  part 
infected  begins  to  itch  and  tingle  and  then  to  burn.  The  skin  in  its  neigh- 
borhood may  develop  vesicles,  and  the  old  wound  may  open. 

The  primary  systemic  symptoms  in  man  are  apprehension,  restlessness,  and 
finally  marked  anxiety.  This  is  followed  by  thirst,  but  when  the  water  is 
brought  near  the  patient  he  seems  to  have  great  fear  of  it — hydrophobia. 
This  fear  is  chiefly  due  to  the  pharyngeal  spasm,  which  is  produced  at  the 
sight  of  water,  which,  if  the  patient  tries  to  swallow,  becomes  exaggerated. 
This  spasm  is  the  most  pathognomonic  symptom  of  rabies  in  man. 

Often  the  site  of  the  inoculation  is  red  and  inflamed  and  there  may  be 
local  irritation  or  pain.  This  stage  lasts  about  five  days  and  is  followed  by 
the  stage  of  excitement,  with  labored  respirations  and  spasm  of  the  laryngeal 
and  pharyngeal  muscles.  The  reflexes  are  greatly  exaggerated  and  delirium 
or  mania  may  come  on.  Occasionally  the  jaws  may  be  snapped  together, 
although  snapping  is  said  to  be  characteristic  of  false  rabies.    Very  commonly 


HYDROPHOBIA  265 

the  curious  symptom  of  spitting  develops,  the  patient  ejecting  small  quan- 
tities of  spittal  upon  surrounding  objects. 

Occasionally  paralytic  rabies  occurs  in  man,  but  it  is  very  rare. 

Diagnosis. — It  is  only  in  the  early  stage  of  the  disease  in  either  the  animal 
or  man  that  any  difficulty  can  exist  as  to  its  diagnosis.  As  the  saliva  of  a 
dog  for  several  days  before  it  seems  very  ill  is  virulent,  all  sick  dogs,  ill  of 
unknown  causes,  should  be  regarded  with  suspicion  or  caution.  In  man  the 
history  of  having  been  bitten  will  usually  be  obtainable. 

Occasionally  a  hysterical  person,  after  reading  or  hearing  a  description  of 
rabies,  develops  symptoms  which  resemble  it.  The  fact  that  the  patient  is 
of  this  type,  and  that  threats,  or  inhalations  of  amyl  nitrite,  speedily 
cure  the  ailment  will  permit  a  differentiation.  This  state  is  called  pseudo- 
hydrophobia  or  lyssaphobia.  It  is  important  to  remember  that  symptoms  of 
pseudohydrophobia  or  hysteria  simulating  the  true  disease  often  develop  as 
early  as  twenty-four  or  forty-eight  hours  after  exposure ;  whereas  true  hydro- 
phobia rarely  develops  in  less  than  fourteen  days.  Again,  the  hysterical 
patient  often  presents  the  symptoms  of  the  second  convulsive  stage,  with- 
out having  shown  any  primary  symptoms.  He  is  apt  to  show  a  disposition 
to  bite,  which  is  very  rare  in  true  human  hydrophobia,  and  if  he  barks, 
growls,  or  snaps  it  is  an  imitation  and  not  the  true  disease.  Finally,  should 
the  patient  survive  for  a  period  of  active  symptoms  longer  than  ten  days  the 
case  is  probably  hysteria. 

True  hydrophobia  is  to  be  differentiated  from  tetanus  by  the  presence  of 
marked  lock-jaw  in  the  latter  disease,  and  by  the  fact  that  in  tetanus  there  is 
no  dribbling  of  saliva  and  no  expression  of  terror.  The  convulsions  in  true 
hydrophobia  are  rarely  as  tonic  as  in  tetanus.  The  paralytic  form  of  rabies 
may  resemble  Landry's  paralysis. 

Prognosis. — It  may  be  possible  for  true  hydrophobia  to  permit  of  recovery 
in  man,  but,  if  it  is,  no  case  of  recovery  has  ever  been  reported  in  which 
there  was  undeniable  evidence  that  the  diagnosis  was  correct. 

Treatment. — The  treatment  of  hydrophobia  is  entirely  in  the  line  of  pre- 
ventive medicine,  for,  once  the  disease  is  developed,  curative  measures  are 
not  possible.  As  soon  as  the  bite  is  received  the  wound,  if  a  punctured  one, 
should  be  washed  and  then  sucked  and  the  spittle  expectorated.  If  the  part 
injured  be  an  extremity  a  tourniquet  should  be  used  until  this  is  done.  The 
punctured  wound  should  be  converted  into  an  incised  wound,  and  the  opening 
should  not  be  closed,  but  given  free  drainage  and  kept  open,  well  protected 
from  other  infection,  for  several  weeks.  Where  possible,  without  great 
mutilation,  the  part  should  be  excised  as  is  now  recommended  for  the  pre- 
vention of  tetanus.  The  value  of  caustics  depends  on  the  one  employed. 
Nitric  acid  is  the  best.  If  the  wound  is  incised,  well  washed  with  normal 
saHne  or  with  bichloride  of  mercury,  real  tissue  destroyers  may  be  set 
aside. 

The  specific  and  rational  method  of  treatment  is  that  proposed  and 
instituted  by  Pasteur  by  means  of  attenuated  virus.  This  investigator  found 
that  if  the  virus  of  hydrophobia  is  propagated,  through  the  inoculation  of  a 
series  of  rabbits,  it  increases  in  virulence,  and  the  spinal  cords  of  the  rabbits 
of  the  last  series  of  inoculations  contain  the  poison  in  a  very  active  state. 


266  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

If  these  spinal  cords  are  preserved  under  certain  conditions  this  degree  of 
virulence  progressively  diminishes.  If  an  emulsion  be  made  from  the 
attenuated  cords  and  a  dog  inoculated  with  it  in  small  amount  the  animal 
survives,  and  if  successively  inoculated  with  virus  of  increasing  virulence 
gradually  becomes  immune  as  larger  doses  are  given,  until  he  is  able  to 
stand  inoculation  with  the  most  virulent  matter  obtained  from  the  cords 
of  rabbits.  This  same  process  is  now  employed  for  the  treatment  of  a 
man  who  has  been  bitten,  the  endeavor  being  made  to  produce  an  artificial 
immunity  before  the  stage  of  incubation  following  the  bite  is  completed. 

Two  methods  of  producing  immunity  to  hydrophobia  are  now  employed. 
One  is  known  as  the  "simple"  and  the  other  as  the  "intensive."  In  both 
methods  spinal  cords  of  infected  animals  are  employed  in  gradually  increas- 
ing strength  until  finally  what  is  known  as  a  three-day  cord — that  is,  one 
which  has  been  kept  three  days — is  administered  subcutaneously.  In 
the  "simple"  method  nineteen  injections  are  given  in  fourteen  days. 

In  those  cases  which  have  severe  lacerated  wounds  of  the  face,  in  which 
not  only  infection  has  taken  place,  but  the  tissues  have  been  devitalized  by 
traumatism,  the  "intensive"  method  is  used.  This  consists  in  the  admin- 
istration of  twenty-eight  injections  in  twenty-one  days.  During  the  first 
three  days  as  many  injections  are  given  in  the  "intensive"  method  as  are 
given  in  five  days  by  the  simple  method. 

Out  of  17,395  cases  treated  at  the  Pasteur  Institute  in  Paris  in  this  manner 
between  1886  and  1895  there  were  139  deaths  from  rabies.  If  the  average 
mortality  after  inoculation  is  in  the  neighborhood  of  20  per  cent.,  as  already 
stated,  it  is  evident  that  instead  of  there  being  139  deaths  there  would  have 
been  approximately  3476  deaths,  which  shows  the  great  value  of  the  plan. 
As  the  treatment  is  absolutely  harmless  if  properly  employed,  the  value  of 
Pasteur's  method  cannot  be  doubted.  It  is,  of  course,  useless  after  the 
malady  is  well  developed. 

After  the  disease  is  established  care  must  be  taken  that  the  patient  does 
not  wound  his  attendants.  His  sufferings  should  be  relieved  by  morphine 
or  chloral  in  sufficient  doses  to  spare  him  from  much  misery.  Nutrient 
enemata  may  be  used  to  help  support  nutrition  if  food  cannot  be  swal- 
lowed. 

Efforts  have  been  made  from  time  to  time  to  provide  an  antirabic  serum. 
Babds  and  Lepp,  in  1889,  Tizzoni  and  Schwarz,  and  later  Tizzoni  and 
Centanni  have  all  endeavored  to  reach  this  much-desired  product.  They 
have  used  virus  which  has  been  attenuated  by  digestion  with  gastric  juice, 
and  their  serum  is  of  such  a  strength  that  in  the  proportion  of  25000  P^^  kilo- 
gram weight  of  rabbit  it  will  protect  against  one  infection  unit  of  virus 
if  administered  subcutaneously  twenty-four  hours  before  the  subdural  injec- 
tion of  virus  is  given  to  an  animal.  An  infection  unit  of  the  virus  is  the 
greatest  dilution  of  any  virus  which  will  surely  kill,  without  prolongation  of 
the  incubation  period,  when  0.012  c.c.  per  kilogram  of  animal  is  admin- 
istered under  the  dura.  These  investigators  believe  that  the  antirabic 
virus  should  be  injected  subdurally,  as  it  is  far  more  efficacious  in  this 
way  than  when  it  is  given  by  the  hypodermic  needle,  and  they  claim  that 
the  subdural  dose  is  12,000  times  as  efficacious  as  the  subcutaneous  dose. 


TETANUS  267 

Unfortunately,  these  investigations  only  give  promise  of  good  for  human 
beings.  Sufficient  statistics  as  to  their  value  have  not  as  yet  been  forth- 
coming. 

TETANUS. 

Definition. — ^Tetanus  is  an  acute  infectious  disease  due  to  the  entrance 
and  development  in  the  body  of  a  specific  organism,  the  bacillus  of  tetanus. 
It  is  characterized  by  the  development  of  rigidity  of  the  muscles  so  that  the 
limbs  are  fixed  and  the  jaw  locked. 

History. — ^Tetanus  has  been  known  for  many  centuries  as  a  disease  that 
occasionally  follows  small  wounds,  but  it  was  not  until  1884  that  Carle  an(] 
Rattone  discovered  that  when  an  animal  showed  symptoms  of  tetanus  it  was 
possible  to  produce  similar  symptoms  in  healthy  animals  by  injecting  virus 
obtained  from  the  first.  In  1885  Nicolaier  obtained  from  the  pus  of  infected 
animals,  bacteria  which,when  inoculated  into  healthy  animals,  caused  tetanus, 
but  he  was  unable  to  isolate  the  organism  absolutely,  although  he  described 
it  as  a  small,  slender  bacillus.  In  1886  Rosenbach  confirmed  Nicolaier's 
discovery,  but  he  also  did  not  get  a  pure  culture  of  the  bacillus  of  the  dis- 
ease. In  1889  Kitasato,  Tizzoni,  and  Cattani  succeeded  in  its  complete 
isolation.  Faber  also  proved  that  he  could  obtain  from  a  culture  of  this 
bacillus  a  toxin  which,  when  injected  into  animals,  caused  symptoms  iden- 
tical with  those  met  with  in  human  beings  suffering  from  this  malady. 

Distribution. — Tetanus  is  met  with  everywhere  in  tropical  and  temperate 
zones.  Its  bacillus  is  particularly  prevalent  in  garden  soil  and  about  stables 
and  dungheaps.  In  the  United  States  it  is  most  prevalent  in  Louisiana, 
New  York,  Pennsylvania,  Texas,  and  Ohio  in  the  order  named.  Wells 
has  shown  that  the  curve  of  deaths  in  this  disease  starts  in  May,  reaches  its 
highest  point  in  July,  and  then  declines  to  October, 

Etiology  and  Frequency. — The  specific  organism,  the  Bacillus  tetani,  is 
4/i  to  5 ft  in  length  and  about  0.4/i  wide;  during  sporulation  one  end  enlarges 
giving  the  organism  a  drumstick  appearance.  This  bacillus  is  an  anaerobic, 
slightly  motile,  flagellated  rod,  possessing  unusually  resistant  spores  and  the 
faculty  of  producing  a  highly  poisonous  toxin.  It  is  frequently  demonstrated 
in  discharges  from  wounds  in  cases  of  tetanus,  and  has  been  found  on  the 
object  producing  the  wound  and  in  freshly  made  wounds. 

The  chief  causative  factor  in  tetanus  is  the  presence  of  a  wound  through 
which  the  specific  germ  may  enter  the  body.  This  wound  may  be  so  insig- 
nificant as  to  be  overlooked.  In  other  cases  the  infection  takes  place  through 
a  break  in  the  mucous  membrane  of  the  mouth.  Accidents  of  this  type 
probably  account  for  the  cases  of  so-called  idiopathic  tetanus.  Small, 
punctured  wounds  are  much  more  apt  to  result  in  the  development  of  the 
disease  than  large  ones  with  free  drainage,  for  the  accumulated  necrotic 
tissues  of  punctured  wounds  afford  approximately  ideal  conditions  for  the 
development  of  the  anaerobic  bacillus.  Within  the  last  few  years  several 
outbreaks  of  tetanus  have  followed  the  use  of  contaminated  vaccine. 

Tetanus  is  not  a  very  common  disease,  but  nearly  every  large  hos- 
pital service  has  presented  to  it  occasionally  an  isolated  instance.     It  has 


268  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

been  epidemic  in  many  hospitals  and  camps;  it  has  also  been  epidemic 
among  newborn  infants,  infection  taking  place  through  the  umbilicus 
and  causing  a  frightful  mortality,  particularly  in  the  West  Indies,  where 
at  times  more  than  60  per  cent,  of  all  children  born  died  within  eight  days 
after  birth  from  its  ravages.  In  this  country  it  is  seen  in  hostlers,  gardeners, 
agricultural  laborers,  men  employed  about  stables,  and  in  children  who  run 
about  with  bare  feet.  By  far  the  most  common  incidence  of  the  disease 
occurs  in  children  who  suffer  from  wounds  produced  by  toy  pistols  and 
fire-crackers.  As  many  as  466  cases  of  this  disease  were  due  to  these  causes 
in  the  celebration  of  the  Fourth  of  July  in  1903  in  the  United  States;  but  it 
is  interesting  to  note  that  owing  to  the  warning  issued  by  medical  men 
against  the  use  of  these  explosives  the  number  of  deaths  due  to  this  cause 
was  only  105  in  1904. 

Prevention. — ^Tetanus  is  to  be  prevented  by  the  excision  or  conversion 
of  all  punctured  woimds  into  incised  wounds  with  free  drainage,  by  the  use 
of  tetanus  antitoxin  as  soon  as  the  wound  is  received,  and,  if  the  disease 
develops  in  a  hospital  or  camp,  by  the  careful  isolation  of  those  who  are  ill 
with  it. 

The  measures  taken  to  destroy  the  bacillus  and  its  spores  outside  the 
body,  as  in  dressings  and  clothing,  must  be  very  radical,  because  the  spores 
are  extraordinarily  resistant  to  those  measures  usually  employed  to  destroy 
pathogenic  germs.  Thus,  the  spores  can  survive  two  hours'  exposure  to 
corrosive  sublimate  1 :  1000,  and  even  survive  exposure  to  boiling  water  if 
the  exposure  is  brief.  So,  too,  fifteen  hours'  treatment  with  1 :  20  of  carbolic 
acid  is  necessary  to  destroy  their  vitality.  Drying  does  not  kill  the  bacillus. 
Miguel  has  produced  the  disease  from  infected  soil  kept  for  eighteen  years. 

Pathology  and  Morbid  Anatomy. — A  most  important  fact  to  be  remem- 
bered in  regard  to  tetanus  is  that  the  specific  organism  primarily  does  not 
spread  through  the  body,  but  develops  at  the  site  of  infection,  and  from  this 
focus  the  toxin  which  produces  the  symptoms  of  the  malady  is  dissemi- 
nated. It  has  been  proved  by  Meyer  and  Ransom  that  the  poison  passes 
to  the  central  nervous  system  through  or  along  the  nerve  trunks.  Another 
fact  of  importance  is  that  the  toxin  combines  with  the  cells  of  the  nervous 
system  with  remarkable  celerity,  and  having  done  so  forms  so  firm  a  com- 
bination that  it  cannot  be  dislodged,  and  in  consequence  the  subsequent  use 
of  antitoxin  often  fails. 

The  tetanic  convulsions  are  not  due  to  any  influence  of  the  poison  on  the 
nerves  or  muscles,  but  upon  the  spinal  cord  and  brain. 

In  cases  of  death  from  tetanus  there  are  no  characteristic  changes  in  the 
tissues  of  the  nervous  system. 

Symptoms. — ^The  symptoms  of  tetanus  are  so  characteristic  that  they  can 
hardly  be  mistaken  for  any  other  disease  save  hysteria  and  strychnine 
poisoning.  The  dominant  symptom  is  the  state  of  rigidity  of  the  voluntary 
muscles,  which,  when  the  disease  is  well  developed,  are  practically  constantly 
contracted,  although  at  intervals  they  relax  and  contract  spasmodically, 
causing  the  well-developed  convulsions  of  the  disease.  It  is  a  curious  fact 
that  the  earliest  symptoms  often  emanate  from  the  muscles  nearest  the  focus 
of  infection,  but  very  commonly  they  originate  in  the  muscles  of  the  jaw 


TETANUS  269 

and  neck,  producing  the  symptom  called  "lock-jaw,"  that  is,  a  state  in 
which,  by  reason  of  the  spasm  in  the  masseter  muscles,  the  lower  maxilla 
is  firmly  pressed  against  the  upper  jaw. 

The  contraction  of  the  facial  muscles  in  the  spasm  gives  the  face  a 
peculiar  expression  of  painful  mirth,  or  risus  sardonicus,  and  it  is  a  note- 
worthy fact  that  this  expression  may  be  the  first  warning  of  an  oncoming 
attack  of  the  disease,  for  as  the  patient  attempts  to  show  his  tongue  to  the 
physician  who  is  inquiring  as  to  his  general  health,  the  physician  is  startled 
to  see  the  facial  muscles  produce  this  strange  expression. 

The  muscles  of  the  back  and  abdominal  wall  are  rigid  to  the  touch,  and 
pain  and  oppression  due  to  spasm  of  the  diaphragm  may  be  present  when 
the  disease  is  well  developed.  The  muscles  of  the  hand  are  the  least  affected 
of  all  the  voluntary  muscles,  as  a  rule. 

If  the  more  powerful  muscles  contract  forcibly  the  patient's  body  is  arched, 
resting  on  his  heels  and  the  occiput;  this  is  called  opisthotonos.  If  the 
muscles  of  the  anterior  part  of  the  body  are  the  more  powerfully  contracted 
he  may  be  arched  forward — emprosthotonos. 

Pain  in  the  affected  muscle  is  not  severe  as  a  rule,  but  is  rather  the 
aching  due  to  prolonged  strain  and  weariness.  Sometimes,  however,  it  is 
severe.  There  may  be  alarming  spasm  of  the  glottis  or  fixation  of  the 
respiratory  muscles  endangering  life,  and,  indeed,  in  severe  cases,  this  is 
the  cause  of  death,  particularly  when,  by  reason  of  exhaustion,  the  patient 
is  unable  to  withstand  asphyxia  for  any  length  of  time. 

The  mind  usually  remains  clear  till  the  time  of  death.  The  temperature 
is  moderate  if  the  convulsions  are  moderate,  and  high  if  they  are  severe, 
ranging  from  100°  to  106°.  The  pulse  varies  in  speed,  becoming  rapid 
during  a  seizure.     Finally  it  becomes  feeble  from  exhaustion. 

Diagnosis. — Tetanus  rarely  is  as  sudden  in  onset  as  is  strychnine  poison- 
ing, and  it  very  rarely  causes  death  so  rapidly.  It  affects  the  muscles  of 
the  face  primarily,  which  strychnine  very  rarely  does.  There  is  usually  a 
history  of  punctured  wound  in  one  case  or  of  the  ingestion  of  poison  in  the 
other.  In  strychnine  poisoning  the  convulsions  are  followed  by  periods  of 
complete  relaxation,  whereas  in  tetanus  constant  spasm  with  exacerbations 
are  present. 

In  hysteria  the  ecstatic  facies  of  the  patient,  the  presence  of  clonic  move- 
ments, the  fact  that  the  patient  is  a  woman  of  a  neurotic  type,  and  that 
laughing  and  crying  are  often  present,  aid  greatly  in  the  diagnosis.  Further 
areas  of  anaesthesia  are  often  present  in  hysteria  and  inhalations  of  nitrite 
of  amyl  may  cause  relaxation  followed  by  sobs  and  tears  as  the  spasm  is 
relieved  by  the  drug. 

Tetany  rarely  presents  such  severe  contractions,  but  it  may  do  so.  The 
spasms  are  often  locaHzed,  and  if  they  occur  in  children  signs  of  rickets  or 
gastric  dilatation  may  be  present.  Tetany  practically  never  causes  death, 
and  it  affects  chiefly  the  hands  and  feet,  which  tetanus  does  not. 

Prognosis. — The  prognosis  in  tetanus  depends  very  greatly  upon  the 
severity  of  the  paroxysms  and  upon  the  virulence  of  the  infection.  In  virulent 
infections  death  comes  as  early  as  the  second  day  and  usually  by  the  sixth. 
It  is  essential  that  two  forms  of  the  disease  be  recalled  in  studying  this  ques- 


270  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

tion.  There  is  an  acute  form  with  a  very  high  mortaUty  of  80  per  cent., 
and  a  chronic  form  in  which  recovery  takes  place  in  a  large  percentage, 
about  50  per  cent.    The  mortality  is  very  high  in  children  in  all  cases. 

Treatment. — Before  everything  else  in  the  treatment  of  tetanus  must  be 
considered  the  use  of  tetanus  antitoxin.  Its  value,  however,  is  chiefly 
limited  to  those  cases  in  which  it  can  be  administered  as  soon  as  the  inocu- 
lating wound  occurs,  or  within  a  short  time  after  this.  Its  failure  to  be  of 
value  when  employed  after  the  symptoms  are  well  developed  is  not  due  to 
any  lack  of  power  on  the  part  of  the  tetanus  antitoxin,  but  to  the  fact  that 
the  tetanus  toxin  so  rapidly  and  firmly  combines  with  the  nervous  proto- 
plasm of  the  brain  and  spinal  cord  that  it  is  impossible  for  it  to  be  disasso- 
ciated from  this  protoplasm,  and  therefore  the  antitoxin  cannot  combine 
with  it  and  prevent  it  from  damaging  the  central  nervous  system. 

When  children  are  wounded  by  means  of  toy  pistols  tetanus  antitoxin 
should  be  injected  at  once,  since  the  proportion  of  cases  in  which  tetanus 
develops  from  this  injury  is  very  large,  and  by  the  prompt  administration 
of  the  remedy  the  disease  may  be  prevented  from  producing  its  character- 
istic symptoms.  Thus  in  1903,  out  of  53  cases  of  so-called  Fourth  of  July 
tetanus  treated  without  antitoxin  16  died,  whereas  in  1904,  out  of  36  cases 
treated  with  antitoxin  none  died.  In  1216  cases  of  tetanus  treated  by 
antitoxin,  Packard  and  Wilson  found  that  the  mortality  was  42.2  per  cent., 
and  Moschowitz  in  461  cases  treated  in  this  way  found  a  mortality  of  40.3 
per  cent.  As  the  death  rate  of  acute  tetanus  is  about  80  per  cent,  and  of 
chronic  tetanus  about  50  per  cent.,  it  is  evident  that  antitoxin  saves  many 
lives.  Even  after  tetanic  symptoms  have  developed  tetanus  antitoxin 
should  still  be  used,  as  it  may  be  of  some  value. 

A  suggestion  has  been  made  that  in  severe  cases  the  patient  be  trephined 
and  the  antitoxin  injected  by  the  hypodermic  needle  between  the  mem- 
branes of  the  brain  or  into  a  cerebral  ventricle.  It  does  not  seem  that  this 
measure  offers  sufficient  promise  of  usefulness  to  justify  so  serious  a  method 
of  treatment.  If  the  symptoms  are  very  severe,  and  doubt  exists  as  to  the 
rapidity  with  which  the  antitoxin  can  be  absorbed  from  the  subcutaneous 
tissues,  it  may  be  advisable  to  inject  it  into  the  cerebrospinal  fluid,  inserting 
the  needle  between  the  fourth  and  the  fifth  lumbar  vertebrae.  In  this  way 
it  will  reach  the  spinal  centres  quite  rapidly  without  exposing  the  patient  to 
a  surgical  operation.  The  needle  should  be  introduced  according  to  the 
directions  given  in  the  section  on  Cerebrospinal  Meningitis,  and  proof  that 
it  has  entered  the  membranes  of  the  cord  assured  by  the  discovery  that  a 
few  drops  of  cerebrospinal  fluid  drip  from  its  external  orifice.  The  syringe 
containing  the  tetanus  antitoxin  is  then  attached  to  the  needle  and  the  injec- 
tion is  made.  According  to  Luckett  it  is  best  to  withdraw  a  considerable 
quantity  of  cerebrospinal  fluid  before  injecting  the  antitoxin. 

Still  more  recently  the  use  of  antitoxin  injected  into  the  nerve  trunks 
supplying  the  part  of  the  body  through  which  the  infection  has  taken  place 
has  been  tried  with  satisfactory  results,  the  idea  being  that  the  infection 
spreads  along  the  nerve. 

The  wound,  by  means  of  which  tetanus  infection  has  possibly  taken  place, 
should,  if  small,  be  excised,  or  if  it  is  large  it  must  be  thoroughly  cleansed 


GLANDERS  271 

first  with  normal  salt  solution  or  some  antiseptic  liquid,  care  being  taken, 
if  an  antiseptic  is  employed,  that  it  is  not  used  in  sufficient  strength  to  in 
any  way  interfere  with  the  vitality  of  the  tissues  with  which  it  comes  in 
contact,  since  it  is  probable  that  the  vitality  of  these  tissues  is  of  greater 
value  in  protecting  the  individual  against  infection  than  are  the  ordinary 
antiseptic  drugs.  If  the  wound  is  a  punctured  wound,  it  should  be  con- 
verted into  an  incised  wound  in  order  that  the  tetanus  bacillus  may  be 
thoroughly  washed  out  of  it  and  that  free  drainage  may  be  provided.  This 
is  exceedingly  important.  Nothing  aids  in  the  production  of  tetanus  so 
certainly  as  the  closure  of  such  a  wound  in  its  early  stages.  Wounds  should 
be  allowed  to  heal  by  granulation,  as  this  is  the  surest  way  to  prevent  the 
development  of  the  disease. 

After  the  disease  is  developed  the  patient  must  be  fed  with  nutritious 
and  easily  digested  foods  in  order  that  his  nutrition  may  be  maintained. 
In  the  rapid  type  of  tetanus  death  usually  comes  so  soon  that  great  emacia- 
tion does  not  occur.  But  in  the  more  chronic  form  the  question  of  nutrition 
must  be  constantly  kept  in  mind. 

If  the  jaws  are  so  locked  that  food  cannot  be  introduced  into  the  mouth,  one 
or  more  teeth  should  be  removed  in  order  that  a  stomach  tube  may  be  passed, 
or  a  rubber  tube  may  be  passed  by  way  of  the  nostril,  as  in  feeding  insane 
patients  who  refuse  to  take  nourishment.  Humphrey  has  gone  so  far  as  to 
recommend  in  these  cases  that  a  gastrostomy  be  performed,  the  tube  intro- 
duced, and  the  patient  nourished  through  the  operative  wound.  This  seems, 
however,  an  unnecessarily  heroic  method  when  the  tube  can  be  used. 

The  severity  of  the  tetanic  seizures  can  be  to  some  extent  modified  by  the 
administration  of  full  doses  of  chloral  and  the  bromides,  which  act  as  seda- 
tives to  the  motor  and  sensory  portions  of  the  spinal  cord.  These  remedies 
are,  however,  in  no  way  curative,  but  simply  symptomatic  in  that  they 
diminish  to  some  extent  the  force  of  the  convulsions  without  in  any  way 
influencing  the  deleterious  influence  of  the  poison  upon  the  system. 

Care  should  be  taken  that  the  activity  of  the  kidneys  is  maintained  by  the 
administration  of  mild  diuretics  and  by  providing  the  patient  with  plenty  of 
water.  The  state  of  the  bladder  should  also  be  watched,  as  retention  of 
urine  is  not  uncommon.  To  prevent  this,  repeated  catheterization  should 
be  resorted  to. 

Under  the  name  of  "  Kopf-tetanus,"  or  head  tetanus,  a  modified  form  of 
the  disease  sometimes  occurs.  It  is  said  to  be  particularly  apt  to  take  place 
after  injuries  to  the  face.  In  these  instances  the  spasm  is  chiefly  confined 
to  the  muscles  of  the  neck  and  face,  but  often  extends  to  the  abdominal 
muscles,  and  there  is  frequently  spasm  or  paralysis  of  the  glottis,  which  not 
rarely  becomes  a  most  serious  symptom.  In  some  instances  the  disease 
gradually  spreads  until  it  becomes  like  an  ordinary  case  of  tetanus.  It  is 
to  be  treated  by  the  employment  of  antitoxin  and  other  antitetanic  measures. 

GLANDERS. 

Definition.— Glanders  is  a  disease  which  is  usually  met  with  in  the  horse, 
but  it   may  also   affect   man.      It  is  due  to   the  presence  of   the  Bacillus 


272 


DISEASES  DUE  TO  A  SPECIFIC  INFECTION 


mallei.  When  it  appears  as  nodular  masses  in  the  nostrils  of  the  horse  it 
is  called  "  glanders,"  but  when  these  nodules  are  in  the  skin  it  is  called 
"  farcy."     Analogous  types  occur  in  man. 

Etiology. — The  Bacillus  mallei  is  usually  conveyed  to  man  while  caring 
for  a  horse  suffering  from  glanders,  and  enters  his  body  through  some 
break  in  the  skin.  It  may  also  find  its  way  into  the  system  by  way  of  the 
nasal  mucous  membrane.  Rarely  one  person  is  infected  by  another  by 
contact  and  through  a  wound.  The  bacillus  is  a  slender  organism,  somewhat 
thicker  in  proportion  to  its  length  than  the  bacillus  tuberculosis,  with 
rounded  ends.  It  is  easily  stained  with  anihne  dyes,  but  is  equally  readily 
decolorized  by  feeble  acids  or  alcohol.  It  can  be  readily  cultivated  outside 
the  body. 


Fig.  43 


Character  of  the  cutaneous  eruption  in  human  glanders.  The  variation  in  size  and  general  lack  of 
umbilication  are  noteworthy  points  in  differentiating  it  from  that  of  smallpox.  On  account  of  shrink- 
age the  skin  and  pustules  appear  more  wrinkled  than  they  did  before  removal  from  the  body.  (Pho- 
tograph, natural  size,  by  Roman  Mercado,  assistant  photographer  of  the  Bureau  of  Animal  Indus- 
try, U.  S.) 

Pathology  and  Morbid  Anatomy. — ^The  Bacillus  mallei  produces  a  circum- 
scribed infiltration  of  the  tissues  with  accumulations  of  leukocytes  and 
connective-tissue  cells,  which  resemble  macroscopically  small  miliary 
tubercles,  but,  as  Baumgarten  has  shown,  these  nodules  histologically 
occupy  a  position  midway  between  tubercles  and  miliary  abscesses.  The 
surrounding  tissues  are  infiltrated  with  blood  or  show  many,  or  few,  petechial 
extravasations.  After  a  short  time  they  undergo  necrotic  changes,  and 
as  they  break  down  abscesses  are  formed,  which  by  necrosis  of  the  over- 
lying tissues  are  changed  into  ulcers,  which  may  be  superficial  or  deep. 
Like  tuberculosis,  the  infection  tends  to  spread  along  the  lymphatics  and 
eventually  the  bacilli  may  reach  the  blood  and  be  distributed  in  the  viscera, 
causing  nodules  in  various  organs.  Such  nodules  occur  in  the  testicles, 
lungs,  spleen,  liver,  and  kidneys,  and  sometimes  the  bones  are  affected, 
causing  an  osteomyelitis. 


ACTINOMYCOSIS  273 

When  the  nodules  break  down  secondary  infections  perpetuate  the  sup- 
puration, the  specific  bacilli  become  much  diminished,  and  it  may  be 
impossible  to  discover  them  by  staining,  because  at  this  period  they  lose 
their  property  of  being  readily  stained. 

Symptoms. — Acute  glanders  develops,  in  about  four  days  after  inoculation, 
with  general  wretchedness,  some  fever,  and  the  appearance  at  the  site  of 
infection  of  a  circumscribed  red  swelling.  This  is  followed  in  a  few  days 
by  breaking  down  of  the  granulomatous  mass,  in  ulceration  of  the  nasal 
mucous  membrane,  and  the  discharge  of  muco-pus  from  the  anterior  nares. 
Secondary  infection  of  the  lymph  glands  in  the  neck  may  occur,  and  if  the 
process  is  severe  the  nose  may  become  necrotic.  Cough  and  dysphagia  may 
be  present.  Upon  the  face  and  about  the  joints  there  develops  an  array 
of  papules  which  as  they  become  pustules  may  very  closely  resemble  the 
eruption  of  smallpox.     A  septic  pneumonia  often  comes  on. 

Death  comes  to  such  cases  almost  invariably  by  the  end  of  a  week  or 
ten  days. 

In  rare  instances  the  process  becomes  subacute  or  chronic,  and  the  nasal 
discharge,  unless  accompanied  by  the  severe  symptoms  described,  may  make 
a  diagnosis  difficult,  if  not  impossible,  by  the  ordinary  methods  of  observation. 

When  the  inoculation  is  by  the  skin,  producing  farcy,  the  same  acute 
localized  swelling  takes  place  and  the  neighboring  lymphatics  become 
inflamed  and  swollen.  Not  only  does  this  occur  as  it  does  in  most  acute 
local  infections  which  are  severe,  but  small  nodules  are  found  scattered 
along  the  neighboring  lymphatics  forming  the  so-called  "farcy  buds." 
These  undergo  necrosis,  and  sloughs  form.  A  septic  arthritis  may  develop. 
The  nasal  passages  escape,  as  a  rule,  in  farcy.  Death  takes  place  in  the 
majority  of  these  cases  in  from  ten  to  twelve  days. 

Chronic  farcy  lasts,  like  chronic  glanders,  for  a  longer  period  of  time  than 
the  acute  disease,  sometimes  for  years.  It  presents  the  picture  of  multiple 
abscesses  and  sloughs,  associated  with  more  or  less  general  septicaemia, 
death  taking  place  from  this  cause.    Very  rarely  recovery  occurs. 

Diagnosis. — Glanders — that  is,  infection  of  the  nasal  mucous  membrane 
by  the  Bacillus  mallei — can  scarcely  be  mistaken  for  any  other  disease. 
Farcy  must  be  separated  from  multiple  abscesses  and  carbuncles.  This  is 
done  by  the  history  of  exposure,  the  distribution  of  the  "farcy  buds,"  and, 
finally,  by  the  injection  of  mallein,  which  produces  a  reaction  as  does 
tuberculin  in  the  tuberculous. 

Treatment. — The  swellings  should  be  promptly  opened  and  free  drainage 
provided.  If  possible  the  local  focus  should  be  well  removed  by  excision 
or  by  the  cautery.  A  nutritious  diet  should  be  given  and  stimulants  used 
if  needed.  Mallein  has  been  used  as  a  curative  agent,  but  nearly  all  acute 
cases  die,  do  what  we  will. 

ACTINOMYCOSIS. 

Definition. — ^This  is  a  chronic  infectious  disorder  produced  by  the  Sirepto- 
thrix    actiiiomyces,  sometimes  called  the  "ray  fungus."     It  is  far  more 
common  in  cattle  than  in  man,  and  in  cattle  it  usually  affects  the  lower  jaw, 
18 


274  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

producing  a  tumor  or  growth  which  gives  the  disease  the  popular  name 
"lumpy  jaw."  In  other  cases  the  tongue  is  involved,  producing  the  so-called 
"wooden  tongue." 

Etiology. — The  actinomycotic  infection  may  be  conveyed  from  cattle  to 
man  by  the  hands  of  the  individual,  or  by  straws  used  for  picking  the  teeth, 
whereby  infection  of  the  jaw  occurs.  Direct  transmission  from  man  to  man, 
or  beast  to  beast,  or  beast  to  man  does  not  appear  to  be  of  very  frequent 
occurrence;  apparently  both  are  infected  independently  by  some  common 
route  or  source,  the  exact  character  of  which  often  cannot  be  determined. 
Grain  which  has  been  soiled  by  the  slobber  of  an  infected  animal  may  infect 
other  cattle.  Cereals  are  thought  by  some  to  be  the  most  frequent  carriers 
of  the  disease  to  man  and  beast. 

The  organism  appears,  in  the  discharges  from  the  areas  of  infection,  as  a 
minute,  rounded  mass  so  tiny  as  to  be  microscopic  in  some  instances,  but  in 
others  as  aggregated  masses,  called  granules,  which  are  as  large  as  a  pin's 
head.  These  masses  are  yellowish-white,  resembling  particles  of  sulphur 
or  iodoform,  grayish  or  drab  in  hue,  and  even  with  slight  magnification 
often  appear  in  groups  or  clumps  of  radiating  filaments,  which  have  caused 
the  organism  to  be  called  the  "ray  fungus."  Each  terminal  filament  in 
some  stage  of  its  evolution  develops  a  bulbous  end. 

Pathology  and  Morbid  Anatomy. — In  the  lower  animals  the  disease  produces 
a  slow,  suppurative,  and  proliferative  process,  which  results  in  the  develop- 
ment of  large  fungous  growths,  which  may  in  part  become  calcareous.  From 
these  growths,  which  are  usually  situated  primarily  in  the  jaw,  secondary 
extensions  occur,  so  that  the  fungus  is  found  in  the  tissues  of  the  tongue  and 
pharynx,  and  even  in  the  lungs,  the  intestines,  and  in  the  nearly  related 
glands  and  skin.  When  the  disease  affects  man  it  does  not  so  commonly 
involve  the  jaw,  but  results  in  the  development  of  abscesses  which  often 
change  into  ulcers  or  form  fistulse.  These  may  lead  to  the  deeper  tissues, 
although  the  disease  is  usually  superficial. 

Histologically  the  new  tissue  may  closely  resemble  sarcoma,  for  which 
it  is  often  mistaken,  but  its  richness  in  pus  cells  and  resemblance  to  gran- 
ulation tissue,  combined  with  the  presence  of  the  fungus,  should  prevent 
this  error. 

The  lower  jaw  is  more  frequently  attacked  than  the  upper;  cutaneous  or 
subcutaneous  forms  occur  and  invasion  of  the  alimentary  and  respiratory 
organs,  both  primarily  and  as  a  secondary  process,  is  not  uncommon.  A 
chronic  bronchitis  actinomycotica  and  cerebral  actinomycosis  are  among 
the  rarer  manifestations  of  the  disease. 

Symptoms. — The  symptoms  of  actinomycosis  in  man  depend  to  a  great 
extent  upon  the  part  of  the  body  which  is  affected.  When  the  infection 
takes  place  through  a  carious  tooth  or  by  ulcer  of  the  gum  the  jaw  is  invaded, 
and  the  tissues  covering  it  become  swollen.  To  such  an  extent  may  this 
sweUing  increase  that  the  neck  and  face  may  be  involved.  In  these  tissues 
suppuration  ensues  and  pus  is  discharged  from  chronic  and  somewhat 
puckered  sinuses,  which  heal  in  one  place  only  to  break  out  elsewhere. 
Rarely  the  disease  may  spread  to  the  fauces  and  to  the  tongue. 

By  the  swallowing  of  the  fungus  it  may  infect  the  intestines  and  even 


MYCETOMA  275 

the  liver,  and  in  all  these  organs  it  often  causes  the  formation  of  abscesses. 
It  has  been  found  in  the  stools  in  these  cases. 

Actinomycosis  affects  the  lungs  even  more  frequently  than  the  alimentary 
tract,  and  produces  symptoms  of  subacute  bronchitis  or  bronchiectasis  or 
even  those  of  pulmonary  abscess.  The  patient  suffers  from  cough  and 
from  fever,  and  expectorates  purulent  material  in  which  the  micro-organism 
is  often  found.  The  pulmonary  lesions  are  not  very  acute  in  their  course, 
but  rather  chronic,  life  usually  being  prolonged  in  these  cases  for  a  year 
or  even  longer  than  this.  Rare  cases  of  brain  abscess  have  been  recorded 
as  the  result  of  the  organism  reaching  this  organ.  Howard  has  been  able 
to  find  only  four  primary  cases  beside  his  own,  and  thirteen  secondar)- 
cases.  Such  cases  must  not  be  confused  with  those  equally  rare  instances 
of  strep tothrix  infection  which  Musser  has  recently  reported. 

Diagnosis. — The  disease,  when  the  jaw  is  affected,  must  be  separated  from 
ordinary  necrosis  and  from  sarcoma.  In  the  first  the  swelling  is  not  so 
widespread  and  the  sinuses  not  so  numerous.  In  the  second  condition  there 
is  no  suppuration,  the  growth  is  usually  more  rapid,  and  the  surface  is  not 
so  fluctuating.  An  examination  of  the  pus  in  those  cases  in  which  it  escapes 
will  decide  the  diagnosis  by  revealing  the  ray  fungus.  It  is  to  be  remembered 
that  secondary  pyogenic  infection  and  extensive  necrosis  may  render  the 
detection  of  the  specific  fungus  difficult  if  not  impossible,  and  undoubted 
cases  are  on  record  in  which  for  relatively  long  periods  the  characteristic 
organism  was  absent.  Search  for  the  germ  is  most  likely  to  be  rewarded 
during  recrudescence  in  old  lesions  and  in  newly  formed  nodules  or 
extensions,  when  they  are  freshly  opened. 

Treatment. — This  is  largely  surgical  when  the  growth  is  so  placed  as  to 
permit  of  its  being  attacked  by  this  means.  The  mass  and  the  surrounding 
tissues  should  be  excised  and  all  dead  bone  and  infected  tissue  removed, 
after  which  drainage  should  be  maintained  and  the  sinuses  irrigated  with 
weak  solutions  of  odine  or  of  iodoform  in  oil.  When  the  pleura  is  involved 
iodoform  injections  are  particularly  useful.  Iodide  of  potassium  is  also  an 
effective  drug  when  given  internally  in  doses  of  from  20  to  60  grains  a  day, 
it  being  thought  tha,t  in  its  liberation  of  iodine  it  acts  as  a  specific  against 
the  ray  fungus. 

Periods  of  marked  improvement  and  even  apparent  cure  should  not 
cause  relaxation  in  treatment,  nor  do  they  justify  a  too  hopeful  prognosis, 
as  a  recrudescence  of  lesions  long  obsolescent  is  of  frequent  occurrence. 


MYCETOMA   (MADURA  FOOT,  FUNGUS  FOOT  OF  INDIA). 

This  is  a  mycotic  disease,  usually  invading  one  or  both  feet  and  rarely 
appearing  in  other  parts  of  the  body.  It  is  most  commonly  observed  in 
India.  Sporadic  cases  occur  in  other  parts  of  Asia,  in  Europe,  and  in  South 
America.  A  number  of  cases  have  been  reported  in  the  United  States. 
Two  varieties  of  the  disease  are  recognized:  the  melanoid,  or  mycetoma 
with  black  granules,  and  the  ochroid,  with  white  or  yellow  granules.  They 
are  due  to  distinct  varieties  of  streptothrix  (Streptothrix  madurce  and  Strepto- 
thrix  mycetomas).     The  disease  is  closely  related  to  actinomycosis;  indeed, 


276  DISEASES  DUE   TO   A  SPECIFIC  INFECTION 

some  of  the  cases  reported  in  the  United  States  as  mycetoma  are  undoubted 
cases  of  actinomycotic  feet. 

The  disease  commonly  attacks  one  foot;  beginning  as  a  firm,  hard  nodule 
on  the  sole,  which  gradually  softens  and  discharges  an  oily,  fetid  pus  con- 
taining the  black  or  yellow  granules.  The  sinus  thus  formed  persists. 
Other  nodules  appear  and  go  through  the  same  course.  The  foot  gradually 
enlarges  and  the  sole  is  greatly  thickened.  The  disease  attacks  the  deeper 
tissues  until  eventually  all  structures,  including  the  bones,  are  converted 
into  a  greasy,  yellowish  mass.  The  appearance  of  the  fungus  foot,  with  the 
thickened  sole,  the  toes  strongly  extended  upward,  and  the  plantar  and  dorsal 
surfaces  covered  with  the  button-like  orifices  of  the  sinuses,  is  character- 
istic. Occasionally,  the  disease  shows  some  tendency  to  the  formation  of 
secondary  deposits,  spreading  along  the  lymphatic  vessels.  The  diagnosis 
between  mycetoma  and  actinomycosis  rests  on  the  microscopic  character 
of  the  organisms. 

Treatment. — The  treatment  consists  of  conservative  resection  in  early 
cases  and  amputation  in  older  cases. 


SYPHILIS. 

Definition. — Syphilis  is  a  contagious  disease,  the  cause  of  which  is  as  yet 
undiscovered.  It  is  sometimes  called  "  Lues,"  "  Pox,"  or  "  Lues  Venerea." 
It  occurs  in  two  forms,  the  acquired  and  the  hereditary,  and  is  characterized 
in  the  different  stages  of  its  progress  by  a  greater  number  of  pathological 
changes  in  the  tissues  of  the  body  than  any  other  known  malady.  It  has 
been  said  that  he  who  knows  the  whole  pathology  of  syphilis  and  tubercu- 
losis knows  all  pathology.  This  is,  of  course,  an  exaggerated  statement,  but 
it  emphasizes  the  fact  that  the  disease  presents  lesions  in  many  different 
tissues. 

The  acquired  form  is  usually  divided  into  three  stages,  called  the  primary, 
secondary,  and  tertiary,  and  to  these  Fournier  has  added  a  fourth  group  of 
affections,  apparently  quite  separate  from  any  of  the  foregoing,  which  he 
calls  the  parasyphilitic  or  metasyphilitic  affections. 

The  primary  stage  is  characterized  by  the  development  of  a  chancre  or 
hard  sore,  also  called  the  "initial  lesion";  the  secondary  stage  by  the  appear- 
ance of  eruptions  and  lymphatic  swellings,  and  by  ulceration  of  the  mucous 
membranes.  The  third  stage  consists  in  the  growth  of  tumor-like  masses, 
called  gummata,  and  pathological  changes  in  the  bones  and  in  the  nervous 
and  vascular  systems.  In  the  parasyphilitic  forms  there  is  atrophy  of  the 
cells  of  the  part  involved  and  overgrowth  of  connective  tissue. 

History. — The  history  of  syphilis  is  not  definite.  Certain  investigators 
believe  that  it  is  one  of  the  most  ancient  maladies,  but  it  was  not  clearly 
recognized  as  a  separate  affection  in  Europe  until  1494.  Those  who  wish 
to  look  into  this  question  should  consult  Syphilis  in  Ancient  and  Prehistoric 
Times,  by  Buret,  translated  by  Ohmann-Dumesnil. 

Distribution. — Syphilis  is  found  all  over  the  world,  and  in  its  frequency 
and  virulence  is  not  modified  materially  by  climate  or  geographical  con- 


SYPHILIS  277 

ditions,  but  it  is  worthy  of  note  that  the  disease  is  unknown  among  savage 
peoples  who  have  not  come  in  contact  with  civiUzed  communities. 

Etiology. — No  one  seems  to  doubt  the  micro-organismal  nature  of  syphihs, 
although  a  demonstrated  etiological  agent  is  wanting.  A  great  number  of 
organisms  have  at  various  times  been  regarded  as  the  cause  of  syphilis, 
among  them  being  the  bacteria  described  by  Lustgarten,  Van  Niessen, 
Lisle  and  Jullien,  and  the  parasites  studied  by  Dohle  and  by  Schiiller. 
None  has  been  proved  an  etiologic  factor.  Siegel  describes  a  small  body, 
the  cytoryctes  luis,  which  he  finds  in  the  blood  of  syphilitics  and  regards 
as  the  cause  of  the  disease.  His  findings  lack  confirmation.  A  distinct  ad- 
vance in  the  investigation  of  the  disease  was  made  in  1903,  when  Metschni- 
koff  and  Roux  succeeded  in  producing  characteristic  lesions  in  the  higher 
apes  by  inoculating  syphilitic  virus  from  human  beings;  this  has  since  been 
many  times  repeated.  Early  in  1905Schaudinn  and  Hofi^mann  described  a 
small  spiral  organism  which  they  found  constantly  in  primary  and  secondary 
syphilitic  lesions  and  which,  because  of  its  indifferent  staining  qualities, 
they  termed  the  Spirochceta  pallida.  Recently  they  have  given  it  the  name 
Treponema  pallidum.  Their  findings  have  since  been  confirmed  by  hun- 
dreds of  observers  in  all  parts  of  the  world.  No  authentic  instance  of  the 
organism  in  tertiary  lesions  is  on  record.  It  is  found  in  the  artificially 
produced  lesions  in  apes  and  highly  important  is  its  presence  in  the  blood 
and  tissues  of  infants  dead  from  hereditary  syphilis.  I.evaditi  has  made 
extensive  studies  of  these  cases  and  finds  the  organism  in  greatest  numbers 
in  the  liver,  lung,  and  suprarenal  glands  respectively.  It  exhibits  a  prefer- 
ence for  the  perivascular  tissues  rather  than  for  the  blood  stream  and  is 
found  in  and  without  the  vessel  walls  in  enormous  numbers.  Many  are 
intracellular,  especially  in  epithelial  cells.  The  organism  is  4  to  14//  long 
does  not  exceed  0.5^«  in  thickness  and  possesses  numerous  pronounced 
spirals.  It  is  actively  motile,  but  flagella  have  not  been  positively  demon- 
strated. The  specificity  of  this  parasite  is  regarded  by  Metschnikoff  and 
many  others  as  being  abundantly  proven  and  they  accept  it  as  the  un- 
doubted cause  of  syphilis.  Some  investigators  as  yet  hold  more  conserva- 
tive views.  It  may  at  least  be  said  that  evidence  in  favor  of  the  specificity 
of  the  organism  is  constantly  accumulating. 

In  the  vast  majority  of  cases  syphilis  is  acquired  by  sexual  intercourse, 
although  a  large  number  of  cases  of  acquired  syphilis,  due  to  non-sexual 
contact  with  syphilitic  persons  or  their  garments  when  infected  by  dis- 
charges, have  been  recorded.  (See  Bulkley  on  Syphilis  Insontium.)  Obstet- 
ricians, midwives,  and  nurses  have  often  contracted  the  disease  through  a 
break  in  the  skin  of  the  finger.  Wet-nurses  have  been  infected  through  the 
nipples  by  syphilitic  infants,  and  drinking  utensils,  knives,  forks,  spoons, 
pipes,  and  dental  instruments  have  conveyed  the  poison  to  the  mouths  of 
innocent  persons.  The  disease  can  be  transmitted  by  kissing  and  by  the 
drinking  cup.  Primary  lesions  of  syphilis  have  also  been  produced  in  the 
mouth  by  perverted  sexual  practices. 

The  virus  of  the  disease  is  active  in  the  transmission  of  the  malady  through- 
out the  primary  and  secondary  stages,  and  during  this  time  all  secretions 
from  the  lesions  of  these  stages  are  capable  of  producing  the  disease  in 


278  DISEASES  DUE  TO  A   SPECIFIC  INFECTION 

another  person,  provided  that  they  be  brought  in  contact  with  a  solution 
of  continuity  in  the  skin  or  mucous  membrane.  Infection  does  not  take 
place  through  healthy  skin  or  mucous  membrane,  but  the  break  in  the 
surface  may  be  so  slight  as  to  be  overlooked.  The  blood  of  the  patient 
during  the  secondary  stage  is  capable  of  spreading  the  disease  by  inoculation, 
but  notwithstanding  this  fact  it  is  noteworthy  that  the  secretions  of  the 
various  glands  do  not  contain  the  poison  unless  they  are  contaminated  by 
discharges  from  local  syphilitic  lesions. 

The  acquired  disease  is  not  conveyed  by  the  discharges  from  syphilitic 
sores,  or  by  the  blood  of  a  syphilitic,  if  five  years  have  elapsed  since  the  date 
of  primary  infection;  indeed,  in  most  cases  the  virus  ceases  to  be  capable  of 
inoculating  another  person  at  the  end  of  two  years  after  infection.  This  rule 
holds  true,  even  although  the  patient  may  be  suffering  from  syphilitic  sores  or 
other  active  lesions  at  the  time  of  contact.  On  the  other  hand,  the  spermato- 
zoids  may  indirectly  transfer  the  poison  from  the  man  to  woman  by  the  fetus. 

A  person  who  is  suffering,  or  has  suffered,  from  acquired  syphilis  is  protected 
against  a  second  infection  in  the  vast  majority  of  instances,  although  a  few 
cases  have  been  recorded  which  seem  to  throw  doubt  upon  the  statement 
of  some  syphilographers  that  the  protection  is  absolute.  This  immunity 
is  developed  at  once  after  primary  infection,  as  early  as  the  development 
of  the  primary  lesion  or  chancre,  and  in  some  cases  even  earlier  than  this. 
In  the  case  of  a  person  who  has  inherited  syphilis  from  one  or  both  parents 
the  protection  against  acquired  infection  is  absolute,  even  if  no  signs  of  the 
hereditary  disease  be  present. 

Hereditary  syphilis  may  come  to  a  child  through  one  or  both  parents. 
When  the  father  only  is  syphilitic,  the  term  "  sperm  inheritance  "  is  employed, 
and  when  the  mother  only  is  syphilitic  it  is  called  "germ  inheritance."  A 
syphilitic  male  may  transmit  syphilis  to  his  offspring  without  manifesting  at 
the  time  of  intercourse  any  symptoms  of  syphilis  and  without  producing  in 
the  mother  any  signs  of  the  disease.  It  is  also  possible  for  him  to  have  a 
healthy  child;  that  is,  he  may  fail  to  transmit  the  infection.  This  depends 
largely  upon  the  stage  of  the  malady,  its  virulence  and  activity,  and  the 
value  of  any  antisyphilitic  treatment  that  may  have  been  instituted  for  the 
father's  benefit  before  conception,  and  for  the  benefit  of  the  mother  and 
child  after  conception. 

A  woman  suffering  from  syphilis  may  or  may  not  bear  a  syphilitic  child, 
and  if  active  antisyphilitic  treatment  during  pregnancy  is  maintained,  the 
child  is  likely  to  escape.  It  is  also  possible  for  a  mother  who  contracts 
syphilis  during  her  pregnancy  to  give  birth  to  a  non-syphilitic  child,  but  it 
is  also  possible  for  the  child  to  contract  primary  syphilis  from  a  mucous 
patch  as  it  passes  through  the  birth  canal.  It  is  interesting  to  note,  however, 
that  while  the  syphilitic  mother  is  not  always  able  to  confer  immunity  to 
primary  infection  upon  her  child,  so  that  it  cannot  be  infected  by  the  disease 
before  or  after  birth,  it  is  possible  for  the  syphilitic  foetus  in  utero  to  confer 
immunity  upon  its  mother,  or,  to  express  it  differently,  given  a  child  m 
utero  by  a  syphilitic  father,  that  child  may  be  syphilitic  at  birth,  but  its 
mother  may  not  have  been  infected  during  pregnancy,  and  is  protected 
against  syphilitic  infection  subsequently.     This  is  known  as  Colles'  law. 


SYPHILIS  279 

That  immunity  to  syphilis  can  be  so  acquired  is  proved  by  the  fact  that  if 
a  syphihtic  baby  nurses  at  its  mother's  breast  she  will  not  contract  syphilis, 
even  if  its  mouth  be  filled  by  mucous  patches,  but  if  that  infant  is  nursed 
by  an  innocent  wet-nurse  it  can  produce  syphilis  in  that  nurse. 

From  what  has  been  said  so  far  it  is  evident  that  a  syphilitic  father  or 
syphilitic  mother  may  be  the  parent  of  a  syphilitic  or  non-syphilitic  child. 
If  both  parents  are  syphilitic,  the  probability  of  the  child  being  infected  is 
twice  as  great  as  if  one  parent  is  affected. 

Prevention. — The  prevention  of  syphilis  is  one  of  the  great  social  questions 
of  the  age  that  has  not  been  solved.  In  many  cities  prostitution  has  been 
licensed  in  order  that,  by  governmental  and  medical  control,  prostitutes 
suffering  from  syphilis  might  be  treated  and  prevented  from  plying  their 
vocation  while  capable  of  transmitting  the  disease.  This  plan  when  insti- 
tuted has  not  checked  the  dissemination  of  syphilis,  since  it  continues  to 
spread  through  illicit  intercourse  carried  out  with  unlicensed  women  who 
will  not  be  classed  as  registered  prostitutes. 

Syphilis  may  also  be  prevented  by  forbidding  intercourse  on  the  part  of 
persons  suffering  from  the  disease,  and  by  instructing  the  non-syphilitic  to 
avoid  intercourse  while  any  break  exists  in  the  mucous  membrane  or  skin 
of  the  external  genitals.  Careful  regard  to  cleanliness  after  intercourse  is 
of  some  protective  value. 

Frequency. — It  is  almost  impossible  to  determine  the  prevalence  of  syphilis, 
since  the  living  keep  its  presence  secret  and  the  physician  rarely  returns  a 
death  as  due  to  it,  but  to  some  indirect  result  of  it. 

In  1874  Dr.  F.  R.  Sturgis  estimated  that,  out  of  a  population  of  942,292 
in  New  York  City,  50,450  were  suffering  from  syphilis. 

In  an  appendix  to  Sanger's  History  of  Prostitution,  1892,  it  was  estimated 
that  100,000  persons  out  of  a  population  of  1,800,000  had  syphilis. 

At  the  present  time  the  population  of  Greater  New  York  is  about  3,560,000, 
and  assuming  that  the  rate  of  increase  of  the  disease  has  kept  pace  with 
the  increase  in  population  there  would  be  nearly  200,000  syphilitics  in  that 
city.    These  estimates  are  not  made,  however,  on  a  statistical  basis. 

A  committee  appointed  by  the  Medical  Society  of  the  County  of  New 
York  for  the  study  of  measures  for  preventing  venereal  diseases,  addressed 
a  circular  letter  to  all  the  physicians  in  Greater  New  York  asking  them  to 
report  the  number  of  cases  of  gonorrhoea  and  syphilis  which  they  had  treated 
from  May  1,  1900,  to  May  1,  1901.  Of  the  4750  physicians  to  whom  the 
letter  was  sent,  678  forwarded  statistics  of  their  cases.  The  total  number 
of  cases  of  syphilis  reported  was  7200.  Assuming  that  as  many  cases  occurred 
in  the  practice  of  the  physicians  who  sent  no  reports  as  in  the  practice  of 
those  who  forwarded  statistics,  calculations  would  show  that  50,400  cases 
of  syphilis  were  under  treatment  in  private  practice  during  the  period  of 
time  which  the  investigation  covered.  As  many  patients  go  from  one  phy- 
sician to  another,  it  is  not  improbable  that  some  of  the  reported  cases  may 
have  figured  twice  in  the  statistics;  but  the  committee  believed  that  the 
number  which  did  so  was  more  than  offset  by  the  large  class  of  patients  who 
take  treatment  from  advertising  quacks. 

Of  forty-five  dispensaries  and  charitable  institutions  visited  by  the  com- 


280  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

mittee  nine  refused  to  give  any  information.  An  inspection  of  the  records 
of  the  remaining  thirty-six  showed  that  7607  cases  of  syphiKs  had  been 
treated  during  the  year. 

Burre  shows  by  statistics  that  the  morbidity  of  syphiHs  among  the  inmates 
of  the  Hcensed  houses  of  prostitution  in  Paris  has  fallen  from  30  per  cent, 
in  1873  to  0.25  in  1902.  On  the  1st  of  January,  1873,  1126  public  women 
were  registered,  and  during  the  year  338  cases  of  syphilis  were  recorded 
from  among  the  number.  On  the  1st  of  January,  1902,  429  public  women 
were  registered,  and  only  1  case  of  syphilis  was  observed  among  them  dur- 
ing the  year.  Burre  attributes  this  decrease  in  syphilis  to  the  more  general 
dissemination  of  knowledge  concerning  the  infectious  nature  of  the  disease 
and  to  the  adoption  of  hygienic  measures  for  its  prevention,  which  at 
present  are  largely  practised  by  all  the  licensed  prostitutes.  He  also  lays 
some  stress  upon  the  matter  of  obligatory  elementary  education,  believing 
that  it  may  have  served  to  make  the  prostitutes  more  intelligent  as  a  class 
than  they  were  thirty  years  ago.  His  statistics  illustrate  very  well  the  fallacy 
of  collecting  cases  and  drawing  conclusions  from  them  without  due  care. 
Surely  no  one  supposes  that  the  number  of  prostitutes  in  Paris  has  dimin- 
ished in  the  proportion  of  nearly  75  per  cent. 

R.  W.  Taylor  states  that  most  of  the  cases  of  syphilis  which  he  has  seen 
in  hospitals  are  from  tenement  houses  and  have  not  contracted  the  disease 
from  regular  prostitutes,  which  illustrates  the  difficulty  of  preventing  its 
spread  by  licensing  women  of  the  town. 

Pathology  and  Morbid  Anatomy. — As  already  stated,  syphilis  may  in  its 
various  stages  of  development  affect  almost  every  tissue  of  the  body.  Some 
of  these  manifestations  are  not  distinguishable  from  lesions  resulting  from 
other  causes,  and  hence  their  syphilitic  character  can  only  be  established, 
if  at  all,  by  the  exclusion  of  other  factors  and  the  associated  presence  of 
recognizable  luetic  phenomena. 

The  'primary  lesion  of  syphilis,  called  the  chancre,  develops  at  the  point 
of  infection,  and  is  usually  characterized  by  an  obliterative  endarteritis  with 
spheroidal  cell  infiltration  of  the  surrounding  connective  tissue,  and  by  the 
formation  of  connective-tissue  cells  which  are  particularly  numerous  about 
the  bloodvessels.  As  a  result  of  the  vascular  changes  and  associated  lessened 
nutrition  and  possibly  the  action  of  the  syphilitic  poison,  with  or  without 
added  infection,  superficial  and  usually  central  necrosis  occurs  and  an  ulcer 
results. 

Soon  after  the  formation  of  the  chancre,  just  described,  the  secondary 
stage  develops.  The  lymph  nodes  all  over  the  body,  but  notably  those 
adjacent  to  the  initial  lesion,  become  enlarged  and  inflamed,  and  inflam- 
matory and  degenerative  or  necrotic  processes  develop  in  the  skin,  in  the 
mucous  membranes,  and  in  the  bones  and  viscera. 

Following  this  so-called  secondary  period  of  the  disease  there  develops 
the  tertiary  stage,  in  which  the  periosteum  and  the  internal  viscera  suffer 
from  peculiar  growths  of  newly  formed  tissue.  A  most  constant  lesion  is 
characterized  by  the  formation  of  a  new  tissue  consisting  of  spheroidal  and 
polyhedral  cells  and  scattered  giant  cells,  which  are  commonly  abnormal, 
poorly  supplied  with  bloodvessels,  and  having  a  marked  tendency  to  necrosis, 


SYPHILIS  281 

especially  coagulation  necrosis,  and  hyaline  degeneration  in  their  earlier 
stages,  and  later  caseation  closely  resembling  that  seen  in  tuberculosis.  The 
growth  of  this  new  tissue  is  usually  in  circumscribed  nodes,  and  it  is  in  these 
masses  that  the  necrotic  and  degenerative  processes  just  named  occur  most 
markedly  or  are  most  evident.  These  "  gummaia  "  may  grow  to  consider- 
able size.  They  appear  as  dirty-white,  firm  masses  which,  on  section,  often 
are  found  to  be  caseous  at  the  centre,  where  the  new  tissue  has  undergone 
necrotic  change. 

Syphilis  produces  grave  changes  in  the  hlccdvcssels,  and  no  other  patho- 
logical process  impairs  the  general  vascular  system  so  markedly,  except  it 
be  renal  disease.  A  syphilitic  arteritis  develops  with  diffuse  overgrowth 
of  fibrous  tissue  in  the  adventitia,  and  even  gummata  may  form  along  the 
vessels.  The  arteritis  also  involves  the  middle  coat  and  even  the  endothelial 
lining  of  the  vessels,  and  so  narrows  or  occludes  them.  This  of  course 
diminishes  the  blood  supply  to  the-,  various  organs  and  increases  the  labor 
of  the  heart.  The  heart  muscle  also  suffers  from  a  myocarditis  characterized 
by  overgrowth  of  its  connective  tissues,  and  the  pericardium  and  endocar- 
dium may  be  thickened  for  a  like  reason,  but  gumma  of  the  heart  is  very 
rarely  produced.  The  changes  in  the  heart  are,  therefore,  almost  entirely 
due  to  the  effects  of  the  disease  on  the  vessels  which  supply  it,  and  upon  the 
changes  which  occur  in  the  aorta  and  the  peripheral  vessels.  In  other  words, 
while  arteritis  may  result  in  myomalacia  cordis  the  conspicuous  change  is  a 
fibrosis  of  the  heart  muscle.  The  aortitis  and  general  arteritis  result  in 
increased  cardiac  and  vascular  stress. 

In  the  secondary  stage  of  syphilis  an  acute  syphilitic  nephritis  has  been 
described.  Later  on  a  destructive  overgrowth  of  connective  tissue  develops 
in  association  with  the  vascular  changes  just  described,  and  gummatous 
growths  occur  in  the  kidneys. 

The  liver  is  very  commonly  affected  by  the  formation  of  gummata  or  by 
connective-tissue  proHferation,  which  produce  grave  interference  with  its 
function.  These  changes  take  place  in  both  the  acquired  and  in  the  heredi- 
tary form  of  the  disease.  This  overgrowth  of  connective  tissue  occurs  in 
two  types.  It  is  developed  between  the  lobules  constituting  an  interlobular 
or  perilobular  cirrhosis,  and  between  the  cellular  columns  forming  an  intra- 
lobular cirrhosis.  In  some  instances  these  connective-tissue  formations 
consist  in  large,  firm  bands  which  run  in  various  directions  through  the  liver 
and,  in  contracting,  draw  in  the  capsule  of  Ghsson  and  so  cause  great 
distortion  of  its  surface.  (See  Fig.  44.)  Not  rarely  gummata  are 
enclosed  by  these  bands.  In  the  earlier  stages  and  milder  forms  of  syphilitic 
hepatic  cirrhosis  the  changes  cannot  be  considered  pathognomonic,  but  in 
the  exaggerated  form,  just  described,  typical  syphilitic  changes  occur.  As 
secondary  lesions  of  the  liver  amyloid  disease  and  atrophy  of  its  paren- 
chyma are  occasionally  observed.     (See  Cirrhosis  of  the  Liver.) 

The  lesions  in  the  lungs  consist  in  gummata  which  are  often  surrounded 
by  exudative  material,  as  in  pneumonia.  These  gummata  may  contain  a 
cheesy  area  as  in  tuberculosis  and,  by  pressure,  may  cause  secondary  altera- 
tions." A  second  change  is  overgrowth  of  fibrous  tissue  around  the  bronchi 
which,  associated  with  catarrhal  processes  involving  their  mucosa,  distorts 


282 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


these  tubes,  causing  narrowing  at  some  points  and  at  others  bronchiectases. 
Infarctions  may  occur  because  of  the  obUterative  changes  in  the  bloodvessels. 
A  true  syphihtic  phthisis  presenting  symptoms  resembling  tuberculous  pul- 
monary phthisis,  but  in  which  tubercle  bacilli  are  not  present,  may  occur, 
but  it  is  exceedingly  rare.  It  is  true  that  cases  have  been  reported  in 
which  gummata  in  the  lungs  have,  hke  tubercles,  undergone  softening  of  a 
caseous  type,  and  Wilks  has  recorded  an  instance  in  which  this  process  had 
gone  on  to  the  development  of  a  cavity.    Virchow  and  Fowler  have  recorded 


Fig.  44 


Nodular  syphilis  of  Ihe  liver.     (Kasl  and  Rumpler.) 


similar  cases.  These  cases,  however,  although  they  may  produce  physical 
signs  of  cavity  do  not  present  the  characteristics  of  pulmonary  phthisis  in  the 
sense  of  pulmonary  tuberculosis,  nor  do  those  instances  in  which  bronchi- 
ectatic  cavities  develop  as  the  result  of  syphilitic  fibroid  changes  in  the 
lungs  do  so,  even  though  the  physical  signs  may  be  similar.  The  main 
pathological  difference  in  the  two  states  is  this — viz.,  that  in  tuberculosis 
there  is  not  only  a  destruction  of  the  tubercle  by  softening,  but  the  inter- 
vening tissue  is  infiltrated  with  exudate  which  soon  becomes  tuberculous 


SYPHILIS  283 

and  proceeds  to  necrosis.  This  does  not  occur  in  syphilis.  In  rare  cases 
syphihs  of  the  king  and   tuberculosis  may  be  coincident. 

In  the  hereditary  syphihs  of  infancy  a  lobar  or  bronchopneumonia  in 
which  the  pulmonary  tissues  show  red,  gray,  and  white  exudates,  according 
to  the  stage  of  the  local  disease,  is  sometimes  met. 

The  lymph  nodes  in  cases  of  syphilis  are  always  affected  by  an  over- 
growth of  connective  tissue  after  the  primary  infection.  In  the  third  stage 
gummatous  masses  may  develop  in  them. 

Next  to  changes  produced  in  the  organs  of  circulation  syphilis  manifests 
its  gravest  changes  in  the  central  nervous  system.  The  meninges  may  be 
the  seat  of  gummata  with  or  without  the  presence  of  chronic,  indurative 
overgrowth  of  connective  tissue. 

In  the  brain  it  causes  gummata  manifesting  the  symptoms  of  brain  tumor; 
it  also  produces  a  syphilitic  inflammation  which  is  associated  with  the  forma- 
tion of  a  gelatinous  tissue,  and  finally  and  most  frequently  it  gives  rise  to 
serious  degenerative  changes  in  the  arteries  which  interfere  with  the  nutri- 
tion, and  later  by  rupturing  bring  about  cerebral  hemorrhage.  It  also  causes 
gumma  of  the  cord  and  its  membranes,  which  usually  have  their  origin  in 
the  tissues  of  a  bloodvessel  or  in  the  pia  arachnoid.  Rarely  it  affects  the 
peripheral  nerves,  through  pressure,  as  they  emerge  from  the  cerebrospinal 
sheaths.  In  the  spinal  cord  it  causes  degenerative  changes  of  cells  and 
fibres  and  overgrowth  of  the  sustentacular  tissue. 

The  parasyphilitic  affections,  paresis,  meningoencephalitis,  locomotor 
ataxia,  etc.,  will  be  discussed  with  diseases  of  the  nervous  system. 

Symptoms. — The  symptoms  of  acquired  syphilis  are  best  described  as 
they  appear  in  the  three  stages  of  the  disease. 

First  Stage. — In  from  twelve  to  twenty-one  days  after  exposure  and 
infection  the  patient  develops  at  the  site  of  original  contact  with  the  virus  a 
small  papule  or  pimple  which  has  an  area  of  indurated  tissue  about  its 
base,  the  so-called  primary  lesion  or  hard  chancre.  Further  examination 
of  the  patient  will  reveal  the  fact  that  the  inguinal  glands  are  slightly 
enlarged. 

This  period  of  primary  syphilis  lasts  from  three  to  ten  days  or  two  weeks, 
and  is  followed  by  the  development  of  the  secondary  stage. 

Second  Stage. — In  the  secondary  stage  we  find  fever  as  an  early 
symptom,  which  varies  in  its  degree  very  greatly  in  different  patients.  In 
some  instances  it  is  so  mild  as  to  be  overlooked;  in  others  it  may  rise  to  a 
point  as  high  as  104°  or  even  105°.  The  more  common  febrile  movement 
is  one  in  which  the  temperature  for  some  days  stays  in  the  neighborhood  of 
101°.  When  the  fever  intermits,  being  fairly  high  at  one  period  and  then 
breaking  sharply,  it  may  mislead  the  physician  into  a  diagnosis  of  malarial 
infection  or  acute  sepsis.  I  have  seen  several  cases  in  which  a  diagnosis  of 
typhoid  fever,  malarial  fever,  or  tuberculosis  was  made  when  in  reality  the 
disease  was  early  secondary  syphilis. 

The  skin  eruptions  of  the  secondary  stage  consist  chiefly  of  the  roseola,  the 
development  of  which  often  marks  the  onset  of  the  secondary  stage.  This 
roseolous  rash  may  occur  in  limited  areas  or  be  widely  distributed  over  the 
body  and  even  involve  the  face.     On  one  occasion  a  woman  with  a  well- 


284  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

developed  syphilitic  roseola  presented  so  scarlet  a  visage  that,  although  she 
was  veiled,  she  caused  the  other  patients  to  leave  my  waiting-room  in 
alarm,  they  thinking  that  she  had  scarlet  fever.  As  a  rule,  however,  the 
rash  is  not  so  marked  on  the  face. 

In  other  cases,  in  place  of  roseola  there  develops  a  macular  syphilide, 
characterized  by  the  appearance  of  reddish-brown  or  copper-like  macules 
scattered  over  the  trunk. 

As  the  secondary  stage  advances  the  eruption  may  be  papular  and 
finally  pustular,  and  at  this  time  it  may  closely  resemble  that  of  true 
variola.  In  still  other  cases  a  squamous  or  scaly  eruption  appears  which 
differs  from  psoriasis  in  that  it  is  not  chiefly  on  the  extensor  surfaces  as  is 
ordinary  psoriasis,  and  in  addition  it  is  frequently  copper-colored. 

At  the  point  of  junction  between  the  mucous  membrane  and  the  skin,  as  at 
the  anus  or  at  the  angles  of  the  mouth,  "mucous  patches, "  or  ulcers,  develop, 
and  upon  the  skin  in  the  neighborhood  of  these  lesions  warty  growths  of  a 
flat  character,  the  so-called  syphilitic  condylomata,  appear.  Mucous  patches 
on  the  buccal  mucous  membrane  and  tongue  also  appear. 

There  is  nearly  always  some  falling  of  the  hair  in  secondary  syphilis. 
Sometimes  this  falling  is  well  distributed;  in  other  cases  it  is  in  patches — 
syphilitic  alopecia. 

A  serious,  oftentimes  painful  complication  at  this  stage  is  syphilitic  iritis. 
If  the  treatment  is  not  active  sight  may  be  lost. 

A  rapid  development  of  anaemia,  which  often  becomes  quite  marked,  not 
as  to  haemoglobin,  but  as  to  the  number  of  the  red  cells  present,  is  often 
observed. 

The  secondary  stage  lasts  from  twelve  to  eighteen  months,  and  is  usually 
followed  by  a  period  during  which  the  symptoms  are  modified  or  entirely 
disappear,  the  virulence  of  the  disease  seeming  to  have  spent  itself,  but 
even  if  no  syphilitic  symptoms  are  present  a  child  begotten  at  this  time  will 
usually  suffer  from  hereditary  syphilis. 

Third  Stage. — In  the  great  majority  of  untreated  cases  the  malady  pro- 
ceeds to  the  so-called  tertiary  stage.  This  is  characterized  by  the  presence  of 
skin  lesions,  which  are  more  severe  than  those  of  the  secondary  period,  such  as 
tuberculous  and  ulcerous  formations  of  a  subacute  or  chronic  character.  There 
is  an  overgrowth  of  connective  tissue  in  different  parts  of  the  body,  as  in 
the  secondary  period,  and  multiple  gummata  are  often  present  in  numbers, 
developing  in  the  skin,  in  the  subcutaneous  tissues,  in  the  muscles,  and  in 
the  internal  viscera,  particularly  in  the  liver.  When  in  the  skin  they  often 
slough  and  produce  ulcers,  and  in  the  internal  organs  they  become  filled  with 
fibrous  tissue  and  undergo  contraction  in  the  manner  already  described. 

Last,  but  by  no  means  least,  of  the  changes  due  to  syphilis  in  its  tertiary 
stage,  we  meet  with  lesions  of  the  nervous  system.  These  changes,  as  a 
rule,  are  late  manifestations  of  the  disease,  occurring  some  years  after  the 
infection.  Rarely  they  may  appear  as  early  as  within  the  first  six  months, 
usually  within  the  first  ten  years,  seldom  as  late  as  twenty  years. 

Syphilis  in  certain  cases  may  seem  to  possess  great  virulence  and  become 
destructive  in  its  course,  almost  from  the  onset.  The  chancre  may  rapidly 
ulcerate  and  spread,  the  fever  may  be  marked,  and  the  ansemia  severe.    The 


SYPHILIS  285 

skin  lesions  become  pustular,  even  in  the  secondary  stage,  and  form  deep 
ulcers,  which,  in  turn,  cause  scars  as  they  heal.  Destructive  changes  rapidly 
develop  in  the  bones  and  viscera.  The  patient  may  die  within  a  few  months 
of  the  infection.  In  these  cases  there  is  usually  a  lowered  vital  resistance 
which  permits  the  disease  to  progress  unopposed. 

In  other  cases  the  symptoms  are  remarkably  mild.  The  chancre  is  so 
small  that  it  is  overlooked,  the  patient  truthfully  stating  years  afterward  that 
he  has  never  had  a  primary  lesion.  The  rose  rash  may  not  occur,  or  be  so 
faint  and  fleeting  as  not  to  attract  notice,  and  the  primary  anremia  may  be 
entirely  absent.  Syphilis  may  end  in  complete  recovery  at  the  close  of  the 
secondary  stage,  but  such  a  fortunate  result  is  rare,  unless  active  treatment 
has  been  instituted. 

It  is  a  fact  worthy  of  note  that  nervous  lesions  seem  to  occur  more 
frequently  in  cases  which  have  presented  mild  secondary  symptoms  than  in 
those  who  have  had  severe  secondary  and  tertiary  lesions  of  internal  viscera. 

Three  intracranial  conditions  due  to  syphilis  may  produce  violent  head- 
ache, namely,  arteritis,  meningitis,  and  gumma.  When  arteritis  is  thecause, 
giddiness,  weakness  of  groups  of  muscles,  difficulty  of  speech,  and,  it  may 
be,  signs  of  general  paresis  develop.  On  the  other  hand,  when  the  ocular 
muscles  are  affected  and  an  optic  neuritis  is  present,  meningitis  is  the  more 
likely  condition,  particularly  if  there  is  spasmodic  contraction  of  certain 
cranial  muscles  and  fever.  Neuroretinitis  is  present  in  meningitis  and  in 
gumma,  but  is  not  commonly  present  in  arteritis.     (See  Meningitis.) 

The  symptoms  of  syphilis  of  the  brain  depend  very  largely  upon  the  site 
of  the  lesion,  for,  as  already  stated  in  the  section  on  the  Morbid  Anatomy 
of  Syphilis,  these  lesions  may  be  at  the  base,  on  the  convexity,  or  in  the 
membranes.  By  far  the  most  common  symptom  of  cerebral  syphilis  is 
headache,  which  is  usually  diffuse  and  constant,  but  if  the  meninges  are 
involved,  or  a  gumma  is  causing  pressure,  it  may  be  exceedingly  severe  and 
characterized  by  what  are  known  as  "crashing  pains."  Patients  with  cere- 
bral syphilis  are  often  unduly  somnolent.     (See  Diagnosis.) 

When  gummatous  growths  form  at  the  base  of  the  brain  the  symptoms 
are  those  due  to  interference  with  the  cranial  nerves,  such  as  squint,  optic 
atrophy,  and  facial  paralysis.  When  the  convexity  of  the  brain  is  aflected 
the  symptoms  are  those  of  localized  or  Jacksonian  epilepsy,  or  of  petit  mal. 
Sometimes  the  epileptic  seizure  is  general.  Fournier  laid  down  as  a  law 
that  epilepsy  beginning  in  adult  years  is,  nine  times  out  of  ten,  syphilitic. 
A  third  form  of  cerebral  syphilis  is  that  in  which  there  are  psychical  disorders, 
such  as  melancholia  or  delusions  of  grandeur.     (See  Paresis.) 

Spinal  syphilis  manifests  itself  as  the  result  of  the  presence  of  gummata  or 
of  connective-tissue  changes  in  the  cord.  When  the  lesion  is  a  gumma 
the  symptoms  are  those  of  pressure  on  the  cord.  When  connective-tissue 
changes  occur  the  signs  are  those  of  spastic  paralysis  of  the  lower  limbs,  with 
markedly  exaggerated  reflexes,  low  muscle  tension,  and  vesical  disturbances. 
Often  the  disorder  of  the  functions  of  the  bladder  is  the  first  sign  of  spinal 
difficulty.  The  bladder  may  lose  its  expulsive  power  or  incontinence  may 
occur.  As  a  parasyphilitic  affection  locomotor  ataxia  is  the  most  common 
nervous  disease.     (See  Locomotor  Ataxia.) 


286  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Diagnosis. — The  diagnosis  of  acquired  syphilis  is  readily  made  if  the 
patient  presents  the  well-developed  symptoms.  In  many  cases,  however, 
these  are  not  manifested.  The  indurated  base  of  the  chancre  is  an  invalu- 
able sign  if  the  chancre  has  not  been  cauterized,  and  the  presence  of  enlarge- 
ment of  the  lymph  nodes  in  the  groin  and  in  the  great  chain  of  nodes  in 
the  neck  is  also  a  useful  diagnostic  point.  The  presence  of  secondary 
syphilitic  roseola,  and  fever  with  sore  throat,  and  mucous  patches  are  diag- 
nostic. In  some  cases,  however,  the  secondary  symptoms  never  develop  or 
are  so  mild  as  to  be  overlooked,  yet  well-marked  tertiary  signs  develop  later. 
The  employment  of  mercury  or  iodide  of  potassium,  followed  by  the  dis- 
appearance of  the  symptoms,  is  a  therapeutic  test,  but  such  a  result  is  not 
a  pathognomonic  sign  of  syphilis. 

Prognosis. — ^The  outlook  in  acquired  syphilis  as  to  severity  of  attack  and 
ultimate  recovery  depends  largely  upon  the  state  of  the  general  health,  and 
the  promptness  with  which  specific  treatment  is  instituted.  Much  depends 
also  upon  the  faithfulness  of  the  patient  in  carrying  out  the  treatment  for  a 
sufficient  length  of  time.  In  the  great  majority  of  cases  active  and  skilful 
treatment  permits  a  favorable  prognosis  as  to  complete  cure,  and  even  as  to 
the  safety  of  future  marriage.  In  the  maHgnant  cases,  or  those  in  which 
tertiary  lesions  have  already  formed,  we  can  only  hope  to  modify  the  progress 
of  the  malady,  or  perhaps  arrest  it  without  being  able  to  remove  all  signs 
of  its  invasion.  Gummatous  growths  may,  however,  be  removed  by  treat- 
ment, even  in  the  tertiary  stage. 

Hereditary  Syphilis. — ^The  symptoms  of  hereditanj  syphilis  may  be  present 
at  birth,  the  skin  being  already  the  site  of  syphilitic  eruptions,  of  which  pem- 
phigus neonatorum — that  is,  a  bleb-like  eruption  about  the  wrists  and  ankles 
— is  typical.  The  liver  and  spleen  are  usually  enlarged,  and  the  child  may 
be  wasted  and  poorly  nourished.  In  other  instances  the  child  manifests  no 
lesions  at  birth,  but  within  its  first  six  months  of  life  develops  syphilitic 
rhinitis,  or,  as  it  is  called,  "snuffles."  This  is  accompanied  or  followed 
by  cutaneous  lesions,  of  which  the  most  frequent  is  mucous  patches  about 
the  anus  and  in  the  mouth.  It  may  waste  away  from  so-called  syphilitic 
marasmus,  developing  a  syphilitic  rosary  at  its  costocartilaginous  junctures, 
as  in  rickets.  The  ends  of  the  long  bones  are  the  victims  of  syphilitic 
epiphysitis.  If  the  child  lives  to  reach  the  period  of  second  dentition  its 
teeth  may  be  notched — the  so-called  "Hutchinson"  or  "peg"  teeth.  This 
malformation  does  not  appear  in  the  milk  teeth.  In  many  cases  of  heredi- 
tary syphilis  in  infancy  the  child  looks  like  an  old  man,  whereas  in  hereditary 
syphilis  of  early  adult  life  the  patient  often  looks  very  immature — "syphilitic 
infantilism."  Children  having  hereditary  syphilis  are  prone  to  suffer  from 
syphilitic  keratitis,  from  deafness,  and  from  bone  lesions  which  develop 
after  several  years  of  life.  The  periosteum  is  thickened  and  even  nodular 
in  its  appearance,  particularly  on  the  tibia. 

x\nother  lesion  is  deformity  of  the  fingers,  in  which  they  become  thickened 
at  the  base  and  taper  rapidly  to  the  tip,  being  somewhat  pear-shaped  or 
top-shaped — the  so-called  syphilitic  dactylitis. 

Treatment. — Divergent  views  have  existed  in  regard  to  the  proper  treat- 
ment of  syphilis  in  its  early  stages.     A  certain  number  of  practitioners  of 


SYPHILIS  287 

experience  have  insisted  that  it  is  unwise  to  administer  mercury  to  a  patient 
suffering  from  a  suspicious  primary  lesion  until,  by  the  development  of 
secondary  symptoms,  the  diagnosis  of  syphilis  is  absolutely  confirmed;  since 
if  we  do  not  wait  for  these  symptoms,  the  possibility  exists  that  a  patient  who 
has  not  really  acquired  syphilis  may  be  condemned  to  the  belief  that  he  has 
been  inoculated,  and  this  may  cause  him  great  mental  suffering  during  the 
rest  of  his  life. 

Another  group  of  practitioners  have  strongly  urged  a  view  directly  opposed 
to  this,  claiming  that  we  have  no  right  to  permit  the  disease  to  become  thor- 
oughly engrafted  upon  the  patient's  system  without  instituting  measures 
for  its  relief,  or  at  least  for  the  diminution  of  the  severity  of  the  infection. 
The  leaders  in  this  line  of  thought  have  advocated  the  excision  of  the 
chancre  in  the  belief  that  by  so  doing  the  primary  focus  of  infection  was 
removed.  It  must  be  remembered,  however,  that  the  primary  lesion  does 
not  develop  until  two  or  three  weeks  after  the  actual  inoculation,  and,  there- 
fore, although  it  appears  at  the  site  of  inoculation,  there  is  good  reason  to 
believe  that  it  is  not  a  source  from  which  still  further  infection  takes  place, 
but  rather  a  localized  manifestation  that  inoculation  has  been  accomplished. 
Nearly  always  there  can  be  found  in  the  adjacent  lymphatics  evidence  that 
they  are  affected  as  early  as  the  chancre  appears.  The  question  as  to  whether 
the  chancre  should  be  excised  must,  therefore,  be  left  to  the  judgment  of  the 
individual  physician,  with  the  statement  that  it  is  possible,  but  not  probable, 
for  the  excision  to  have  some  influence  for  good. 

It  is  with  those  who  believe  in  the  immediate  administration  of  anti- 
syphilitic  treatment  as  soon  as  the  chancre  is  developed  that  I  agree.  It  does 
not  seem  to  me  rational  to  permit  the  disease  to  run  on  uncontrolled  until 
he  who  runs  may  read  that  infection  has  taken  place.  While  it  is  true  that 
the  chancre  at  times  is  not  sufficiently  characteristic  to  enable  us  to  make 
a  positive  diagnosis  that  it  is  true  syphilis,  we  are  justified  in  such  a  case 
in  considering  that  it  is  such  and  proceeding  at  once  to  the  relief  of  the 
patient. 

The  main  treatment  during  the  primary  and  secondary  stage  of  syphilis 
must  consist  in  the  administration  of  full  doses  of  the  protiodide  of  mercury, 
which  should  be  given  in  the  form  of  uncompressed  tablet  triturates  in  the 
dose  of  J  of  a  grain  three  times  a  day,  increased  by  one  or  two  quarters 
each  day,  until  the  patient  manifests  distinct  evidences  of  the  full  systemic 
effect  of  the  drug,  as  evidenced  by  some  looseness  of  the  bowels  or  by  the 
development  of  tenderness  of  the  teeth  and  slight  salivation.  It  is  impor- 
tant when  this  drug  is  given  that  tablet  triturates,  and  not  compressed  tablets, 
are  employed,  as  the  compressed  tablets  are  often  unabsorbed,  because  of 
their  hardness,  and  frequently  cause  irritation  of  the  stomach,  whereas,  the 
properly  made  tablet  triturate  rarely  does. 

As  soon  as  the  patient  manifests  any  of  the  symptoms,  mentioned  as  indic- 
ative of  the  fact  that  he  is  using  all  of  this  drug  which  he  can  well  bear,  it  is 
proper  to  diminish  the  dose  one-half,  and  keep  it  at  this  point,  provided  that 
this  dose  seems  competent  to  prevent  the  development  of  further  syphilitic 
manifestations.  If,  however,  this  half  dose  is  not  sufficient  for  this  purpose, 
the  drug  must  be  given  in  ascending  doses  the  second  time,  and  if  the 


288  DISEASES  DUE   TO  A  SPECIFIC  INFECTION 

syphilitic  manifestations  are  at  all  malignant  it  may  be  necessary  to  continue 
it,  even  if  opium  or  bismuth  have  to  be  given  to  control  diarrhoea. 

It  is  essential  in  the  use  of  the  protiodide  of  mercury  in  syphilis,  first, 
that  the  stomach  shall  not  be  disordered,  because  it  is  of  vital  importance 
that  the  patient  should  be  able  to  take  full  quantities  of  highly  nutritious 
food,  in  order  that  by  maintaining  his  vitality  his  own  vital  processes  may 
aid  him  to  combat  the  infection. 

It  is  also  essential  that  great  care  be  taken  against  the  development  of  mer- 
curial stomatitis.  If  this  condition  once  develops,  it  is  often  difficult  to  cure 
it  while  the  mercury  is  continued,  and  it  frequently  will  prevent  the  patient 
from  taking  sufficient  doses  of  the  drug  to  favorably  influence  his  syphilitic 
infection.  If  the  patient  is  directed  to  take  the  greatest  possible  care  as  to 
cleanliness  of  his  mouth,  to  use  a  tooth-brush  and  some  antiseptic  dentifrice 
after  each  meal,  to  keep  particles  of  food  from  between  the  teeth  by  the 
use  of  floss  silk,  and,  finally,  if  he  also  be  given  a  prescription  calling  for  10 
grains  of  chlorate  of  potassium  and  10  drops  of  tincture  of  myrrh  in  an  ounce 
of  elixir  of  calisaya,  which  is  to  be  diluted  one-half  with  water,  and  used 
as  a  mouth-wash  night  and  morning,  it  will  be  found  that  he  will  be  able  to 
take  much  larger  doses  of  mercury  than  if  these  measures  are  delayed  until 
some  evidences  of  mercurial  sore  mouth  present  themselves. 

Should  the  manifestations  of  syphilis  be  virulent,  then  it  is  necessary  to  give 
the  drug  to  the  patient  not  only  in  the  form  of  the  protiodide  by  the  mouth, 
but  to  use  blue  ointment  rubbed  into  the  skin  at  least  once  a  day,  in  the  dose 
of  about  1  drachm,  choosing  a  different  spot  each  time  for  the  rubbing,  and 
exercising  great  care  that  the  rubbing  is  continued  long  enough  to  actually 
cause  the  absorption  of  the  mercury.  Usually  a  hot  Turkish  bath  or,  if  this 
is  impossible,  an  ordinary  hot-water  bath  should  be  taken  before  the  mercurial 
ointment  is  used,  in  order  that  the  skin  may  be  rendered  pliable  and  put  in 
such  a  state  that  the  mercury  can  be  readily  taken  up  by  the  tissues  beneath 
it.  The  entrance  of  mercurial  ointment  into  the  body  may  also  be  aided  by 
smearing  it  on  a  flannel  binder  and  placing  this  about  the  patient's  waist. 

In  other  instances,  in  addition  to  the  internal  and  external  use  of  mercury,  or 
in  place  of  one  of  them,  hypodermic  injections  of  mercury  may  be  employed. 
For  this  purpose  one  of  the  best  preparations  is  corrosive  sublimate  dissolved 
in  normal  salt  solution  and  given  in  the  dose  of  -J  of  a  grain,  injected  deeply, 
but  gently,  into  the  loose  cellular  tissues  of  the  buttocks  or  back,  or,  better 
still,  into  the  body  of  the  greater  muscles,  such  as  the  gluteus.  Great  care 
must  be  exercised  that  antisepsis  is  complete,  since  otherwise  the  irritant 
drug,  although  antiseptic  in  itself,  may  cause  abscess.  This  injection  should 
not  be  given  oftener  than  every  two  or  three  days.  In  other  instances 
gray  oil  may  be  used,  prepared  by  rubbing  2  drachms  of  lanolin  with  a 
sufficient  quantity  of  chloroform  to  form  an  emulsion,  continuing  the  rubbing 
until  most  of  the  chloroform  is  evaporated,  then  adding  metaflic  mercury  to 
the  extent  of  4  drachms,  and  rubbing  again  until  the  mixture  is  complete. 
This  strong  gray  ointment,  diluted  still  further  by  the  addition  of  equal  parts 
of  olive  oil,  may  be  injected  in  the  dose  of  1  or  2  minims  every  second  or  third 
day  in  the  same  manner  as  corrosive  sublimate. 

Still  another  way  of  getting  mercury  into  the  body  is  by  means  of  the  sub- 


SYPHILIS  289 

limation  of  calomel.  The  patient,  being  stripped  of  all  clothing,  is  wrapped 
in  a  blanket  and  placed  upon  a  chair  with  a  wooden  seat.  Under  this  chair 
is  placed  an  alcohol  lamp  and  over  it  a  disk  of  metal  upon  a  small  iron 
stand,  on  which  20  grains  of  calomel  is  laid.  Upon  this  stand  is  also  placed 
a  tincupful  of  water.  The  heat  of  the  lamp  vaporizes  the  water  and  sub- 
limes the  calomel,  and  the  mercury,  being  deposited  upon  the  skin  of  the 
patient,  is  absorbed.  This  method  of  treatment  is  useful  for  the  relief  not 
only  of  the  systemic  symptoms,  but  also  for  the  syphilitic  eruption  of  the 
skin.  A  similar  plan  of  sublimation  can  be  carried  out  with  inhalations,  the 
patient  holding  his  face  eighteen  inches  away  from  the  pan  and  inhaling  the 
fumes.  If  this  is  done  mucous  patches  in  the  mouth  are  very  frequently 
rapidly  healed,  but  after  each  employment  of  sublimation  and  inhalation, 
the  mouth  should  be  well  rinsed  with  water,  in  order  that  an  excess  of  mer- 
cury may  not  remain  there  and  produce  stomatitis.  In  many  cases  the  best 
results  are  produced  by  a  plan  of  treatment  in  which  both  the  iodide  of 
potassium   and  protiodide  of  mercury  are  given  together  or  alternately. 

The  treatment  of  the  tertiary  stage  of  syphilis  consists  chiefly  in  the  admin- 
istration of  iodide  of  potassium  or  iodide  of  sodium  or  iodide  of  strontium, 
in  as  full  doses  as  the  patient  can  well  bear,  but  should  evidences  of  gum- 
matous growth  in  the  brain  present  themselves  the  iodide  is  not  sufficiently 
active  in  its  action,  and  mercury  should  be  given  with  it. 

The  dose  of  the  iodides  varies  greatly  with  the  susceptibility  of  different 
individuals.  As  a  rule,  tertiary  syphilis  is  not  benefited  by  giving  less  than 
100  grains  a  day,  I  have  had  a  patient  under  my  care  who  would  take  800 
grains  a  day  with  great  benefit,  with  no  other  disagreeable  symptoms  than 
the  development  of  an  intense  acne.  But  we  rarely  meet  with  instances 
where  these  enormous  doses  must  be  taken. 

The  proper  way  to  administer  the  drug  is  to  order  a  saturated  solution  of 
iodide  of  sodium  dissolved  in  the  strength  of  1  grain  to  the  minim  of  water, 
and  direct  that  10  minims  of  this  be  given  in  a  dessertspoonful  of  the  com- 
pound syrup  of  sarsaparilla  three  times  a  day  an  hour  after  meals,  being 
increased  each  day  from  1  to  5  minims  at  a  dose.  If  careful  attention  is  paid 
to  the  diet  and  to  the  condition  of  the  bowels,  patients  who  would  not  be 
able  to  take  large  doses  at  first  soon  become  fairly  immune  so  far  as  untoward 
effects  are  concerned,  and  can  take  effective  quantities  within  a  brief  period 
of  time. 

Hereditary  syphilis  is  to  be  treated  by  the  active  employment  of  mercury. 
In  babies  suffering  from  syphilis,  gray  powder  may  be  given  in  the  dose  of  2 
grains  two  or  three  times  a  day,  and  mercurial  ointment  may  be  rubbed  into 
the  abdomen  and  on  the  inside  of  the  thighs  and  smeared  upon  the  abdom- 
inal binder  of  the  child.  This  will  prove  a  most  advantageous  plan  of  treat- 
ment. The  change  in  the  nutrition  and  appearance  of  the  infant  under  these 
circumstances  is  little  less  than  marvellous. 

The  diet  should  be  carefully  regulated,  and,  if  the  digestion  will  stand 
it,  cod-liver  oil  should  be  given  internally.  The  employment  of  the  mer- 
curial ointment  produces  an  active  systemic  influence  without  disordering 
digestion,  and  is,  therefore,  particularly  advantageous  when  hereditary 
syphilis  is  being  treated  in  infants. 
19 


290  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 


TUBERCULOSIS. 

Definition. — Tuberculosis  is  an  infectious  disease  caused  by  the  presence 
in  the  body  of  the  Bacillus  tuberculosis.  It  is  characterized  by  a  local 
inflammatory  process  followed  by  the  development  of  areas  of  necrosis. 
While  the  lesions  produced  by  the  disease  are  varied,  the  typical  manifes- 
tation is  the  formation  of  small  nodules  v^^hich  appear  as  gray,  or  v^hite,  or 
sometimes  yellowish  bodies  called  tubercles.  It  is  because  of  these  tubercles 
that  the  name  "tuberculosis"  is  applied  to  the  malady. 

Etiology. — The  chief  etiological  factors  in  this  disease  are  the  specific 
bacillus  and  the  presence  of  a  favorable  state  in  the  tissues  of  the  individual 
for  the  growth  of  the  germ.  As  the  disease  is  constantly  present  all  over  the 
world,  except  in  a  few  scattered  areas,  the  specific  germ  is  always  at  hand, 
and  as  a  large  number  of  causes  produce  a  condition  of  the  tissues  which 
is  favorable  to  their  development  the  disease  is  only  too  prevalent. 

The  bacillus  of  tuberculosis  appears  as  a  straight,  slightly  curved  or  bent 
rod  with  rounded  ends,  devoid  of  motility,  and  reproducing  itself  by  fission ; 
the  often  expressed  belief  that  it  is  a  spore-bearing  organism  is  not 
unequivocally  established.  It  stains  with  the  ordinary  aniline  dyes  and  by 
Gram's  method.     (See  Pathology.) 

The  Bacillus  tuberculosis  enters  the  body  by  several  pathways,  of  which 
the  most  common  is  undoubtedly  the  respiratory  passages.  It  also  gains 
access  by  way  of  the  alimentary  canal  with  the  food,  and  occasionally  by 
accidental  inoculation.  Recent  studies  have  shown  that  the  tonsils  and 
lymphoid  tissues  of  the  pharynx  are  portals  through  which  the  tubercle 
bacillus  frequently  enters.  The  position  of  the  tonsils  exposes  them 
to  both  air-borne  and  food-borne  infection,  and  their  crypts  and  lymphatic 
communications  afford  favorable  opportunities  for  the  entrance  and  dis- 
semination of  the  micro-organism.  Very  rarely  true  hereditary  transmission 
takes  place  by  the  passage  of  the  bacillus  through  the  placenta  or  possibly  by 
the  infection  of  the  ovum  by  this  organism.  Such  instances  are,  however, 
so  rare  that  they  are  curiosities  in  medicine. 

When  the  infection  takes  place  by  inhalation  it  usually  occurs  by  the  bacilli 
being  dissipated  through  the  air  in  the  form  of  dust,  or  by  their  expulsion  in 
small  masses  of  sputum  which,  falling  on  pillows,  bedding,  or  clothing,  are 
easily  taken  into  the  respiratory  passages  when  the  sputum  dries.  Fliigge 
has  shown  that  when  a  patient  coughs  with  his  mouth  open  the  ejected  air 
may  contain  droplets  holding  the  bacillus,  thereby  rendering  the  immediate 
neighborhood  of  the  sufferer  especially  dangerous.  There  can  be  no  doubt 
of  these  facts,  for  they  are  proved  by  the  very  great  frequency  of  the  disease 
in  the  lungs,  particularly  when  opportunity  exists  for  infection  by  dust, 
and  by  the  fact  that  susceptible  animals  can  be  infected  by  this  disease  if 
forced  to  breathe  dust  which  has  been  contaminated  by  dried  tuberculous 
sputum. 

Kingsford  found  in  analysis  of  339  cases  that  216,  or  63.7  per  cent., 
occurred  by  inhalation,  65,  or  19.1  per  cent.,  by  ingestion,  and  17  per  cent, 
were  of  doubtful  origin. 


TUBERCULOSIS  291 

That  tuberculous  infection  by  way  of  the  aUmentary  tract  occurs  very 
commonly  as  the  result  of  drinking  milk  from  tuberculous  cows,  or  milk  that 
has  been  contaminated  by  the  sputum  from  tuberculous  human  beings  has 
long  been  held.  The  infection  of  milk  by  coughing  or  sneezing  by  persons 
suffering  from  this  disease  occurs  quite  frequently.  The  milk  of  a  tuber- 
culous cow  will  convey  the  infection  even  if  local  tuberculous  lesions  are 
not  present  in  the  udder,  and  the  bacillus  may  be  found  in  butter  made 
from  such  milk.  The  fact  that  tuberculosis  is  so  frequently  found  in  the 
mesenteric  glands  of  young  children  is  significant  in  this  connection.  Infec- 
tion by  the  meat  of  a  tuberculous  animal  can  only  occur  if  the  meat  actually 
contains  the  bacilli  and  is  eaten  uncooked.  This  form  of  infection  is 
probably  very  rare  except  when  sausages  made  from  what  are  known  as 
Bologna  cows^  are  eaten  in  a  raw  or  half-cooked  state. 

Medical  publications  have  teemed  during  the  last  few  years  with  rather 
heated  debates  as  to  the  communicability  of  bovine  tuberculosis  to  man. 
In  the  minds  of  some  bacteriologists,  in  Germany  in  particular,  this  question 
is  still  sub  judice,  but  the  majority  of  those  best  qualified  to  judge  now  agree 
that  no  doubt  can  exist  of  its  transference,  particularly  from  the  udders  of 
tuberculous  cows  to  the  mesenteric  glands  of  children  who  drink  the  milk 
from  these  animals. 

Raw,  Theobald  Smith,  and  others  have  maintained  that  man  is  subject  to 
two  forms  of  tuberculosis,  one  derived  from  members  of  his  own  zoological 
group  and  another  due  to  infection  by  the  bovine  bacillus.  The  wide 
distribution  of  tuberculosis  in  the  animal  kingdom,  the  morphological, 
cultural,  and  pathogenic  differences  in  the  bacillus  found  under  different 
conditions,  and  the  generally  admitted  possibility  of  ranging  these  organisms 
in  a  scale,  or  at  least  in  closely  allied  groups,  explain,  at  least  in  part,  the 
different  phenomena  as  seen  in  man. 

The  mere  presence,  however,  of  the  tubercle  bacillus  is  not  the  only  requi- 
site for  the  development  of  tuberculosis,  for  as  already  stated  the  tissues  must 
be  in  a  favorable  state  for  its  growth.  This  favorable  state  is  produced  by 
any  cause  which  impairs  vital  resistance  and  prevents  the  body  from  destroy- 
ing invading  micro-organisms  soon  after  they  enter  it.  Of  these  causes, 
aside  from  diseases  which  impair  the  general  health,  we  find  the  most 
potent  are  bad  air,  particularly  that  due  to  poor  ventilation  when  large 
numbers  of  persons  are  crowded  together;  lack  of  exercise,  so  that  all  parts 
of  the  lungs  are  not  thoroughly  expanded;  and,  lastly,  those  conditions  of 
air  and  soil  which  are  associated  with  excessive  humidity,  particularly  if 
there  be  much  dust  in  the  atmosphere,  as  in  large  cities. 

In  addition  to  these  causes,  which  increase  the  susceptibility  of  all  persons, 
we  also  find  that  certain  individuals  inherit  conditions  which  undoubtedly  pre- 
dispose them  to  this  disease.  They  belong  to  two  classes :  those  who  by  inheri- 
tance possess  faulty  thoracic  development,  or  bad  chest  configuration,  so  that 
the  apices  of  the  lungs  never  expand  properly,  and  those  who  seem  to  inherit 
a  condition  of  the  tissues  which  is  unable  to  cope  with  the  infection  when  it 
takes  place.    Both  these  causes  are  often  present  in  one  case.    Such  persons 

1  A  Bologna  cow  is  an  animal  so  feeble  and  wasted  that  it  cannot  be  used  for  milking,  breeding,  or  for 
the  providing  of  ordinary  butchers'  meat.     It  is  killed  and  used  lo  make  sausage. 


292  DISEASES   DUE   TO   A    SPECIFIC  INFECTION 

are  usually  lightly  built  and  have  small  bones  and  delicate  features,  with  a 
thin  skin  and  superficial  veins  about  the  temples.  It  is  a  mistake,  however, 
to  think  that  this  configuration  is  always  present,  for  another  type  exists  in 
which  the  bony  structures  are  large  and  the  muscles  powerful,  the  so-called 
"lanky"  type,  in  which  tuberculosis  is  very  apt  to  run  a  rapid  course.  Every 
clinician  of  experience  has  been  astonished  to  find  active  tuberculosis  of  the 
lungs  in  heavy  and  powerfully  built  men,  and  has  seen  more  than  one 
generation  of  the  same  family,  though  strongly  built,  succumb  to  this 
malady,  although  promising  in  early  life  to  escape  all  danger  from  it.  In 
these  instances  the  vital  resistance  to  infection  is  poor,  although  the  physique 
may  seem  excellent. 

The  influence  of  age  upon  the  development  of  the  disease  is  distinct,  but 
it  is  not  sufficiently  powerful  to  confer  immunity  upon  any  period  of  life. 
In  the  first  ten  years  of  life  tuberculosis  is  quite  common,  affecting  the 
lymphatic  system  most  frequently,  the  bones  being  also  commonly  involved, 
and  more  rarely  the  membranes  covering  the  brain.  After  puberty  the 
pulmonary  tissues  are  the  parts  which  are  affected  in  the  majority  of  cases, 
and  this  predisposition  of  the  lungs  to  the  disease  persists  throughout  the 
rest  of  life,  although  after  the  thirty-fifth  year  the  frequency  of  pulmonary 
tuberculosis  rapidly  decreases,  so  that  in  persons  over  fifty  years  of  age  it 
is  really  very  uncommon  as  a  new  ailment,  unless  they  have  been  specially 
exposed  by  occupation  to  infection  by  the  malady.  The  only  cases  I  have 
seen  of  primary  pulmonary  tuberculosis  which  began  in  persons  of  over 
fifty  years  of  age  were  miners  and  grinders. 

The  sexes  are  about  equally  affected  by  tuberculosis. 

Of  the  races,  negroes  and  North  American  Indians  are  very  susceptible, 
and  half-breed  negroes  and  half-breed  Indians  are  peculiarly  prone  to  the 
malady.  I  have  had  opportunities  of  studying  the  frequency  of  tuberculosis 
among  both  of  these  classes  and  have  been  impressed  by  this  well-recognized 
fact.  Perhaps  this  susceptibility  is  due  to  the  fact  that  the  white  father  is 
usually  a  degenerate,  or  one  whose  vitality  is  impaired  by  alcohol  and  abuse. 

Of  the  occupations  which  favor  the  development  of  tuberculosis  may  be 
named  knife-grinding,  mining,  weaving,  and  other  pursuits  which  cause 
large  quantities  of  dust  to  enter  the  lungs.     (See  Pneumonoconiosis.) 

AH  the  infectious  diseases  which  diminish  the  vitality  of  the  patient  pre- 
dispose him  to  infection  by  this  bacillus.  Thus,  pneumonia,  particularly  that 
of  the  catarrhal  type,  not  rarely  causes  pulmonary  tuberculosis  to  develop, 
and  influenza  renders  the  patient  especially  prone  to  its  development.  In 
many  cases  the  catarrhal  process  provides  the  centre  in  which  a  new,  or 
an  old  and  slumbering,  infection  can  become  active.  Among  the  acute 
infections,  measles  and  whooping-cough  are  active  predisposing  factors, 
causing  catarrhal  pneumonia  or  exhaustion  and  diminished  vitality.  Dia- 
betes melhtus  very  commonly  ends  in  a  rapid  and  fatal  tuberculosis. 

A  very  important  point  is  the  relation  of  injury  to  the  development  of 
tuberculous  lesions.  There  can  be  no  doubt  that  trauma  to  the  chest  wall 
may  be  followed  by  an  outbreak  of  pleural  or  pulmonary  tuberculosis,  that 
injuries  to  the  joints,  even  if  seemingly  trivial,  may  cause  tuberculous  arthritis, 
and  blows  on  the  abdomen  may  incite  tuberculous  peritonitis  or  tuberculosis 


TUBERCULOSIS  293 

of  the  retroperitoneal  or  mesenteric  glands.     (See  also  article  on  Pneumonia 
for  traumatic  lesions  of  the  thorax  followed  by  pulmonary  disease.) 

Prevention. — In  the  prevention  of  tuberculosis  the  most  important  factor 
is  the  destruction  of  the  bacillus  as  soon  as  it  leaves  the  body  of  the  patient 
This  is  by  no  means  as  easy  to  accomplish  as  would  appear  at  first  sight, 
since  it  is  often  expelled  in  enormous  numbers  by  sneezing  and  coughing. 
The  moustache  or  beard  of  the  consumptive  is  a  veritable  nest  of  infection, 
and  his  bed-clothing  may  be  equally  virulent  unless  he  holds  something  in 
front  of  his  face  when  he  coughs. 

All  sputum  should  be  received  into  rags,which  should  be  burned  in  a  hot  fire 
before  they  become  dry,  or  into  a  paper  spit-cup  which  can  be  burned.  If  a 
china  cup  is  used,  it  should  always  contain  bichloride  of  mercury  solution. 

Largely  through  the  efi'orts  of  Dr.  Herman  Biggs,  of  New  York,  the 
health  department  of  that  city  has  been  active  during  the  last  ten  years  in 
stamping  out  tuberculosis,  or  consumption.  Under  an  ordinance,  physicians 
are  required  to  report  every  case  of  this  disease  that  comes  under  their  care. 
In  the  poorer  districts  of  the  city  this  is  followed  by  inspection,  and,  if 
necessary,  disinfection  of  the  quarters  occupied  by  the  sick  man,  and  this 
again  has  been  supplemented  by  the  distribution  of  circulars  in  which 
directions  are  given  whereby  the  patient  can  take  precautions  against  the 
infection  of  his  family,  and  the  family  can  protect  themselves. 

The  second  great  preventive  of  tuberculosis  is  sunlight,  for  sunlight 
destroys  the  bacillus.  If  this  were  not  the  case  our  streets  would  infect 
more  thousands  than  they  do.  Sunlight  not  only  destroys  the  bacillus,  but 
increases  the  vital  resistance  of  the  patient  and  of  the  uninfected  as  well. 
The  absence  of  sunlight  and  the  presence  of  bad  air  are  the  most  potent 
auxiliaries  to  the  disease.  This  is  shown  by  the  prevalence  of  the  malady 
in  tenement  houses,  in  prisons,  and  in  asylums  which  are  badly  arranged  or 
managed.  These  facts  have  not  only  been  proved  on  a  gigantic  scale  by 
unintentional  tests  with  human  beings,  but  experimentally  as  well,  particu- 
larly by  Trudeau,  who  inoculated  two  sets  of  rabbits  with  the  bacillus 
tuberculosis.  He  kept  one  set  in  a  dark  cellar  and  these  animals  suffered 
an  unusually  high  mortality.  The  other  set  he  turned  out-of-doors,  and 
these  animals  survived  or  were  affected  only  by  a  modified  form  of  the  disease. 

In  those  who  have  an  hereditary  predisposition  to  the  disease  or  who  have 
a  faulty  thoracic  development,  out-door  life  is  in  many  cases  an  absolute 
necessity  to  prevent  the  disease. 

It  is  proven  that  tuberculosis  can  be  conveyed  from  animals  to  man,  and 
it  would  seem  unwise  to  give  up  such  precautionary  measures  as  careful 
inspection  of  cattle  in  slaughter-houses  and  the  proper  control  of  cows 
supplying  milk,  and  especially  when  the  latter  is  to  be  used  as  an  infant 
food. 

Frequency.— The  prevalence  of  tuberculosis  in  its  various  forms  is  very 
great.  About  one  death  in  every  seven  is  due  to  this  cause,  and  when  we 
add  to  this  fact  the  additional  statement  that  a  very  large  proportion  of 
those  who  die  of  other  diseases  show  more  or  less  well-developed  tuberculous 
lesions,  it  becomes  evident  that  tuberculosis  contributes  to  the  death  of  a 
still  larger  proportion  of  persons.    Thus  Schlenker  in  100  autopsies  made 


294  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

on  adults  and  children  dying  of  various  diseases  found  that  65  per  cent, 
had  tuberculosis.  Biggs  found  it  in  60  per  cent,  of  his  postmortems,  and 
out  of  4000  consecutive  autopsies  in  Breslau  about  1300  showed  tuberculosis. 
These  statistics,  which  give  some  conception  of  the  ordinary  prevalence  of 
the  disease,  are  outclassed  in  an  extreme  degree  by  the  reports  of  Naegeli 
in  Zurich,  who  found  in  the  Pathological  Institute  of  that  Canton  that 
500  consecutive  autopsies  revealed  tuberculosis  in  some  form  in  97  per  cent. 
This  percentage  held  true  of  adults  as  well  as  of  children.  Naegeli  also 
found  that  tuberculosis  is  very  rare  in  the  first  twelve  months  of  life,  un- 
common up  to  the  age  of  five  years,  but  so  frequent  from  five  to  fourteen 
years  that  it  was  found  in  one-third  of  all  bodies  examined.  In  studying 
these  statistics  of  Naegeli  it  must  be  remembered  that  in  many  of  the  autop- 
sies tuberculosis  was  not  the  cause  of  death,  and  in  some  cases  was  present 
in  such  a  very  slight  degree  that  only  careful  search  revealed  its  presence. 
Burrell  believes  that  about  70  to  80  per  cent,  of  all  persons  who  reach  the 
age  of  forty  years  have  or  have  had  some  form  of  the  disease. 

The  far  greater  frequency  of  tuberculosis  in  cities  as  compared  to  country 
districts  and  villages  is  shown  by  the  statistics  of  Paris,  in  which  the  number 
of  cases  per  thousand  is  4.9  per  cent.;  whereas  in  662  villages  in  France  it 
is  only  1.81  per  cent. 

Notwithstanding  these  facts  it  is  interesting  to  note  that  in  many  parts 
of  the  world  tuberculosis  has  undergone  a  most  remarkable  decrease  in  its 
frequency,  although  the  mortality  rate  of  1  in  7  still  holds  true  for  nearly 
all  cities.  In  New  York  the  mortality  has  decreased  from  4.6  to  2.6  per 
thousand  in  ten  years,  and  a  similar  fall  of  about  40  per  cent,  has  occurred 
in  Philadelphia  in  that  time.  Abbott  has  shown  that  in  1853  the  mortality 
of  pulmonary  tuberculosis  in  Massachusetts  was  42  per  10,000  inhabitants, 
whereas  in  1895  it  was  21.8  per  10,000  inhabitants.  The  decrease  in 
the  entire  United  States  has  been  from  25  per  10,000  in  1890  to  19  per 
10,000  in  1900.  Hiller  has  shown  that  at  the  present  rate  of  decrease 
the  disease  will  be  extinct  in  Prussia  in  1927  and  in  England  about  1947. 
In  Prussia  the  mortality  fell  from  31  per  10,000  in  1886  to  19  per  10,000 
in  1901,  and  in  England  it  has  fallen  50  per  cent,  in  the  last  forty  years. 

A  very  great  difference  in  frequency  is  found  in  different  races.  Thus, 
in  the  United  States  the  death  rate  in  those  of  English  descent  is  15  per 
10,000,  whereas  for  the  Irish  it  is  43,  and  59  for  the  colored  race. 

Occupation  also  makes  great  differences;  thus,  the  death  rate  among 
tradespeople  is  17  per  10,000,  among  barbers  33  per  10,000,  book-keepers 
40,  and  stone-cutters  54  per  10,000. 

The  average  age  at  death  from  pulmonary  tuberculosis  is  thirty-five  years, 
but  the  actual  incidence  of  the  disease  is  from  fifteen  to  thirty-five  years. 

The  relative  frequency  of  the  different  forms  of  tuberculosis  is  difficult 
to  determine.  Statistics  of  deaths  from  tuberculosis  in  Ireland  from  the 
years  1891  to  1901  show  the  following  figures  as  to  the  relative  frequency: 

Pulmonary  tuberculosis  .         .         .         .         .         .21.35  per  10,000 

Tuberculosis  of  the  mesenteric  glands      .         .         .2.2      "         " 

Tuberculous  meningitis 2.25    "         " 

Other  forms  of  tuberculosis 2.3      "         " 


TUBERCULOSIS  295 

Some  difference  exists,  however,  between  the  frequency  of  primary  and 
secondary  lesions.  Thus,  Heller,  of  Kiel,  found  but  1.45  per  cent,  of  primary 
intestinal  tuberculosis,  but  37.8  per  cent,  in  which  the  principal  lesion  was 
abdominal. 

Pathology  and  Morbid  Anatomy.— As  already  stated,  when  discussing  the 
etiology  of  tuberculosis,  the  bacillus  enters  the  body  usually  through  the 
respiratory  mucous  membrane,  or  through  that  of  the  ahmentary  canal.  It 
is  possible,  however,  for  infection  to  take  place  through  the  skin,  but  this 
is  usually  followed  by  a  localized  lesion  and  rarely  by  visceral  disease.  The 
results  which  accrue  from  the  entrance  of  the  bacillus,  in  the  manner  indi- 
cated, vary  greatly  with  the  virulence  of  the  micro-organism,  the  vital 
resistance  of  the  individual  and  the  organ  or  part  in  which  the  primary 
localization  of  the  bacillus  takes  place.  The  effect  of  the  bacillus  upon  the 
local  tissues  is  to  cause  an  accumulation  of  cells  in  the  immediate  neighbor- 
hood, followed  in  favorable  cases  by  repair  or,  under  less  promising  condi- 
tions, by  necrosis.  This  aggregation  of  cells,  composed  of  lymphoid,  hyaline, 
endothehal,  and,  it  may  be,  giant  cells,  and  containing  the  bacillus,  is  the 
histological  or  rather  anatomical  characteristic  of  the  disease,  and  is  called 

a  tubercle.  . 

In  the  great  majority  of  instances  the  pathological  process  which  is 
induced  is  inflammatory  in  type,  and,  as  already  stated,  the  lungs  and  their 
adjacent  lymph  nodes  are  the  parts  which  are  usually  affected  m  adults, 
whereas  in  young  children  the  gastrointestinal  tract  and  its  adjacent  glands 
are  commonly  involved  either  alone  or  with  the  structures  just  mentioned. 
When  the  collection  of  the  cells  is  small  the  growth  is  said  to  be  a  miliary 
tubercle,  because  it  is  thought  to  be  the  size  of  a  millet-seed;  but  when  a 
single  tubercle  grows  to  be  so  large  as  to  be  called  a  nodule  its  growth  to 
these  proportions  is  accomplished  by  the  addition  of  a  number  of  miliary 
tubercles  This  growth  usually  is  Hmited,  in  the  mihary  tubercle  or  nodule, 
by  the  fact  that  an  exudate  takes  place,  as  part  of  the  inflammatory  process 
which  the  bacilh  produce,  which  prevents  the  spread  of  the  bacilli  to 
adjacent  areas,  and  so  limits  the  field  occupied  by  the  micro-organisms 

As  the  disease  progresses  this  exudate  becomes  organized  and  is  finally 
developed  into  a  dense  fibroid  or  cicatricial  tissue,  which  acts  as  a  protective 
barrier  against  the  spread  from  that  particular  area  of  invasion.  This  barrier 
in  a  great  number  of  cases  remains  effective  and  in  a  sense  impnsons  or 
restricts  the  production  of  poisons  and  lessens  their  dissemination,  \\ithm 
this  limited  zone  of  action  the  bacterial  products  cause  necrosis  and  m 
the  dead  tissue  the  germ  is  suppressed  or  actually  destroyed.  After  the 
local  necrotic  process  is  complete  the  necrotic  contents  are  more  or  less  fully 
absorbed  and  only  a  cicatrix  remains  to  mark  the  site  of  the  original  lesion, 
or  if  this  does  not  take  place  the  caseous  and  degenerated  mass  undergoes 
calcification.     In  either  instance  a  natural  process  tends  to  bring  about  a 

^^If'for  any  cause  this  protective  barrier  is  removed  by  absorption  while 
the  imprisoned  bacilli  are  still  alive,  or  if  the  wall  which  is  formed  is  incom- 
plete, the  bacilh  escape  and  speedily  infect  adjoining  or  distant  areas  being 
conveyed  by  the  lymph  or  blood  streams.    Such  is  the  explanation  of  those 


296  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

cases  in  which  a  patient  who  has  suffered  from  some  acute  infection,  hke 
pneumonia,  typhoid  fever,  or  influenza,  speedily  develops  tuberculosis  during 
convalescence,  although  the  acute  illness  may,  by  confining  him  to  a  healthful 
and  well-ventilated  room,have  protected  him  from  any  recent  infection. 

In  still  other  cases  the  protective  barrier  of  surrounding  exudate  is  not 
formed  and  the  amalgamation  of  tubercles  produces  a  nodule  which  undergoes 
necrosis  and  softening  and  its  bacterial  contents  become  diffused  into  the 
surrounding  tissues,  thus  spreading  the  infection.  In  still  a  third  type  of  cases 
the  lesions  consist  in  a  diffuse  exudative  process,  with  little  or  no  tubercle 
formation,  and  as  a  consequence  we  find  that  it  is  possible  for  the  entrance 
of  the  tubercle  bacillus  to  be  followed  by  a  tuberculous  pneumonia  or  pulmo- 
nary consolidation,  tuberculous  serositis,  or  lymphadenitis,  the  lesion  not 
containing  the  characteristic  tubercle.  In  other  words,  in  certain  instances 
the  tuberculous  inflammation  is  so  intense  and  the  poison  formed  by  the 
bacilli  is  so  abundant  or  virulent,  or  the  resistance  of  the  soil  so  inadequate, 
that  no  attempt  at  protection  is  made,  but  instead  there  occurs  a  profuse 
exudative  process  which  is  extremely  liable  to  undergo  necrosis,  and  this 
results  in  rapid  breaking  down  not  only  of  the  exudate  itself,  but  of  the 
involved  tissues  as  well. 

Under  certain  admittedly  unusual  conditions  the  tubercle  bacillus  becomes 
distinctly  pyogenic  and,  rapidly  developing  in  the  lung,  produces  not  only  the 
degenerative  and  necrotic  changes  peculiar  to  tubercle  formation,  but  fills  the 
air  vesicles  with  pus,  serum,  and  dead  epithelial  cells  and  leukocytes,  a  state 
in  which  the  part  involved  speedily  goes  on  to  widespread  destruction.  It 
is  also  to  be  recalled  that  in  nearly  all  cases  of  tuberculous  disease  infection 
by  other  pyogenic  organisms,  such  as  the  staphylococcus  and  streptococcus, 
aids  in  producing  local  inflammation  and  pus,  and  leads  to  the  formation 
of  toxins  which  cause  local  and  general  impairment  of  vitality. 

In  some  cases,  on  the  other  hand,  the  bacilli,  in  the  presence  of  the  resist- 
ance offered,  do  not  seem  capable  of  originating  an  acute  inflammatory 
process,  nor  do  they  cause  the  formation  of  tubercles  with  caseation,  but 
produce  a  condition  in  which  an  excessive  formation  of  connective  tissue 
occurs,  which  prevents  the  rapid  spread  of  the  disease  and  constitutes  a 
form  of  infection  called  chronic  hyperplastic  tuberculosis  in  the  intestine 
or  in  the  lung  which  is  closely  allied  to  fibroid  phthisis,  so  called ;  but  this 
fibroid  process  is  by  no  means  entirely  dependent  upon  the  presence  of  the 
bacillus  tuberculosis,  since  other  causes  may  produce  it. 

It  is  fully  established  that  the  action  of  the  tubercle  bacillus  in  the  human 
organism  is  due  to  its  poisons,  a  number  of  which  have  been  described. 
The  early  coagulation  necrosis  and  subsequent  caseation  are  clearly  the 
result  of  bacillary  toxins.  The  tendency  to  fibrosis  seen  in  many  cases  has 
been  thought  to  be  due  to  a  sclerogenous  toxin  and  the  frequent  cheesy 
disintegration,  so  commonly  present,  to  a  caseogenous  poison;  it  is  probable, 
however,  that  the  same  noxious  agent  in  some  individuals  induces  caseation 
and  in  those  more  resistant  to  its  action  a  fibroid  or  fibrocalcareous  change. 
Progressing  caseation  may  be  looked  upon  as  an  evidence  to  low  resistance, 
while  fibrosis,  with  or  without  calcification,  indicates  strong  reparative  and 
antagonistic  powers  on  the  part  of  the  afi'ected  tissues. 


TUBERCULOSIS  297 

With  these  preliminary  remarks  we  may  proceed  to  a  discussion  of  the 
various  manifestations,  pathological  and  clinical,  which  are  to  be  met  with 
in  persons  affected  by  this  disease. 

Acute  Miliary  Tuberculosis. — By  acute  miliary  tuberculosis  is  meant 
a  condition  in  which  a  single  organ,  or  a  number  of  organs,  or  perhaps 
the  whole  body,  is  infected  by  the  Bacillus  tuberculosis,  causing  the  forma- 
tion of  innumerable  tubercles  of  the  type  already  described.  It  arises  not 
by  the  inhalation  of  dust  laden  by  bacilli,  but  by  the  escape  of  bacilli  in 
large  numbers  from  some  infected  focus,  as,  for  example,  a  caseous  lymphatic 
gland.  The  escape  takes  place  into  a  bloodvessel,  and  in  a  few  hours  at 
most  the  bloodvessels  of  the  neighboring  parts,  or  perhaps  of  the  entire 
body,  are  swarming  with  bacilli,  so  that  in  a  very  brief  space  of  time  the 
lungs,  the  liver,  and  other  parts  are  found  studded,  or,  as  it  has  been  well 
expressed,  "stuffed,"  with  miliary  tubercles.  The  caseous  gland  or  primary 
cheesy  nodule  which  gives  origin  to  this  acute  secondary  infection  is  usually 
so  situated  that  it  is  adherent  by  inflammatory  products  to  a  vein,  commonly 
the  pulmonary  vein  or  one  of  its  branches,  or  to  the  thoracic  duct,  or  the 
superior  cava.  By  a  process  of  extending  necrosis  the  soft  contents  of  the 
gland,  laden  with  tubercle  bacilli,  break  into  the  vessel  or  duct.  Sometimes 
an  active  tuberculosis  of  the  wall  of  the  bloodvessel  is  present,  so  that  tubercles 
may  be  found  in  the  intima.  Councilman  has  observed  a  tuberculous  aortitis 
apparently  resulting  from  infection  through  the  vasovasorum. 

Weigert  has  divided  the  results  of  this  vascular  invasion  by  the  bacilli 
into  three  classes:  (1)  that  in  which  all  the  organs  of  the  body  become 
filled  with  tubercles  of  the  miliary  type;  (2)  that  in  which  the  disease,  though 
widely  disseminated,  nevertheless  appears  in  multiple  but  widely  separated 
foci;  and  (3)  that  in  which  the  tubercles  are  not  so  numerous,  their  growth 
is  more  chronic,  and  their  size  causes  them  to  be  classed  as  nodules.  This 
is  manifestly  an  artificial  division  which  is  not  closely  adhered  to  under 
natural  conditions,  for  the  process  may  represent  all  these  types  in  one 
case,  while  in  other  instances  it  may  be  impossible  to  tell  to  which  class 
the  case  belongs  because  the  lesions  shade  into  one  another. 

Symptoms. — The  symptoms  of  widely  diffused  miliary  tuberculosis  are  to 
be  carefully  studied  because  they  simulate  those  of  enteric  fever  and  other 
typhoid  states  so  closely  that  not  rarely  an  erroneous  diagnosis  is  made. 
The  chief  manifestations  may  be  said  to  be  those  of  profound  toxsemia 
without  any  localized  lesion  to  explain  the  illness,  which  begins  with  the 
general  wretchedness  common  to  the  early  stages  of  all  acute  infections  and 
which  is  followed  by  fever,  rising  each  evening  to  102°  or  103°.  The  pulse 
is  unduly  rapid,  and  there  are  often  profuse  sweats.  In  such  cases  there 
are  three  symptoms  which,  while  not  pathognomonic  by  any  means,  are 
nevertheless  of  some  value  in  separating  this  condition  from  typhoid  fever. 
The  fever  is  often  irregular,  sometimes  breaking  with  a  profuse  sweat.  In 
other  cases  it  is  higher  in  the  morning  than  at  night.  The  pulse  is  often 
exceedingly  rapid  in  the  early  stages,  a  phenomenon  which,  as  a  rule,  is  not 
observed  in  typhoid  fever.  The  temperature  does  not  resist  cold  sponging 
in  the  first  week  as  does  that  of  typhoid  fever,  but,  on  the  contrary,  falls  with 
great  rapidity  to  below  normal.     Later  there  is  the  absence  of  rose  spots 


298  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

to  lead  one  to  a  correct  opinion,  and  careful  examination  of  the  lungs  may 
reveal  some  area  of  infiltration  or  softening,  or  of  dulness  on  percussion 
which  should  arouse  suspicion. 

Additional  differential  factors  are  as  follows:  There  is  absence  of  the 
Widal  reaction.  This  reaction,  however,  often  does  not  appear  in  typhoid 
fever  until  after  the  tenth  day.  Tubercle  bacilli  may,  by  spinal  puncture, 
be  found  in  the  cerebrospinal  fluid,  and  in  some  instances  the  ophthal- 
moscope will  reveal  tubercles  in  the  choroid.  Rarely  the  bacillus  can  be 
demonstrated  in  the  blood  or  urine.  Enlargement  of  the  spleen,  the  diazo 
reaction  in  the  urine,  the  presence  of  active  diarrhoea  or  severe  constipation, 
and  the  fever  are  not  differential  points  in  favor  of  typhoid,  for  they 
all  appear  in  miliary  tuberculosis.  Unlike  typhoid  fever,  herpes  labialis 
may  be  present  in  acute  miliary  tuberculosis. 

In  other  instances  the  disease  has  a  much  more  abrupt  onset.  The 
patient  is  seized  with  a  chill  followed  by  high  fever,  or  rapid  pulse,  pro- 
found prostration,  and  copious  sweats.  Emaciation  proceeds  with  remark- 
able rapidity.  The  aspect  of  the  patient  is  profoundly  toxic  or  septic  and  his 
expression  anxious.     The  tongue  is  dry  and  the  cheeks  flushed. 

When  miliary  tuberculosis  involves  the  lungs  the  pulmonary  symptoms 
are  chiefly  those  of  diffuse  acute  bronchitis,  although  careful  examination 
may  reveal  at  one  apex,  or  at  both,  some  impairment  of  resonance  due 
perhaps  to  an  ancient  infection.  The  general  symptoms  are  distinctly 
asthenic,  as  already  described,  and  added  to  them  there  ai-e  fine  rales  over 
the  greater  part  of  the  chest  and  a  degree  of  dyspnoea  far  out  of  propor- 
tion to  the  lesions  which  can  be  discovered.  The  respirations  may  be  unduly 
rapid.  The  cyanosis  is  very  pronounced,  the  cough  constant,  and  the  patient 
may  seem  surprisingly  ill  considering  that  no  cause  can  be  discovered.  The 
sputum  may  be  rusty  or  blood-streaked,  or  a  true  haemoptysis  may  develop. 
Auscultation  may  reveal  pleural  friction  due  to  tuberculosis  of  the  pleura, 
and  as  the  case  progresses  widely  distributed  rales  may  be  heard  in  the 
back  and  front  of  the  chest.  In  these  cases  great  mental  anxiety  is  often 
a  marked  symptom  unless  the  disease  attacks  a  child,  when  the  patient 
usually  lies  limp  and  apathetic  and  perhaps  stuporous. 

These  patients  usually  die  in  from  one  to  three  months,  but  cases  are 
occasionally  met  with  in  which  death  ensues  as  early  as  the  fourteenth  day. 
In  still  other  instances  the  case  becomes  less  fulminating  in  character, 
the  symptoms  moderate,  and  the  patient  passes  into  ordinary  subacute 
pulmonary  tuberculosis.  Acute  tuberculous  bronchopneumonia  is  more 
frequently  seen  in  children  than  in  adults. 

Diagnosis. — ^The  diagnosis  is  not  difficult  in  the  pulmonary  form  if  there 
is  a  history  of  an  old  tuberculous  lesion  elsewhere,  or  if  the  marked  cyanosis 
as  compared  to  the  apparent  limited  area  of  disease  is  considered.  Here 
again  the  presence  of  tuberculous  foci  may,  if  found,  show  that  an  acute  con- 
dition is  imposed  upon  an  older  one.  The  physician  must  not  be  led  into 
the  belief  that  the  lungs  are  normal  because  he  is  able  to  elicit  a  clear  and 
resonant  percussion  note  on  the  chest  wall,  for  a  compensatory  emphysema 
often  is  present  in  these  cases. 

When  the  miliary  process  chiefly  or  entirely  involves  the  meninges  the 


TUBERCULOSIS  299 

symptoms  are  of  course  cephalic  in  large  degree,  and  we  have  that  grave 
state  known  as  acute  tuberculous  meningitis  present. 

Spinal  puncture  to  determine  the  cause  of  the  disease  is  a  most  valuable 
aid.  If  tuberculosis  is  present  the  cerebrospinal  fluid  will  be  turbid  and 
occasionally,  if  it  is  placed  in  a  centrifuge,  the  bacilli  can  be  found,  or  some 
of  the  fluid  may  be  injected  into  a  guinea-pig,  which  will  develop  tubercu- 
losis, if  this  be  the  cause  of  the  illness. 

From  typhoid  fever  of  the  meningeal  type  tuberculous  meningitis  is  sepa- 
rated by  the  presence  of  spots,  by  the  diazo  reaction,  and  the  Widal  test. 
Again,  the  diagnosis  of  tuberculous  meningitis  may  be  confirmed  if  a  focus 
of  primary  tuberculosis  can  be  found  in  the  other  organs  as  in  the  lungs, 
the  bones,  or  the  mesenteric  glands. 

Prognosis. — The  prognosis  is  always  fatal,  although  cases  said  to  have 
recovered  have  been  reported 

Treatment. — The  treatment  consists  in  the  use  of  nutritious  food  and 
stimulants  and  in  the  relief  of  restlessness  by  chloral  or  the  bromides. 

Glandular  Tuberculosis. ^ — Glandular  tuberculosis,  or  tuberculosis  of  the 
lymphatic  glands,  is  the  condition  whidi  was  formerly  called  "scrofula" 
before  Koch  demonstrated  the  existence  of  the  tubercle  bacillus.  It  is  now 
known  that  no  such  disease  exists  as  scrofula,  or  scrofulosis,  in  the  sense 
of  a  separate  entity. 

Tuberculosis  of  the  lymph  glands  is  often  a  very  mild  form  of  the  infection 
and  the  mortality  from  its  presence  is  very  low.  Indeed,  it  may  be  said  that 
if  the  infection  does  not  escape  to  other  parts  of  the  body  life  will  not  be 
seriously  jeopardized. 

In  studying  this  state  it  must  be  recalled  that  one  of  the  important  functions 
of  the  lymph  nodes  is  to  arrest  and  perhaps  destroy  such  micro-organisms 
as  may  endeavor  to  enter  the  general  system.  As  soon  as  pathogenic 
germs  enter  a  healthy  gland  one  of  several  processes  takes  place.  In  a 
strong  individual  with  great  vital  resistance  the  gland  becomes  enlarged 
and  active  in  an  evident  endeavor  to  destroy  the  invaders.  In  this  it  may 
succeed,  or  the  few  bacilh  which  escape  are  caught  and  destroyed  by 
other  adjacent  glands.  If  the  infection  is  virulent  and  the  vital  resistance 
is  below  par,  the  battle  is  more  prolonged,  the  inflammation  in  and  about 
the  gland  is  more  active,  and  the  general  system  may  be  saved  by  the  addi- 
tional safeguard  of  a  wall  of  protective  tissue  thrown  around  the  infected 
gland  to  protect  the  rest  of  the  body.  In  still  other  cases  the  glands  go 
on  to  caseation  and  the  necrotic  contents  escape  externally  or  even  internally. 
It  is  a  noteworthy  fact,  however,  that  this  so-called  pus  is  usually  sterile 
or  contains  bacilli  in  such  small  numbers  as  to  be  demonstrable  only  by 
inoculation  experiments.  Again,  if  the  infection  wins  the  battle  and  the 
gland  undergoes  caseation,  it  is  still  possible  for  the  area  to  be  surrounded  by 
a  fibrous  barrier  which  walls  up  the  caseous  mass  and  its  bacilli  and  protects 
the  body  even  though  the  gland  is  destroyed. 

When  the  protective  processes  fail  the  bacilli  pass  the  h^llph  nodes,  or  a 
caseous  gland  in  juxtaposition  to  a  bloodvessel  breaks,  and  general  tuber- 
culosis ensues  as  already  described. 

Tuberculous  infection  of  the  lymph  nodes  takes  place  in  four  chief  areas : 


300  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

the  cervical  glands,  the  mediastinal  glands,  and  the  mesenteric  and  retro- 
peritoneal glands.  In  the  first  class  the  infection  takes  place  through  the 
tonsils,  in  the  nasopharynx,  or  because  of  the  presence  of  bad  teeth  or  a  break 
in  the  gums.  The  mediastinal  glands  suffer  by  the  entrance  of  the  bacillus 
through  the  mucous  membrane  of  the  larynx,  bronchial  tubes,  or  smaller 
bronchioles,  while  the  abdominal  lymphatics  receive  their  infection  from 
the  intestines. 

The  diagnosis  of  cervical  adenitis  is  not  difficult,  although  occasionally, 
when  the  disease  is  bilateral  and  the  swelling  is  great,  the  possibility  of 
Hodgkin's  disease  may  have  to  be  considered. 

The  involvement  of  the  mediastinal  glands  by  tuberculous  infection 
results  in  a  spread  of  the  disease  to  the  retroperitoneal  lymphatics  or  in 
the  growth  of  the  tissues  affected  to  such  a  degree  that  lymphatic  tumors 
may  be  formed  which  cause  serious  symptoms  by  pressure.  Thus,  the 
recurrent  laryngeal  nerve  may  be  pressed  upon  and  laryngeal  spasm  result, 
or  the  superior  vena  cava  or  pulmonary  vein  suffers  from  compression,  and 
in  a  similar  manner  bronchial  obstruction  may  ensue.  More  important, 
however,  than  the  pressure  symptoms  are  possible  perforation  by  ulceration 
of  the  bronchi  or  trachea,  or  even  of  the  bloodvessels  with  rapid  diffusion 
of  the  infection  all  through  the  body.  So,  too,  it  is  possible  for  bacilli  to 
enter  the  lung,  to  pass  to  the  lymphatics,  to  cause  disease  in  these  glands, 
and  finally  cause  pulmonary  tuberculosis,  pleural  tuberculosis,  or  pericar- 
dial tuberculosis  by  softening  and  rupture  into  these  parts  through  the 
adhesions  which  are  formed. 

In  diseases  of  the  retrobronchial  glands  auscultation  over  the  upper  end 
of  the  sternum,  when  the  head  is  w^ell  thrown  back,  may  reveal  a  tracheal 
hum,  and  careful  percussion  may  elicit  some  dulness. 

\Vhen  the  mesenteric  and  retroperitoneal  glands  are  involved,  producing 
what  is  called  "tabes  mesenterica,"  the  child  is  ansemic,  poorly  nourished, 
has  constipation  alternating  with  diarrhoea,  and  presents  an  enlarged  abdo- 
men ("pot-belly").  The  size  of  the  belly  as  compared  to  the  rather  wasted 
arms,  legs,  and  thorax  is  noteworthy,  and  careful  palpation  may  occasionally 
reveal  enlarged  glands  deeply  situated  in  the  abdominal  cavity.  This  con- 
dition is  to  be  separated  from  tuberculosis  of  the  peritoneum  and  from 
consumption  of  the  bowels,  for  both  of  these  structures  are  usually  free 
from  the  disease  in  these  cases,  although  they  may  be  infected  by  softening 
of  the  glands  themselves.  These  lesions  probably  exist  in  a  far  larger  pro- 
portion of  cases  than  is  generally  thought,  and  end  by  a  process  of  fibrosis 
and  calcification,  for  the  involvement  of  these  glands  is  met  with  in  many 
cases  at  autopsy  when  death  is  due  to  another  cause,  and  when  no  sus- 
picion of  tuberculous  infection  has  been  present. 

Treatment  of  Glandular  Tuberculosis.  —  Tuberculosis  of  the  retrobron- 
chial glands  and  of  the  retroperitoneal  glands  can  be  treated  only  by 
sunshine  and  fresh  air  with  residence  by  the  sea,  and  by  the  internal 
use  of  tonics,  of  syrup  of  the  iodide  of  iron  and  cod-liver  oil  to  combat 
ansemia. 

Persistent  enlargement  of  the  cervical  glands  demands  their  surgical 
removal,  not  their  incision,  but  their  excision,  because,  as  has  already  been 


TUBERCULOSIS  301 

stated,  a  tuberculous  focus  is  always  a  threatening  focus.  On  the  other 
hand,  it  cannot  be  denied  that  large  numbers  of  very  heahhy  adults  bear 
scars  showing  that  they  have  had  cervical  adenitis  in  early  life.  In  these  cases 
the  battle  between  vital  resistance  and  tuberculous  infection  has  been  won 
by  the  individual. 

Tuberculosis  of  the  Serous  Membranes.— Tuberculosis  of  the  serous 
membranes  may  be  divided  into  the  acute  and  chronic  forms.  The  acute 
is  further  subdivided  into  (a)  an  acute  serofibrinous  form,  macroscopically 
identical  or  indistinguishable  from  serofibrinous  serositis  arising  from 
other  causes;  (h)  an  acute  miliary  tuberculous  serositis  due  to  the  invasion  of 
the  serous  membrane  by  tubercle  bacilli  and  the  formation  of  miliary  tuber- 
cles. The  two  forms  just  mentioned  may  be  distinct  or  coincident.  The 
chronic  tuberculous  serositis  may  be  (a)  fibrocaseous  or  (h)  fibrohyaline. 
The  former  results  from  the  formation  of  tuberculous  exudates,  in  which 
extensive  caseation  gives  rise  to  cheesy  accumulations  of  various  sizes 
surrounded  by  granulations  or  more  fully  organized  fibrous  tissue.  Marked 
calcareous  change  is  frequently  associated  with  this  form.  The  fibrohyaline 
type  is  characterized  by  marked  thickening,  and  the  formation  of  adhesions 
by  newly  developed  fibrous  tissue  of  a  pecuHar,  grayish,  translucent  form. 
Both  the  chronic  forms  may  occur  together,  and  the  caseous  masses  may 
be  enclosed  by  hyaline  fibrous  tissue  of  the  type  just  mentioned. 

Acute  Meningeal  Tuberculosis. — Meningeal  tuberculosis  is  an  inflammation 
of  the  pia  mater  produced  by  an  infection  of  this  membrane  with  the  bacillus 
tuberculosis  and  accompanied  by  an  effusion  of  lymph,  it  may  be  the  forma- 
tion of  pus,  and  the  development  of  tubercles.  These  tubercles  are  usually 
very  minute,  but  occasionally  are  large  from  the  amalgamation  of  several 
tubercles  into  one.  They  are  most  profuse  at  the  base  of  the  brain,  hence 
the  name  basilar  meningitis,  and  extend  upward  on  its  sides  following 
chiefly  the  vascular  pathways.  In  some  instances,  however,  the  pia  mater 
on  the  convexity  of  the  brain  contains  more  tubercles  than  exist  at  the  base. 
Nearly  always  at  the  base  there  is  a  copious  exudate  of  lymph  which  pro- 
duces a  pearly,  gelatinous  appearance.  The  lateral  ventricles  are  distended 
with  fluid.  Minot  states  that  Robert  "Whytt,  of  Edinburgh,  in  1768,  first 
accurately  described  this  condition,  although  he  had  no  clear  conception 
of  its  cause.  Guersant,  in  1827,  reported  that  the  pathological  appearances 
of  the  membranes  were  of  so  peculiar  a  type  that  he  suggested  the  name 
"granular  meningitis."  In  1830  Papavoine  described  the  disease  as  a  true 
tuberculous  lesion,  and  the  condition  of  moderate  hydrocephalus  which 
existed  with  the  meningitis  was  recognized  as  having  its  origin  in  the  tuber- 
culous infection.  It  was  reserved  for  W.  W.  Gerhard,  of  Philadelphia,  in 
1833,  to  show  not  only  that  this  type  of  meningitis  was  tuberculous,  but  that 
it  was  practically  in  every  instance  secondary  to  some  tuberculous  lesion 
elsewhere. 

Symptoms. — The  symptoms  of  acute  meningeal  tuberculosis  are  very 
characteristic,  whether  it  occurs  in  children  or  adults.  It  is  much  more  fre- 
quently seen,  however,  in  children  between  two  and  seven  years.  These 
symptoms  are  best  divided  into  three  stages  for  study.  At  first  the  parent 
notices  that  the  child  is  unusually  peevish  and  irritable,  or  in  other  cases 


302  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

peculiarly  languid  and  indisposed  to  play.  There  is  little  restful  sleep  and 
the  child  often  has  night  terrors.  The  appetite  is  capricious  and  the  bowels 
irregular.  After  these  symptoms  have  lasted  for  some  days,  during  which 
time  the  tubercles  have  probably  been  deposited  in  the  pia  mater,  the  well- 
developed  symptoms  of  the  disease  appear.  Headache  may  be  constant 
and  is  characterized  by  sharp  exacerbations  of  pain  which  cause  the  child 
to  give  a  peculiar  high-pitched  scream  which  is  quite  characteristic.  Sudden 
attacks  of  vomiting  of  an  explosive  character  may  occur.  At  times  a  fleeting 
delirium  may  be  present. 

It  is  almost  impossible  in  many  of  these  cases  to  exclude  early  typhoid 
fever,  for  a  similar  train  of  symptoms  may  be  presented  in  its  early  stages. 

The  temperature  is  usually  elevated,  rising  as  high  as  102°  or  103°.  The 
pulse  is  slow  and  the  respirations  are  irregular  and  sighing.  Rapid  emacia- 
tion takes  place,  and  if  the  child  be  very  young,  so  that  the  fontanelle  is 
open,  there  may  be  distinct  hydrocephalic  enlargement.  The  patient  now 
lies  stuporous  or  somnolent,  with  the  eyes  half  closed.  Indeed,  the  appear- 
ance may  be  that  of  deep  sleep  with  sighing  breathing. 

In  some  cases  in  which  the  onset  of  the  affection  is  rather  acute,  the  patient 
suffers  from  a  series  of  convulsions.  I  have  seen  such  a  case  with  Dr. 
Brouwer,  of  Tom's  River,  New  Jersey,  while  preparing  this  article,  in  which 
the  child  had  as  many  as  sixty  convulsions  in  twenty-four  hours. 

As  the  exudate  increases  symptoms  of  intracranial  pressure  and  signs  of 
interference  with  the  cranial  nerves  appear,  so  that  squint,  twitching  of  the 
facial  muscles,  and  chewing  movements  of  the  lips  and  jaws  develop. 

Even  as  late  as  this  the  patient  may  be  aroused  and  will  seem  so  much  better 
for  a  time  that  the  friends  are  much  encouraged,  but  a  relapse  inevitably  occurs. 
The  child  is  now  too  stuporous  to  be  roused,  the  eyes  are  filled  with  sticky 
secretion,  and  the  parents  find  solace  in  the  belief  that  even  if  hopelessly  ill 
the  patient  does  not  suffer.  This  solace  is,  however,  occasionally  rudely  dis- 
pelled by  a  shrill,  piercing  cry  which,  interrupting  ^the  profound  stillness,  is 
more  than  usually  startling.  As  death  approaches  the  pulse  becomes  ver^' 
rapid,  probably  from  vagal  paralysis,  the  pupils  no  longer  react  to  light,  and 
the  eyeballs  are  rotated  upward. 

The  duration  of  the  entire  illness  is  about  ten  to  eighteen  days,  as  a  rule, 
but  cases  may  die  as  early  as  the  end  of  five  days,  in  a  convulsive  seizure,  or 
they  may  last  for  several  weeks. 

Diagnosis. — The  diagnosis  of  acute  miliary  tuberculous  meningitis  must 
be  made  with  the  recollection  that  the  following  conditions  simulate  it: 
Acute  meningitis  not  due  to  tubercle  is  rare  in  children,  has  a  more  sudden 
onset,  as  a  rule,  and  ends  in  a  week  in  most  cases.  The  delirium  accom- 
panying it  is  more  marked,  the  febrile  movement  is  more  sharp,  and  there 
is  usually  no  history  of  tuberculosis  in  the  parents,  as  there  is  in  the  tuber- 
culous case  in  many  instances. 

From  cerebrospinal  meningitis  of  the  epidemic  type  it  is  separated  by  the 
sudden  onset  of  that  disease,  by  the  absence  of  its  eruption,  and  by  the 
fact  that  no  cases  of  cerebrospinal  meningitis  have  occurred  in  the  vicinity. 
By  spinal  puncture  the  meningococcus  may  be  obtained  in  one  case  and  the 
tubercle  bacillus  in  the  other,  although  the  latter  is  not  frequently  discovered, 


TUBERCULOSIS  303 

The-  fluid  in  cerebrospinal  fever  contains  polymorphonuclear  cells  and 
hyaline  leukocytes,  while  in  tuberculous  meningitis  recent  studies  seem  to 
show  that  a  lymphocytosis  is  the  rule.     (See  Cerebral  Spinal  Fever.) 

Tuberculous  Pleurisy. — ^Tuberculous  pleurisy  is,  in  the  vast  majority  of 
cases,  secondary  to  tuberculous  infection  in  other  parts.  Most  commonly 
the  primary  focus  is  in  the  lungs  or  in  the  mediastinal  glands.  In  some 
instances  the  process  is  the  result  of  a  general  infection  which  results  in 
miliary  tuberculosis,  and  in  these  instances  it  not  infrequently  happens  that 
the  pleura  is  involved  without  there  being  any  tuberculous  process  in  the 
lungs.  Thus  Hodenpyl,  in  91  autopsies  on  persons  in  whom  the  lungs  were 
free  from  tubercle,  found  miliary  tuberculosis  of  the  pleura  in  41,  both  the 
parietal  and  visceral  layers  being  affected.  He  also  believes  that  miliary 
tuberculosis  of  the  pleura  is  apt  to  undergo  fibrous  changes. 

The  tuberculous  lesions  are  of  three  types.  In  the  first  type  we  find 
scattered  patches  of  tuberculous  deposit  which  are  the  continuation  of  a 
tuberculous  process  in  the  lung  beneath  the  visceral  layer  of  the  pleura, 
or  similar  patches  are  found  which  are  independent  of  lung  involvement, 
or  again  patches  appear  upon  the  parietal  pleura.  In  the  second  type  the 
lesions  are  simply  those  of  a  widespread  miliary  tuberculosis  of  the  pleura, 
and  in  the  third  type,  which  is  representative  of  a  more  chronic  or  slow 
process,  there  is  great  thickening  of  the  pleura,  partly  as  the  result  of  the 
organization  of  formed  exudates  and  also  of  proliferative  changes  in  the 
primitive  serous  layers.  Throughout  this  tissue  and  exudate  miliary  tubercles, 
or  masses  of  miliary  tubercles,  appear.  These  undergo  coagulation  necrosis 
in  some  instances. 

The  presence  of  any  one  of  these  processes  usually  results  in  the  out- 
pouring of  a  certain  amount  of  effusion  which  is  often  serous  and  by  no 
means  rarely  purulent.  When  it  is  serous  it  is  lacking  in  fibrin  and  it  may 
be  tinged  with  blood.  The  physician  should  recall  the  important  clinical 
fact,  in  connection  with  these  tuberculous  pleural  effusions,  that  whether 
they  be  serous  or  purulent,  an  examination  of  the  fluid  will  rarely  reveal 
the  tubercle  bacillus  unless  in  some  manner  these  organisms  are  dislodged 
from  the  pleural  surface  by  scraping.  In  some  cases  the  effusion  is  not 
due  to  the  bacillus  tuberculosis  alone,  but  to  an  associated  infection.  Thus, 
in  the  purulent  type  the  pneumococcus,  streptococcus,  or  staphylococcus 
pyogenes  are  often  found.     (See  Empyema.) 

Reference  has  already  been  made  to  the  fact  that  the  visceral  layer  of  the 
pleura  is  often  infected  by  a  tuberculous  process  in  the  lung  as  a  result  of 
direct  extension.  It  may  be  added  that  in  nearly  every  case  an  inflammatory 
area — that  is,  a  localized  pleuritis — exists  over  the  seat  of  the  disease  in  the 
pulmonary  tissues.  This  condition  often  gives  rise  to  pam  in  the  chest 
and  not  rarely  causes  adhesions  between  the  layers  of  the  pleura.  The 
inflammatory  process,  while  tuberculous  in  origin,  is  not  necessarily  tuber- 
culous in  character,  but  it  often  becomes  tuberculous  as  already  stated. 

Sometimes  when  the  tuberculous  mass  in  the  lung  softens  and  breaks 
down  the  visceral  layer  of  the  pleura  is  perforated  and  sudden  dyspnoea  and 
pain  ensue,  with  the  production  of  pneumothorax.  (See  Pneumothorax 
and   complications  of  Pulmonary  Tuberculosis.)      Through  this  opening 


304  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

infection  with  pyogenic  bacilli  occurs  or  the  Bacillus  tuberculosis  becomes 
pyogenic,  and  as  a  consequence  pyopneumothorax  develops.  (See  Pyopneu- 
mothorax.) 

Tuberculosis  of  the  Pericardium. — Like  tuberculosis  of  the  pleura,  peri- 
cardial tuberculosis  is  usually  secondary  to  primary  infection  elsewhere.  It 
may,  however,  be  primary.  It  occurs  in  two  forms:  the  mihary,  in  which 
the  small  tubercles  are  scattered  or  profuse,  and  in  a  form  in  which  the 
entire  pericardium,  both  in  its  visceral  and  parietal  layers,  is  thickened  by 
an  inflammatory  exudate  which  is  associated  with  the  development  of 
tuberculous  masses  which  undergo  cheesy  change.  In  this  type  the  peri- 
cardial space  may  be  nearly  obhterated  by  the  adhesions  which  are  formed 
between  its  layers.  It  is  a  noteworthy  fact  that  although  the  pericardium 
is  so  near  the  lungs  and  pleura  it  is,  comparatively  speaking,  rarely  infected. 
Out  of  1048  autopsies  Wells  found  tuberculous  pericarditis  only  16  times 
and  in  4500  autopsies  Baginsky  found  it  15  times.  In  1317  autopsies  on 
phthisical  patients  Willigk  found  tuberculosis  of  the  pericardium  11  times. 
Leudet  found  it  8  times  in  299  autopsies.  In  1000  autopsies  Osier  found 
7  cases  of  tuberculous  pericarditis.  Ellis  has  recently  reported  from  the 
laboratories  of  the  Jefferson  Medical  College  a  case  in  which  the  heart,  the 
pericardium,  and  the  mediastinal  tissues  formed  one  large,  adherent  mass 
of  tuberculous  nodules. 

The  symptoms  presented  by  tuberculosis  of  the  pericardium  may  be  so 
slight  that  no  suspicion  of  the  pericardial  disease  exists  during  life,  or  they 
may  resemble  those  of  mediastinopericarditis,  or  adherent  pericardium. 
(See  Adherent  Pericardium). 

Tuberculosis  of  the  Peritoneum. — Aside  from  tuberculosis  of  the  lungs, 
tuberculosis  of  the  peritoneum  is  the  most  frequent  and  most  important 
manifestation  of  tuberculous  infection  met  by  the  physician.  The  statistics 
of  Grawitz  and  Brunn  show  that  in  13,422  autopsies  tuberculosis  of  the 
peritoneum  was  found  284  times. 

In  2802  autopsies  on  tuberculous  subjects,  collected  from  various  sources, 
the  peritoneum  was  involved  in  571,  a  percentage  of  20.36.  These  figures 
represent  all  ages.  Steiner  found  the  peritoneum  affected  in  92  out  of  800 
cases  of  tuberculosis  occurring  in  children,  or  in  11.5  per  cent. 

As  to  the  relative  frequency  of  the  disease  in  adults  and  children  Aldibert's 
statistics,  based  on  326  cases,  are  of  interest.  Of  these  326  cases,  274,  or 
84.05  per  cent.,  occurred  in  adults  and  the  remaining  52,  or  15.95  per  cent., 
occurred  in  children.  It  is  in  a  very  large  proportion  of  cases  secondary 
to  tuberculous  foci  elsewhere.  The  combined  statistics  of  Munstermann, 
Borschke,  and  Pribram,  comprising  437  cases  of  tuberculous  peritonitis  ex- 
amined postmortem,  showed  that  only  3  were  primary. 

A  tuberculous  family  history  is  present  in  53  per  cent,  of  cases.  The 
disease  is  much  more  common  in  the  female  than  in  the  male;  according 
to  Nothnagel  90  per  cent,  of  the  cases  are  females.  Konig's  statistics  make 
it  78  per  cent. 

Tuberculous  peritonitis  is  of  especial  interest  not  only  because  of  its 
frequency  and  gravity,  but  because  it  is,  in  one  type  at  least,  more  readily 
cured  than  any  other  well-developed  form  of  internal  tuberculosis.    It  occurs 


TUBERCULOSIS 


305 


in  three  chief  varieties,  viz.,  as  an  acute  mihary  tuberculosis,  as  a  chronic 
tuberculosis  with  large  nodules  and  adhesions,  and  as  a  still  more  chronic 
form  with  fibroid  changes.  The  relative  frequency  of  the  different  forms 
of  tuberculous  peritonitis  is  shown  by  the  following  facts:  In  46  cases 
which  came  under  the  observation  of  Munstermann,  25  were  exudative, 
21  were  plastic,  and  8  were  chiefly  caseous.  Of  the  21  plastic  cases  8  were 
fibrous.  Herringham  found  fibrous  adhesions  in  18  out  of  50  cases.  Borschke 
found  the  miliary  form  in  16  out  of  226  cases  which  came  to  autopsy. 

The  acute  miliary  form  is  usually  secondary  to  infection  of  the  mesenteric 
and  retroperitoneal  glands,  but  occasionally  in  women  the  infection  comes 
from  the  Fallopian  tubes,  or  in  males  from  the  bladder  or  other  part  of  the 
genito-urinary  apparatus.  The  miliary  tubercles  are  scattered  widely  over 
the   peritoneum   on   both  its  visceral  and    parietal  layers    (Fig.   45),  and 

Fig.  45 


Miliary  tubercles  of  the  surface  of  the  small  bowel  and  mesentery.    (Kast  and  Rumpler.) 

the  surface  of  the  liver  is  often  profusely  peppered  by  these  formations.  In 
these  cases  there  is  a  serous  effusion  into  the  peritoneum  which  in  some 
instances  is  very  profuse,  particularly  if^  the  case  is  rather  subacute  in  the 
rapidity  of  its  course. 

The  mode  of  its  development  is  well  illustrated  by  a  case  I  saw  some  years 
since  with  my  associate,  Dr.  Thornton.  A  girl  of  about  twelve  or  thirteen 
years,  while  in  apparently  perfect  health,  was  bathing  in  a  pond  and  playing 
with  a  small  row-boat,  the  sharp  prow  of  which  struck  her  a  severe  blow 
on  the  epigastrium,  which  made  her  nauseated  and  faint.  She  speedily 
20 


306  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

began  to  lose  weight  and  strength,  became  distinctly  emaciated,  and  rapidly 
developed  a  marked  ascites.  The  abdomen  was  opened  and  every  peritoneal 
surface  was  found  hterally  covered  with  tubercles.  The  fluid  was  allowed 
to  escape,  drainage  was  permitted,  and  perfect  recovery  followed.  Un- 
doubtedly the  blow  on  the  belly  ruptured  a  tuberculous  mesenteric  or  retro- 
peritoneal gland,  and  so  produced  general  peritoneal  infection.  In  such 
a  case  no  nodules  can  be  found  in  the  belly  on  palpation,  but  the  presence 
of  ascites  in  a  child,  or  in  an  adult,  without  any  signs  of  hepatic  disease 
should  lead  the  physician  to  suspect  tuberculosis  of  this  type,  particularly 
if  in  addition  there  is  present  some  fever  of  an  irregular  type,  which  is 
commonly  moderate,  but  which  may  rise  at  times  as  high  as  103°  or  even  104° 

How  opening  the  belly  and  permitting  drainage  cures  these  cases  is  not 
known,  but  the  clinical  fact  that  such  a  result  is  often  achieved  is  not  to  be 
denied,  and  this  holds  true  even  if  this  condition  develops  in  adults.  Walter's 
statistics  show  that  50  per  cent,  of  adults  who  are  subjected  to  laparotomy 
recover,  and  Herzfeld's  statistics  give  a  recovery  percentage  of  62  per  cent, 
for  children.  ^larganecci  gives  85  per  cent.,  von  Krencki  71.5  per  cent. 
Thomas  73  per  cent.     Hall  reports  94  cures  out  of  110  operations. 

The  second  caseous  type  of  peritoneal  tuberculosis  ^^ith  nodules  is  charac- 
terized by  the  presence  of  caseous  masses  of  tubercle  which  tend  to  ulcerate, 
which  are  associated  vnih  seropurulent,  or  purulent,  effusion  in  moderate 
amount,  and  in  which  the  belly  cavity  is  not  distended  by  fluid  nor  the 
intestines  by  gas,  as  in  the  miliary  form  just  described,  but  is  apt  to 
present  a  peculiar  pasteboard  rigidity.  The  effusion  in  these  cases  is 
often  sacculated  by  reason  of  the  fact  that  there  are  formed  adhesions 
which  wall  off  spaces  in  which  the  fluid  collects.  These  spaces  may  be 
between  coils  of  intestine  or  contiguous  mesentery,  between  the  intestine 
and  omentum,  and  between  the  omentum  and  the  parietal  peritoneum. 

In  some  instances  these  sacculations  are  capable  of  containing  but  a  few 
drachms  of  fluid,,  but  in  those  cases  in  which  fairly  large  peritoneal  areas 
are  separated  from  the  general  peritoneum  by  adhesions  very  large  accumu- 
lations of  fluid  may  be  present.  If  this  takes  place  in  the  flanks  or  lower 
zone  of  the  abdomen,  where  it  usually  occurs,  the  S}Tnptoms  may  very 
closely  resemble  ovarian  cyst,  and  many  cases  have  been  operated  upon 
with  the  idea  that  ovarian  disease  was  the  cause  of  the  fluctuating  mass. 
Careful  palpation  under  ether  may  reveal  an  irregular  nodular  edge  to  the 
grow1;h,  or  nodules  elsewhere  may  explain  the  real  state. 

The  chronic  fibroid  type  may  resemble  the  nodular  type  just  spoken  of,  but 
in  it  the  matting  of  the  abdominal  contents  into  a  small  compact  mass  is 
quite  extraordinary,  the  intestines  and  omentum  being  glued  together  in  an 
adhesive  bundle  which  cannot  be  separated.  In  this  type  the  belly  is  often 
remarkably  scaphoid  and  the  degree  of  general  emaciation  extraordinary. 
Some  idea  of  its  degree  may  be  gathered  from  the  illustrations  shown  in 
Figs.  46  and  47. 

The  symptoms  of  chronic  fibroid  peritoneal  tuberculosis  are  characteristic. 
In  addition  to  the  general  emaciation  it  will  often  be  found  that  the  sJcin  over 
the  abdomen  looks  and  feels  pecuharly  rough  and  scurf-like,  or  as  if  there 
was  marked  "goose  flesh"  over  this  part.     In  addition  it  is  often  stained  a 


TUBERCULOSIS 


307 


Fig . 46 


A  case  of  peritoneal  tuberculosis  of  the  fibroid  type  in  a  man  aged  twentj'-onc  years,  with  great  general 

atrophy  and  scaphoid  belly. 


Fig.  47 


Extreme  emaciation  in  a  woman  due  to  thoracic  and  peritoneal  tuberculosis  of  the  fibroid  type. 


308  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

curious  dirty  yellow  or  is  light  brownish  in  hue.  The  abdominal  wall  is 
not  only  hard,  but  the  abdominal  muscles  are  readily  felt  by  the  finger- 
tips, while  deep  palpation  reveals  nodules  or  gives  the  sense  of  abdominal 
vacancy  as  if  the  patient  had  been  eviscerated.  The  temperature  range  is  not 
markedly  febrile,  and  often  is  subnormal,  ranging  from  96°  in  the  morning 
to  99°  at  night. 

It  is  not,  however,  in  these  well-advanced  forms  of  the  disease  that  the 
physician  has  difficulty  in  making  a  diagnosis,  but  in  those  cases  in  which 
there  is  general  impairment  of  health  without  marked  general  emaciation; 
and  it  may  be  without  distinct  abdominal  symptoms  save  obstinate  consti- 
pation, with  occasionally  attacks  of  active  purging,  or  in  those  instances  in 
which  the  patient  is  still  hale  and  robust,  but  suffers  from  some  abdominal 
distress.  These  cases  often  present  a  distinct  abdominal  tumor,  or  tumors, 
composed  of  tuberculous  nodules,  or  of  nodules  combined  with  thickened 
knuckles  of  intestine  which  may  be  so  firmly  held  by  adhesions  of  exuded 
lymph  that  gas  and  feces  produce  a  tumor  that  cannot  be  readily  dispelled 
by  pressure. 

Sometimes  a  tumor  is  met  with  in  the  epigastric  area  extending  across 
the  abdomen  at  this  level,  or  just  above  the  umbihcus,  formed  by  a 
peculiar  rolling  of  the  omentum  as  a  workman  would  roll  up  his  apron 
and  stow  it  under  his  belt.  A  similar  condition  is  sometimes  found  in  carci- 
nomatosis of  the  peritoneum,  but  such  a  roll  is  usually  due  to  tuberculosis. 

\Vlien  the  mesenteric  glands  or  retroperitoneal  glands  are  gravely  infected, 
a  single  nodule  or  several  nodules  may  be  easily  palpated.  When  multiple 
they  are  usually  tuberculous,  but  where  it  is  single  a  careful  exclusion  of 
malignant  growth  must  be  made  by  finding  a  tuberculous  focus  elsewhere 
or  by  the  tuberculin  test. 

Treatment  of  Tuberculosis  of  the  Peritoneum. — The  treatment  of  the 
subacute  or  chronic  forms  of  peritoneal  tuberculosis  consists  in  operation. 
The  first  thing  to  be  looked  for  at  operation  in  peritoneal  tuberculosis  in 
the  female  is  the  Fallopian  tubes,  for  they  are  the  cause  in  the  majority  of 
cases.  If  diseased  they  must  be  removed,  for  such  tubes  will  persistently 
infect  the  peritoneum. 

The  operative  treatment  is  most  successful,  as  a  rule,  when  the  state  is 
characterized  by  sufficient  effusion  to  keep  the  intestinal  coils  apart,  and 
so  prevent  adhesions.  The  operation  consists  in  a  single  opening  of  the 
peritoneal  cavity  and  a  free  entrance  into  it  of  atmospheric  air.  Any  attempt 
to  remove  the  tuberculous  masses  is  useless,  unless  a  single  mass  can  be 
excised  without  damaging  the  tissues  and  without  the  danger  of  setting 
free  bacilli  to  cause  infection  elsewhere.  In  sacculated  cases  the  sac 
should  be  incised,  drained,  and  packed  with  iodoform  gauze.  In  the 
chronic  fibroid  type  operation  will  not  be  productive  of  much  good,  for 
it  cannot  result  in  the  loosening  of  the  shrivelled  omentum  or  of  the  cica- 
tricial contractions  about  the  intestines,  but  in  these  cases  coeliotomy  may 
arrest  the  disease.  AVhen  there  are  sacculations  with  accumulations  of  fluid 
or  pus,  the  operation  is  of  value  in  that  it  evacuates  these  collections  and 
may  arrest  the  process,  but  it  does  not  promise  complete  cure  as  in  the  cases 
with  large  ascites.     (For  statistics  see  page  306.) 


TUBERCULOSIS  309 

The  medical  treatment  consists  in  active  feeding  with  easily  assimilated 
foodstuffs  and  in  the  use  of  cod-liver  oil.  If  anaemia  is  marked  the  syrup 
of  the  iodide  of  iron  may  be  given  in  alternate  weeks  with  the  oil,  and  I 
have  certainly  seen  good  results  follow  the  use  of  nightly  iodoform  inunc- 
tions over  the  abdomen,  a  mixture  of  olive  oil  and  iodoform  in  the  pro- 
portion of  10  grains  to  the  ounce  being  used.  Iodoform  suppositories, 
5  grains  each,  may  also  be  employed. 

Pulmonary  Tuberculosis.— Pulmonary  tuberculosis,  or  pulmonary 
phthisis,  as  it  is  sometimes  called  because  it  causes  such  emaciation  or 
wasting,  is  the  most  prevalent  disease  to  which  man  is  susceptible.  It 
affects,  as  a  rule,  young  adults  or  adolescents  (see  Frequency  of  Tuber- 
culosis), but  it  may  occur  at  any  period  of  life,  being  comparatively  rare 
in  the  first  five  years  of  existence  and  in  the  period  of  well-developed 
old  age. 

As  a  result  of  infection  of  the  lung  by  the  Bacillus  tuberculosis  we  find 
three  types  of  pulmonary  disease:  the  miliary,  the  chronic  or  caseating, 
ulcerative  type,  and  the  so-called  fibroid  type.  Of  these  the  second  form  is 
by  far  the  most  common  and  the  most  important  from  the  clinical  stand- 
point. The  infection  takes  place  as  a  primary  process  through  the  entrance 
of  the  bacillus  by  the  respiratory  passages,  or  secondarily  as  a  result  of  the 
transference  of  the  bacillus  from  some  primary  focus  by  the  bloodvessels 
or  lymphatics. 

Much  discussion  has  arisen  as  to  the  mode  by  which  the  first  focus  of 
tuberculosis  in  the  lung  is  produced.  Birch-Hirschfeld  proved  that,  in  many 
cases  at  least,  the  bacilli  gain  their  primary  lodgement  in  a  bronchiole,  where 
the  lung  is  least  able  to  get  rid  of  foreign  matter  by  coughing,  and  that,  from  a 
primary  tuberculous  lesion  at  this  point  the  rest  of  the  lung  becomes  infected. 
Aufrecht  also  proved  that  the  primary  infection  sometimes  takes  place 
through  the  circulation,  to  which  the  bacilli  gain  access  by  the  tonsils  and 
the  alimentary  canal,  the  pulmonary  focus  being  due  to  a  plugging  of  a 
vessel  by  their  presence. 

Whether  the  means  of  infection  be  respiratory  or  vascular,  the  ultimate 
lesions  are  often  the  same  ;  but  the  early  lesions  differ,  and  the  prognosis 
may  be  governed  to  some  extent  by  the  finding  of  a  primary  focus  elsewhere 
which  is  responsible  for  the  pulmonary  lesions. 

The  early  lesions  of  pulmonary  tuberculosis,  due  to  infection  by  inhalation 
(aerogenous  infection),  are  found  chiefly  in  the  wall  of  a  bronchiole  and  in 
the  alveoli  grouped  around  it  and  forming  lobules.  Either  by  extension  from 
this  infected  lobule  or  by  the  fusion  of  a  number  of  similarly  affected 
lobules,  large  tuberculous  masses  are  speedily  formed.  They  are  also 
characterized  by  the  extension  of  the  tuberculous  infection  to  the  tissues 
around  the  bronchioles,  giving  rise  to  an  extending  bronchopneumonia 
which  is  nodular  in  its  character  owing  to  the  primary  lobular  limitations. 

The  early  lesions  of  the  form  of  tuberculosis  of  the  lung  which  is  due  to 
infection  by  way  of  the  bloodvessels  or  lymphatics  are  found  in  the  walls 
of  the  alveoli — that  is  to  say,  in  the  connective  tissue  between  the  alveoli 
and  in  the  interlobular  capillaries.  The  disease  may  be  well  scattered 
through  both  lungs  in  either  instance,  but  -in  the  first  type  the  patches  are 


310  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

larger,  involving,  it  may  be,  a  lobule  at  a  time,  whereas  in  the  second  form 
they  are  diminutive  and  more  of  the  nature  of  miliary  tubercles  as  observed 
elsewhere.  This  we  would  naturally  expect  from  what  has  been  said  of 
the  cause  of  miliary  tuberculosis.  After  the  disease  has  existed  some 
time  the  areas  of  tuberculous  deposit  in  either  case  may  attain  the  same  size. 

The  discovery  that  there  is  a  primary  seat  of  tuberculosis,  which  has  given 
rise  to  the  pulmonary  lesions,  requires  a  graver  prognosis  because  it  indicates 
that  there  is  more  than  one  focus,  and  because  such  a  primary  lesion  which 
has  caused  pulmonary  disease  by  infection  through  the  vessels  may  have 
caused  other  foci  of  infection  elsewhere  by  the  same  means.  Again,  the 
disease  is  more  apt  to  be  generalized  throughout  the  lung  in  this  case  than 
in  the  inspiratory  form  of  infection. 

Tuberculous  infection  of  the  lung,  therefore,  produces  the  following  changes 
in  the  pulmonary  tissues:  The  gray  and  yellow  tubercles,  which  differ  in 
no  way  from  those  tubercles  already  described  as  occurring  elsewhere, 
become  amalgamated  and  form  caseous  masses,  with,  sooner  or  later,  the 
characteristic  softening  of  the  growth;  if  the  tubercles  do  not  undergo 
necrosis  and  fail  to  coalesce,  the  accompanying  low-grade  irritation  or 
inflammation  may  lead  to  fibroid  changes.  Along  with  these  changes  in  the 
tubercles  themselves  there  is  always  associated  a  considerable  amount  of 
inflammation,  which  often  results  in  the  formation  of  an  exudate  which  fills 
the  air  vesicles  just  as  it  does  in  croupous  or  catarrhal  pneumonia.  Side  by 
side  with  the  development  of  the  tubercles  in  the  lungs,  and  of  the  pneumonic 
exudate,  there  develops  in  the  interstitial  tissues  themselves  a  process  which  is 
tuberculous  and  which  causes  thickening.  This  is  the  so-called  tuberculous 
infiltration  of  Laennec.  The  lung,  therefore,  becomes  solidified,  partly  as 
the  result  of  the  tuberculous  growth,  and  partly  as  a  result  of  the  inflam- 
mation caused  by  the  bacillus. 

Sooner  or  later  a  large  part  of  the  infiltrated  area  undergoes  caseation. 
Around  this  focus  or  area  of  active  tuberculous  process  inflanmiatory 
changes  occur,  which  may  cause  the  neighboring  parts  of  the  lung  to 
present  lesions  like  those  of  catarrhal  pneumonia.  On  making  a  section 
of  such  an  area  the  lung  presents  a  smooth,  homogeneous  surface,  as  does 
a  piece  of  Castile  soap  or  cheese  (Figs.  48  and  49),  but  if  the  process 
is  not  far  advanced  in  caseation  it  may  show  a  peculiar  gelatinous  appear- 
ance, the  so-called  gelatinous  pneumonia. 

The  fourth  condition,  which  is  noteworthy,  is  the  lack  of  bloodvessels  in 
the  diseased  portion  of  the  lung,  for  no  new  ones  are  formed  with  the  morbid 
growth  and  the  ones  naturally  present  are  occluded  by  the  disease  which 
involves  their  coats  and  causes  thrombosis;  the  resulting  thrombus  in  turn 
undergoes  caseation  so  that  the  vessels  disappear  in  the  tuberculous  mass. 
These  vascular  changes  possess  great  interest  for  this  reason,  and  also 
because  by  this  means  the  tubercle  bacillus  may  enter  the  blood  and  infect 
other  points,  or  by  a  process  of  ulceration  of  the  vessel  wall  hemorrhages 
may  occur. 

All  tuberculous  lesions  in  the  lungs  are,  therefore,  very  similar  in  character; 
all  manifest  a  disposition  to  undergo  similar  reparative  or  degenerative 
changes,  the  alterations  being  differences  in  degree  rather  than  in  kind. 


TUBERCULOSIS 


311 


When  the  restrictive  efforts  of  the  affected  organ  are  inadequate  caseation 
extends  until  a  bronchus  is  reached,  through  which  the  products  of  necrosis  are 
removed  by  drainage  and  expectoration.  Air  takes  the  place  of  the  material 
removed,  and  so  a  cavity  is  formed,  the  walls  of  which  are  lined  by  broken- 
down  tubercle-containing  material,  which  continually  softens  (caseation)  and 
melts  down,  thereby  enlarging  the  cavity.  This  cheesy  material  is  loaded  with 
bacilli  in  far  greater  numbers  than  they  exist  in  the  solidified  part  of  the  lung. 
The  cavity  is  also  infected  by  the  pathogenic  bacteria  inhaled  in  the  air,  and 
these  aid  in  the  destructive  local  process  and  increase  the  general  toxaemia. 


Fin.  48 


Caseous  consolidation  in  tlie  upper  lobe  and  bronchiectasis  in  the  lower  lobe.    (Kast  and  Rumpler.) 

It  is  interesting  to  note  that  the  smaller  bronchioles  are  usually  closed 
by  tuberculous  infiltration  as  the  disease  progresses  and  only  the  larger  ones 
remain  patulous.  These  communicate  with  the  cavities  by  small  lateral 
orifices  as  the  tube  courses  along  the  wall  of  the  excavation,  or  open  into 
the  cavity  like  the  small  papilla  of  a  duct.  The  walls  of  the  bronchial  tubes 
which  provide  drainage  for  the  cavities  are  often  the  site  of  tuberculous 
ulceration. 

Tuberculous  cavities  are  of  two  classes,  moist  or  secreting,  and  dry.  The 
first  is  that  met  with  in  the  acute  types  of  the  disease  and  it  often  increases 
in  size  very  rapidly.     The  contents  of  this  cavity  are  usually  composed  of 


312 


DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


caseous  matter,  broken-down  lung-tissue,  pus  cells,  and  tubercle  bacilli,  and 
the  walls  of  the  cavity  suffer  from  active  ulceration. 

The  dry  cavity,  on  the  other  hand,  is  found  in  the  chronic  cases  which 
often  last  for  years;  efforts  at  repair  smooth  the  wall,  in  which  fibrous  tissue 
develops,  and  it  not  rarely  happens  that  by  the  fibroid  process  already 
described  as  occurring  in  this  disease  the  size  of  the  cavity  is  greatly 
decreased.    These  cavities  contain  but  little  material  beyond  a  small  amount 


Fig.  49 


Caseous  consolidation  above.    Red  hepatization  below.    (Kast  and  Rumpler.) 

of  pus,  and  from  their  walls  hemorrhage  may  rarely  occur  as  the  result  of 
erosion  of  large  vessels.  Secondary  cavities  are  due  to  the  spread  of  the 
infection  by  the  vessels  or  bronchi,  and  follow  the  secondary  caseation 
process  already  described. 

We  have  now  passed  over  the  stage  of  pulmonary  infection,  consolidation, 
caseation,  and  disintegration,  and  come  to  the  study  of  the  processes  often 
instituted  in  reparation.    This  is  not  a  part  of  the  tuberculous  process.    The 


TUBERCULOSIS 


313 


small-cell  infiltration  and  exudation  in  the  inflammatory  zone  surrounding 
the  area  of  infection  sometimes  escape  speedy  involvement  in  the  tuberculous 
process,  and  instead  of  degenerating  rapidly  aids  in  the  production  of 
fibrous  tissue.  At  first  it  is  immature  and  imperfect  in  character,  but  as 
time  passes  it  becomes  firm,  dense,  and  fully-formed  fibrous  tissue.  If 
the  tuberculous  focus  is  small  it  may  be  completely  encapsulated  by  this 

Fig.  50 


Left  lung,  superior  lobe  and  upper  part  of  lower  lobe,  the  former  containing  a  number  of  communica- 
ting caverns,  brought  about  by  tuberculous  infiltration,  caseation,  and  evacuation  of  the  contents 
through  the  bronchi:  .4,  aneurysmal  dilatation  of  an  artery  spanning  one  margin  of  a  large  cavity;  B, 
communication  ^ath  another  cavity;  C,  C,  thickened  and  adherent  pleura  between  the  two  involved 
lobes.  The  pleura  over  both  lobes  is  thickened,  and  at  the  autopsy  the  cavity  had  been  obliterated  by 
universal  adhesion;  D,  the  pointer  from  the  letter  D  leads  to  a  small  group  of  tubercles  in  which  casea- 
tion is  just  beginning;  E,  a  fused  group  of  tubercles,  further  advanced  than  at  D. 

fibrous  covering,  with  the  result  that  the  caseous  mass  becomes  calcareous 
or  is  gradually  absorbed  so  that  only  a  puckered  scar  results. 

When  a  cavity  heals  its  walls  undergo  cicatricial  contraction,  but  it  is 
probably  never  obliterated  unless  it  has  been  exceedingly  small  before  the 
healing  process  began. 

The  growth  of  fibrous  tissue  is  most  marked  in  those  parts  of  the  lung 


314  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

which  ordinarily  possess  the  greatest  amount  of  connective  tissue,  as  in  the 
interlobar  and  interlobular  portions  of  the  pulmonary  tissues. 

If  a  large  cavity  is  present  bands  of  fibrous  tissue  may  persist,  and,  stretch- 
ing across  it,  form  trabeculse  (Fig.  60).  At  times  these  trabeculse  consist 
largely  of  good-sized  bloodvessels  which  have  not  been  plugged  by  the 
tuberculous  process.  If  they  are  perforated  by  ulceration,  so  violent  a  hemor- 
rhage may  occur  as  to  cause  death,  even  though  the  process  of  advancing 
cicatrization  is  endeavoring  to  limit  the  progress  of  the  disease.  At  times 
the  lesion  in  the  bloodvessel  develops  into  an  aneurysm,  and  this  may  rupture, 
causing  haemoptysis. 

Finally,  we  find  still  another  process  designed  to  arrest  the  disease  and 
save  the  patient,  namely,  thickening  of  the  pleura  which  protects  the 
pleural  cavity  from  pneumothorax  and  which,  as  it  undergoes  fibroid  change, 
contracts  and  so  acts  as  a  sort  of  fibrous  capsule  of  the  entire  diseased 
lung. 

Fibroid  tuberculosis  of  the  lungs  is  a  very  chronic  condition,  already 
described  from  the  pathological  standpoint,  and  characterized  by  marked 
overgrowth  of  fibroid  tissue  in  the  affected  organ.  A  somewhat  similar  state 
exists  when  no  tubercles  have  been  present.  The  primary  areas  of  tubercu- 
lous invasion  become  invested  by  fibrous  tissues  so  that  tuberculous  broncho- 
pneumonia becomes  gradually  changed  into  one  of  fibrous  overgrowth, 
with  shrinkage  of  the  parts  so  that  the  lung  becomes  much  decreased  in 
size  and  even  the  chest  may  be  sunken  and  deformed.  These  thoracic 
changes  are,  however,  more  marked  in  those  cases  in  which  the  visceral 
pleura  is  also  involved  in  the  cicatricial  or  fibroid  process.  The  disease 
loses  many  of  the  symptoms  of  ordinary  pulmonary  tuberculosis,  and  while 
the  constricted  cavities  may  contain  bacilli  and  the  bronchial  tubes  provide 
copious  material  for  expectoration,  the  process  of  general  wasting  goes  on 
very  slowly  and  the  strength  does  not  decrease  with  any  speed.  Such  con- 
ditions are  usually  seen  in  patients  of  middle  life  and  may  last  for  ten  to 
twenty  years.  Death  finally  comes  from  dilatation  of  the  heart  or  from  an 
acute  complicating  pneumonia  or  a  hemorrhage  from  an  ulcerated  bronchial 
vessel. 

Symptoms  of  Pulmonary  Tuberculosis. — The  onset  of  this,  the  most  com- 
mon type  of  the  disease,  is  often  such  as  to  mislead  the  physician.  In  some 
cases  there  is  no  cough,  but  only  a  slight  rise  of  evening  temperature  preceded 
by  chilly  sensations.  If  the  number  of  cases  in  which  these  symptoms 
have  given  rise  to  the  diagnosis  of  "malarial  poisoning"  could  be  gathered 
together  they  would  be  a  "  mukitude  which  none  can  number."  In  many 
instances  this  error  has  been  a  deserved  reproach  to  the  physician  who 
made  it,  because  he  has  not  searched  for  tuberculosis  as  a  cause  but  has 
simply  prescribed  quinine. 

Another  type  of  onset  is  found  in  those  case^  which  present  insidious 
pleural  effusion.  (See  Pleurisy  with  Effusion.)  In  still  a  third  series  the 
primary  symptoms  are  laryngeal.  As  these  lines  are  written  I  am  sending 
a  case  of  active  tuberculosis  of  the  lungs  to  New  Mexico.  He  was  told  by 
several  skilled  laryngologists  that  his  husky  voice  was  due  to  gout  of  the 
larynx,  whereas  if  they  had  examined  his  chest  marked  signs  of  phthisis 


TUBERCULOSIS  315 

would  have  made  the  diagnosis  evident.  All  cases  presenting  signs  of  per- 
sistent hoarseness  should  cause  the  physician  to  search  for  tuberculosis, 
syphilis,  papilloma  of  the  larynx,  and  aneurysm  of  the  aorta. 

In  the  fourth  type  the  very  earliest  sign  of  the  disease  is  spitting  of  blood. 
There  can  be  no  doubt  that  in  the  vast  majority  of  instances  the  bringing 
up  of  blood  from  the  bronchial  tubes  means  tuberculous  infection.  The  only 
other  causes  which  are  at  all  frequent  in  the  production  of  h^jemoptysis  are 
acute  pneumonia  or  pulmonary  infarction  due  to  cardiac  lesions.  It  not 
infrequently  occurs  that  hsemoptysis  in  the  stage  of  onset  is  scanty  and 
associated  with  no  demonstrable  physical  signs,  the  lesion  being  situated  in 
such  a  position  that  it  readily  perforates  a  vessel.     (See  p.  316.) 

The  symptoms  of  pulmonary  tuberculosis  may  be  divided  for  study  into 
those  which  are  complained  of  by  the  patient,  those  which  can  be  readily 
observed  by  the  physician,  and  those  which  can  be  demonstrated  by  the  aid 
of  physical  diagnosis.  It  must  be  remembered,  however,  that  the  severity 
of  the  symptoms  of  all  kinds  varies  to  an  extraordinary  degree  in  different 
cases  and  at  different  times  in  the  same  case.  It  is  necessary,  therefore,  in 
speaking  of  the  symptoms  to  adhere  to  the  description  of  the  three  types  of 
the  disease  named  when  discussing  its  pathology.  At  the  outset,  however, 
it  may  be  said  that  two  symptoms  are  present  in  all  cases  at  some  period, 
namely,  loss  of  flesh  and  fever. 

It  may  be  said  of  the  fever  of  tuberculosis  that  it  is  usually  moderate, 
varying  from  100°  to  102°,  although  at  times  it  may  reach  103°.  When  the 
temperature  reaches  higher  than  this  it  is  probably  not  due  solely  to  the 
tuberculous  infection,  but  to  septic  or  hectic  fever,  depending  upon  asso- 
ciated staphylococcic,  pneumococcic,  or  streptococcic  infection.  In  all 
instances  in  which  the  fever  is  high  it  is  prone  to  run  a  very  uncertain  and 
aberrant  course,  save  that  it  is  high  at  night  and  low  in  the  morning,  as  in 
nearly  all  fevers,  particularly  that  due  to  sepsis.  It  is  very  easily  broken, 
as  a  rule,  by  the  use  of  any  antipyretic  medicine,  but  this  effect  of  drugs 
is,  of  course,  very  temporary. 

The  loss  of  weight  depends  upon  several  causes  for  its  existence.  The 
loss  of  appetite,  the  cough,  which  is  exhausting  and  sleep  destroying,  the 
sweats,  the  disorders  of  digestion,  and  the  anaemia  are  all  active  factors  in 
decreasing  flesh.  Last,  but  by  no  means  least,  as  a  cause  of  loss  of  weight, 
is  to  be  considered  the  toxcemia  of  the  disease  itself. 

The  rapidity  of  loss  of  flesh  is  sometimes  remarkable,  amounting  to  as 
much  as  four  or  five  pounds  a  week.  This  rapidity  of  loss  is  a  good  guide 
to  the  activity  of  the  tuberculous  process,  for  if  it  be  rapid  the  outlook  as  to 
the  progress  of  the  patient's  illness  is  gloomy.  On  the  other  hand,  gain  in 
weight  is  correspondingly  encouraging  in  that  it  indicates  a  very  slow,  or 
arrested,  progress  of  the  disease. 

A  third  symptom,  often  of  very  great  annoyance  to  the  patient,  is  sweating, 
which  is  particularly  prone  to  occur  at  night.  These  sweats  vary  greatly  in 
severity,  and  seem  to  occur  because  of  the  relaxation  of  sleep,  but  in  many 
cases  their  true  cause  is  the  hectic  or  septic  state  of  the  patient.  If  they  are 
not  severe  enough  to  exhaust  the  patient  or  disturb  his  rest,  they  are  to 
be  regarded  as  an  effort  to  diminish  toxaemia,  but  if  they  become  so  profuse 


316  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

as  to  be  called  colliquative  they  are  deleterious.  At  times  the  sweat  follows 
a  sharp  rise  of  septic  temperature.  It  is  hardly  necessary  to  add  that  profuse 
night  sweats,  while  a  common  symptom  in  well-developed  phthisis,  are  by 
no  means  pathognomonic  of  this  disease. 

Aside  from  the  loss  of  flesh,  fever,  and  sweats,  the  most  constant  symptom 
of  pulmonary  tuberculosis  is  cough.  It  varies  in  its  character  and  in  its 
degree  in  different  cases  of  the  subacute  or  chronic  form  of  the  disease. 
In  the  early  stages  it  is  apt  to  be  worse  on  going  to  bed  or  on  getting  up 
in  the  morning,  and  in  the  early  stages  is  usually  annoyingly  unproductive 
and  persistent.  As  the  disease  advances  and  the  process  of  softening 
begins  to  take  place  in  the  consolidated  part  of  the  lung,  the  cough 
becomes  less  dry  and  more  productive.  When  cavities  are  formed,  marked 
increase  in  morning  cough  is  very  prone  to  occur  in  order  that  the  cavity 
may  be  well  cleared  of  the  accumulations  which  have  occurred  in  it  during 
the  night.  Cough  is  to  be  regarded  as  a  useful  attempt  on  the  part  of  the 
system  to  keep  the  lungs  clear.  Only  when  it  provokes  hemorrhage  or  is 
so  excessive  as  to  cause  exhaustion,  loss  of  sleep,  or  vomiting  is  it  to  be 
regarded  as  an  evil. 

Aside  from  the  general  symptoms  of  tuberculosis  already  described, 
patients  with  pulmonary  tuberculosis  often  have  severe  pain  in  the  chest, 
which  is  due  to  an  extension  of  the  inflammation  to  the  visceral  layer  of 
the  pleura.  They  also  suffer  from  dyspnoea  on  exertion  partly  because  of  the 
diminished  area  of  lung  and  lessened  ability  of  the  blood  to  carry  oxygen, 
partly  from  cardiac  feebleness,  and  partly  because  the  general  nervous 
system  and  the  muscles  are  so  feeble  that  any  exercise  leads  to  exhaus- 
tion. 

The  sputum  is  composed  of  mucopurulent  material  from  the  associated 
chronic  bronchitis,  or  if  the  lung  is  beginning  to  undergo  softening  the 
expectorated  material  is  thin,  with  small,  pale  and  greenish-looking  masses 
in  it — the  so-called  "nummular  sputum."  Sometimes  when  a  cavity  is 
being  emptied  or  there  is  a  marked  bronchorrhoea  the  sputum  is  very 
purulent. 

The  quantity  of  sputum  varies  greatly.  The  average  amount  in  an 
active  case  varies  from  1  to  4  ounces  a  day,  but  I  have  known  a  patient 
with  several  cavities  to  raise  a  pint  or  more  in  twenty-four  hours. 

Complications. — A  frequent  symptom  of  the  ulcerative  type  of  pulmonary 
tuberculosis  is  hcemoptysis,  but  a  large  number  of  cases  pass  through  all 
stages  of  the  disease  without  bringing  up  a  particle  of  blood.  It  is  absent, 
according  to  West,  in  from  20  to  30  per  cent,  of  cases.  Haemoptysis  is  more 
than  three  times  as  frequent  in  males  as  in  females.  The  quantity  of  blood 
lost  varies  from  a  mere  streak  in  the  sputum  to  3  ounces  in  the  average  case. 
Occasionally  it  amounts  to  4  or  6  ounces,  but  a  little  blood  "goes  a  great 
way,"  and  patients  will  state  that  they  have  spit  a  quart  when  only  a  few 
ounces  have  been  raised.  It  is  rare  for  as  large  an  amount  as  a  pint  to  be 
coughed  up  in  twenty-four  hours.  Very  rarely  a  large  gush  causes  death 
by  suffocation.  Sometimes  the  hemorrhage  is  concealed  and  unaccom- 
panied by  blood-tinged  sputum.  If  of  a  dribbling  type  it  may  inundate  a 
large  part  of  the  lung  or  even  fill  a  cavity  and  cause  death  without  any 


TUBERCULOSIS  317 

external  manifestation;  such  cases  are  rare.  A  free  hemorrhage  nearly 
always  means  the  presence  of  an  ulcerating  cavity.  The  blood  in  haemop- 
tysis may  come  from  the  pulmonary  vessels  or  from  the  bronchial  vessels, 
but  it  is  usually  from  the  former.  Flick,  Ravenel  and  Irwin  believe  that 
haemoptysis  is  usually  due  to  pneumococcus  infection. 

All  ages  may  suffer  from  hemorrhage  from  the  lungs,  but  the  period 
from  eighteen  to  thirty-five  is  of  course  that  of  greatest  frequency. 
Hoffnung  has  recorded  a  case  in  a  child  of  ten  months  and  Powell  one  in  a 
child  at  seven  months  of  age. 

The  blood  which  is  expelled  in  true  haemoptysis  is  usually  frothy  and  is 
brought  up  by  coughing.  It  is  also  usually  red  except  in  instances  of  slow 
oozing  into  a  cavity,  when  it  may  appear  as  a  dark  clot  or  clots.  When 
the  bleeding  is  profuse  the  blood  gushes  out  of  the  mouth.  Often  before 
the  spitting  of  blood  actually  takes  place  a  salty,  or  bloody,  taste  in  the 
mouth  is  persistently  present  for  some  time. 

Haemoptysis  due  to  pulmonary  tuberculosis  is  to  be  separated  from 
haematemesis  by  the  fact  that  the  first  occurs  with  coughing  and  the  second 
with  retching  or  vomiting.  It  is  further  differentiated  by  the  fact  that 
the  blood  is  frothy  and  filled  with  mucus  and  bubbles  and  is  usually 
bright  red  in  haemoptysis,  whereas  in  haematemesis  it  is  usually  pure  or 
discolored  by  contact  with  the  gastric  juice.  In  one  state  the  history  of 
pulmonary  disease,  or  the  discovery  of  lesions  in  the  lungs,  reveals  the  seat 
of  the  hemorrhage;  in  the  other  gastric  symptoms  are  present.  In  haemop- 
tysis the  blood  is  often  brought  up  in  small  degree  for  several  days, 
whereas  in  haematemesis  it  is  usually  brought  up  once  or  twice  on  one 
day  and  then  the  bleeding  ceases. 

In  this  connection  it  must  not  be  forgotten  that  haemoptysis,  or  blood 
spitting,  is  not  always  due  to  tuberculosis  of  the  lungs.  It  is  sometimes 
present  in  the  stage  of  onset  in  acute  croupous  pneumonia.  It  is  not  rarely 
met  with  in  thoracic  aneurysm,  and  its  occurrence,  unless  it  be  very  profuse, 
does  not  necessarily  mean  immediate  death  in  the  latter  type  of  cases,  since 
it  not  rarely  happens  that  the  vessel  oozes  blood  for  several  days  before  it 
finally  completely  gives  way.  Sometimes  by  the  pressure  of  the  aneurysmal 
sac  some  small  vessel  may  be  eroded  so  that  the  blood  escapes  from  it  alone. 
Slight  haemoptysis  occurs  in  some  cases  of  malignant  intrathoracic  growth, 
and  swollen  glands  by  pressure  may  rupture  a  neighboring  vessel  and  cause 
leakage  of  blood.  Again,  haemoptysis  often  develops  in  mild  degree  as  a 
result  of  pulmonary  infarction. 

Among  the  other  causes  of  haemoptysis  may  be  mentioned  hemorrhage 
from  a  superficial  vessel  in  a  bronchial  tube  in  bronchiectasis,  and  from 
the  larynx  in  malignant  and  non-malignant  growth  or  tuberculosis  of  this 
organ.  Haemoptysis  is  sometimes  due  to  a  varicose  condition  of  the  veins 
at  the  root  of  the  tongue. 

A  peculiar  form  of  haemoptysis  which  lasts  in  some  cases  for  years  is 
seen  in  Formosa  and  Japan,  due  to  the  presence  of  the  parasite  Para- 
gonimus  Westermanni.     (See  Parasitic  Hfvmoptysis.) 

Although  haemoptysis  in  the  great  majority  of  cases  indicates  pulmonary 
tuberculosis,  it  must  not  be  forgotten  that  this  symptom  sometimes  occurs 


318  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

for  years  without  any  other  signs  of  the  disease  appearing.  I  have  one  case 
in  mind  in  which  the  young  wife  of  a  student  at  the  Jefferson  College  had 
repeated  hemorrhages  during  an  entire  winter  without  any  physical  signs 
being  present,  and  continued  to  have  them  for  many  years  afterward. 
Eight  years  after  they  began  she  still  had  them  on  exertion,  but  was  the 
picture  of  health,  had  no  signs  of  aneurysm  or  tuberculosis,  and  had  gained 
thirty-five  pounds. 

In  regard  to  the  distribution  of  the  cavities  Ewart  has  collected  the  fol- 
lowing interesting  statistics.  In  791  cases  cavity  occurred  at  the  apex  in 
282  cases,  in  the  dorsoaxillary  region  in  227,  in  the  mammary  region  in  189, 
in  the  sternal  region  in  61,  and  at  the  base  in  32. 

Many  of  the  other  complications  of  pulmonary  tuberculosis  in  addition 
to  vomiting,  diarrhoea,  and  haemoptysis  have  already  been  considered  when 
discussing  the  disease  as  it  affects  serous  membranes,  as  in  pleurisy  and 
pericarditis.  The  most  important  is  pneumothorax,  which  follows  the 
perforation  of  the  tuberculous  lesion  into  the  pleura.  It  occurs  in  from  3  to  10 
per  cent,  of  all  cases,  is  often  fatal  if  sudden  in  onset,  and  may  cause  dis- 
tressing dyspnoea.  West  says  that  of  39  cases,  2  died  in  an  hour,  8  others  in 
twenty-four  hours,  and  29  out  of  the  39  inside  of  two  weeks.  The  mortality  is 
about  90  per  cent.  Effusion  usually  speedily  develops.  I  have  seen  great  relief 
follow  gentle  aspiration  of  the  air  from  the  thorax,  but  aspiration  is  to  be 
avoided  save  when  the  pressure  produces  urgent  dyspnoea.  Very  rarely  the 
pneumothorax  develops  insidiously  without  severe  symptoms,  producing  what 
is  called  "latent  pneumothorax."     (See  Pneumothorax.) 

A  still  more  rare  affection  seen  in  some  cases  of  the  chronic  forms  of 
pulmonary  tuberculosis  is  pulmonary  osteoarthropathy  (which  see). 

Diagnosis. — Before  the  physical  signs  of  pulmonary  tuberculosis  are 
dealt  with  the  sites  of  the  lesions  usually  present  may  be  discussed,  so  that 
they  may  be  examined  with  particular  interest  in  every  case.  The  apices 
are  the  parts  affected  in  the  vast  majority  of  cases,  and  it  is  here  that  the 
primary  lesion  is  usually  found,  even  if  other  parts  become  more  severely 
diseased  later  on.  The  process  as  it  extends  is  prone  to  travel  back- 
ward rather  than  forward.  No  satisfactory  explanation  of  this  fact  is 
obtainable. 

Next  to  the  apices  the  upper  part  of  the  middle  lobe  on  the  right  side  is 
most  frequently  the  site  of  infection,  or  the  upper  part  of  the  lower  lobe  on 
the  left  side  is  diseased.  The  area  of  the  upper  part  of  the  middle  lobe 
on  the  right  side  is  one  which  is  often  overlooked,  owing  to  the  fact  that 
it  is  covered  by  the  right  scapula.  Only  when  this  scapula  is  raised  by  the 
hand  being  placed  on  the  top  of  the  head  is  the  spot  of  impaired  reso- 
nance exposed  at  its  lower  margin. 

Tuberculosis  of  the  bases  rarely  occurs  except  after  the  disease  has  lasted 
long  enough  to  involve  the  whole  lung. 

Physical  Signs. — The  two  methods  of  physical  diagnosis  which  give  us 
the  most  information  in  cases  of  pulmonary  tuberculosis  are  percussion  and 
auscultation.  Throughout  that  period  in  which  there  is  consolidation  of 
the  lung  percussion  gives  impaired  resonance  or  dulness  over  all  the  part 
affected,  unless  the  lesion  be  deep  seated,  in  which  case  light  percussion  over 


TUBERCULOSIS  319 

this  part  may  produce  a  sound  which  is  high  pitched  or  shghtly  tympanitic. 
With  the  development  of  cavity  the  percussion  note  over  it  undergoes  a 
change  and  there  is  developed  a  high-pitched  tympanitic  resonance,  which 
careful  percussion  will  show  to  be  surrounded  by  an  area,  or  ring,  of  impaired 
resonance  representing  the  surrounding  area  of  infiltrated  lung-tissue.  At 
times  in  the  neighborhood  of  tuberculous  lesions  in  the  lungs  hyperresonance 
is  developed  on  percussion,  as  the  result  of  a  compensatory  emphysema  of 
the  lung.  If  the  cavity  communicate  with  a  bronchus  and  the  patient  takes 
a  breath  and  holds  it,  with  the  mouth  open,  percussion  may  develop  the 
so-called  "cracked-pot  sound." 

Auscultation  reveals,  in  the  earliest  stages  of  infiltration,  prolongation 
of  expiration  in  the  part  involved.  This  is  a  physical  sign  of  very  great 
importance.  Again,  it  may  reveal  some  harshness  of  the  inspiratory 
murmur  and  both  inspiration  and  expiration  may  be  more  distinct  and 
rougher  than  in  health. 

Occasionally  careful  auscultation  will  also  reveal  a  few  very  fine  rales  on 
forced  inspiration.  In  lesions  of  the  apex  on  the  left  side  such  a  forced 
inspiration  not  rarely  produces  an  inspiratory  sound  which  is  interrupted 
by  the  action  of  the  heart  three  or  four  times  during  the  act  of  drawing  air 
into  the  limg. 

It  must  not  be  forgotten  that  negative  signs  may  be  as  valuable  as  positive 
ones,  and  therefore  if  the  infiltration  produces  an  absence  of  breath  sounds 
at  the  infected  spot  this  may  indicate  disease  as  surely  as  do  the  more 
positive  signs  already  named. 

If  the  physician  hstens  carefully  over  the  area  of  consolidation  with  his 
disengaged  ear  closed  by  his  finger-tip,  and  the  patient  will  say  one,  two, 
three  in  a  stage  whisper,  the  area  of  consolidation  will  give  greater  vocal 
resonance  than  the  same  area  in  the  healthy  lung. 

With  the  development  of  softening  the  fine  dry  rales  which  have  been 
heard  at  first  become  coarse  and  moist,  and  as  a  cavity  is  formed  they  may 
become  even  bubbling  or  gurgling.  These  rales  sometimes  possess  a  curious 
metallic  sound. 

As  the  cavity  is  formed  the  vocal  resonance  over  it  increases  and  may 
become  starthngly  clear,  so  that  when  the  patient  speaks  the  sound  of 
the  voice  is  transmitted  with  great  clearness  through  the  chest  wall.  This 
is  called  pectoriloquy. 

Over  such  a  cavity  cavernous  breathing  is  often  heard,  or,  if  the  cavity  is 
a  small  one,  the  breathing  may  be  hollow,  tubular,  or  amphoric,  as  if  he 
patient  were  blowing  with  his  lips  over  the  mouth  of  an  open  bottle. 

Moist  cavities  also  present  on  auscultation,  in  addition  to  large  moist 
rales,  metalhc  tinkhng  due  to  the  dropping  of  fluid  from  their  walls.  This 
metallic  tinkling  is  to  be  separated  from  the  metallic  tinkling  of  hydro- 
pneumothorax  by  the  absence  of  the  physical  signs  of  fluid  in  a  dependent 
part  of  the  chest,  and  by  the  fact  that  such  a  cavity  is  near  the  upper  part 
of  the  lung  and  so  produces  this  sign  in  the  upper  zone  of  the  chest. 

The  sounds  arising  from  a  dry  cavity  are  blowing  or  amphoric.  When 
such  a  cavity  has  existed  long  enough  for  marked  fibroid  change  to  occur 
it  often  happens  that  the  chest  over  the  affected  part  is  greatly  flattened, 


320  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

and  it  may  be  decreased  in  all  its  diameters.  Compensatory  hypertrophy 
of  the  opposite  lung  causes  an  increase  in  the  size  of  the  chest  on  that  side, 
and  this  emphasizes  the  difference  between  the  two  sides.  Further  than 
this,  the  contraction  process  may  greatly  displace  nearby  organs.  Thus,  if 
the  left  lung  undergoes  this  change,  the  right  lung,  partly  from  enlargement 
and  partly  from  traction,  may  extend  as  far  as  three  inches  to  the  left  of 
the  sternum,  the  heart  may  be  drawn  upward  and  tilted  to  the  left  of  the 
nipple  as  high  as  the  third  interspace.  Even  the  stomach  may  be  drawn 
upward.  On  the  other  hand,  when  the  right  lung  is  affected  by  the  disease 
the  heart  may  be  drawn  to  the  right  under  the  sternum,  the  liver  may  be 
pulled  upward,  and  the  left  lung  drawn  well  over  to  the  right  side  of  the 
chest.  Most  of  these  marked  changes  are  due  to  associated  pleural 
adhesions,  and  these  may  cause  deformity  of  the  entire  chest. 

The  diagnosis  of  cavity  from  bronchiectasis  is  made  by  the  recollection 
that  a  cavity  is  usually  near  the  apex,  and  bronchiectatic  spaces  are  at  the 
base,  as  a  rule,  although  they  may  develop  as  high  as  the  third  or  fourth 
rib.  If  so,  they  are  nearer  the  sternum  than  is  the  cavity.  Again,  in 
cases  of  cavity  the  area  around  the  hollow  space  is  usually  dull  on 
percussion,  whereas  in  bronchiectasis  it  is  usually  hyperresonant  from 
emphysema. 

It  is  to  be  remembered  that  tuberculosis  may  occur  as  a  complication 
of  bronchiectasis,  but  that  well-developed  bronchiectasis  rarely  occurs  in 
tuberculosis  except  in  old  chronic  cases  with  much  contraction  due  to  fibroid 
change. 

Palpation. — Palpation  over  that  portion  of  the  chest  which  is  infiltrated 
by  a  tuberculous  process,  or  in  which  a  cavity  has  already  formed,  also 
presents  very  definite  physical  signs  when  the  patient  speaks,  namely,  a 
marked  increase  in  vocal  fremitus.  If  the  cavity  is  superficial  and  of  any 
size  it  may  be  possible  to  feel  the  bubbling  rales  which  are  produced  by 
its  contents. 

Inspection. — Inspection  of  a  well-advanced  case  of  pulmonary  tubercu- 
losis occurring  in  one  whose  configuration  is  naturally  phthisical  reveals  a 
very  typical  picture,  but  in  those  with  well-developed  chests  very  advanced 
lesions  of  the  lungs  may  be  present  before  any  change  in  the  appearance  of 
the  chest  is  manifest. 

The  physical  signs  of  acute  pneumonic  tuberculosis  are  at  first  the  same 
as  those  of  acute  pneumonia.  There  are  bronchial  or  tubular  breathing, 
dulness  on  percussion,  and  fine  crepitant  rales.  As  the  disease  progresses 
these  signs  become  modified  to  the  extent  that  the  rales  become  coarse  and 
more  moist  in  character,  and  signs  of  softening  are  therefore  developed. 

In  the  diagnosis  of  a  case  of  this  character  it  may  not  be  possible  to 
state  accurately  the  true  cause  of  the  disease  for  several  days,  but  the  fol- 
lowing points  are  of  some  value,  namely,  the  discovery  in  the  history  of  the 
patient,  or  in  the  body  at  the  time,  of  a  tuberculous  infection,  as  of  enlarged 
cervical  glands  or  of  tuberculous  masses  elsewhere,  as  in  a  Fallopian  tube  or  in 
a  testicle  or  joint;  the  general  appearance  of  the  patient  as  to  nutrition,  for 
the  pale,  anaemic  patient  with  the  typical  slim  bones  and  large  joints,  large 


TUBERCULOSIS  321 

orbital  spaces,  and  delicate  features  is  more  apt  to  succumb  to  the  bacillus 
tuberculosis  than  to  the  pneumococcus.  On  the  other  hand,  it  is  to  be 
remembered  that  robust  and  hearty  persons  may  develop  acute  tuberculous 
pneumonia  and  die  in  a  short  period.  The  presence  of  the  pneumococcus 
in  the  sputum  is  of  little  diagnostic  value,  but  the  discovery  of  the  tubercle 
bacillus  will  be  of  great  aid  in  determining  the  cause  of  the  illness. 

Microscopic  Diagnosis. — An  examination  of  the  sputum  by  the  aid 
of  the  microscope  reveals  shreds  of  mucus  mixed  w^ith  particles  of  caseous 
substance  and  small  round  cells,  leukocytes,  and  pus  corpuscles.  Crystals 
of  the  triple  phosphates,  oxalates,  and  of  tyrosin  and  leucin  are  often  present. 
All  these  constituents  of  the  sputum  are,  however,  of  little  importance  as 
compared  to  two  others,  namely,  the  presence  of  elastic-tissue  fibres  pos- 
sessing the  morphology  and  arrangement  of  pulmonary  reticulum,  showing 
that  breaking  down  of  the  lung  is  taking  place,  and  tubercle  bacilli,  the 
presence  of  which  reveals  the  fact  that  they  are  the  cause  of  this  condition. 
The  bacilli  are  indisputable  evidence  of  the  presence  of  the  disease,  but 
their  absence  from  a  specimen  of  sputum  does  not  exclude  tuberculosis, 
because  they  may  happen  to  be  absent  from  that  individual  sample,  or  they 
are  absent  because  the  sputum  does  not  come  from  a  part  of  the  lung  in 
which  breaking  down  is  taking  place.  Even  an  old  cavity,  if  it  is  well 
drained,  may  not  provide  bacilli  constantly. 

Yellow,  elastic  fibres  are  to  be  sought  for  by  spreading  the  sputum  in  a 
thin  layer  on  a  pane  of  glass  placed  over  a  blackened  surface.  A  second 
sheet  of  glass  is  placed  over  this  and  the  sputum  smeared  by  moving  the 
upper  piece  laterally.  The  particles  of  elastic  tissue  are  usually  contained 
in  small  masses  of  yellowish-gray  material,  which,  if  crushed  and  placed 
under  the  microscope,  are  found  to  consist  of  characteristic,  double-contoured, 
interlacing,  yellow,  elastic  fibres,  having  the  arrangement  of  the  pulmonary 
elastica.  Elastic-tissue  stains  are  of  value  in  the  hands  of  experienced 
microscopists.  As  many  meats  are  rich  in  elastic  tissue  which  may  lodge 
in  the  mouth,  the  mere  finding  of  such  structures  in  the  sputum  does  not 
justify  the  diagnosis  of  "  breaking  down  "  of  the  lung.  The  recognition  of 
pulmonary  elastica  must  be  based  on  the  shape  and  arrangement  indi- 
cated. Occasionally  small  pieces  of  calcareous  matter  are  found  in  the 
sputum. 

The  bacilli  are  sought  for  in  the  following  manner:  A  microscope  slide 
is  thoroughly  cleansed  and  dried.  From  the  sputum  spread  out  on  a  glass 
plate,  or  in  a  Petri  dish,  nummular  particles  if  present  are  selected,  or  if 
absent  the  thicker  portion  of  the  sputum  is  spread  in  a  thin  layer  over  the 
surface  of  the  slide  and  allowed  to  dry  spontaneously.  The  dried  film  on 
the  slide,  surface  upward,  is  passed  three  times  through  the  flame  in  order 
to  fix  the  thin  layer  firmly  to  the  slide.  Cover-glasses  may  be  used  instead 
of  slides,  but  possess  no  special  advantages.  Of  the  many  stains  recom- 
mended Ziehl's  carbol-fuchsin  gives  satisfactory  results.  It  is  prepared  by 
dissolving  1  gm.  of  powdered  fuchsin  in  10  c.c.  of  alcohol;  to  this  solution 
90  c.c.  of  5  per  cent,  aqueous  solution  of  carbolic  acid  is  added;  the  stair 
is  ready  for  immediate  use,  and  if  prepared  from  proper  ingredients  keeps 
21 


322  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

well.  The  prepared  stain  is  poured  over  the  slide,  which  is  then  heated 
over  a  Bunsen  burner  or  alcohol  lamp  until  steam  begins  to  rise,  when  the 
heat  is  withdrawn.  After  staining  five  minutes  the  excess  is  poured  off  and 
the  slide  freely  washed  in  clean  water.  It  is  then  flooded  with  Gabbett's 
solution,  which  consists  of  1.5  gm.  of  methylene  blue  dissolved  in  100  c.c, 
of  a  25  per  cent,  aqueous  solution  of  sulphuric  acid.  This  is  allowed  to  act 
for  one  minute;  it  is  then  poured  off  and  the  slide  washed  in  water;  if  any 
of  the  red  dye  be  retained  the  application  of  the  Gabbett  solution  is  repeated 
until  all  macroscopic  e\'idence  of  the  fuchsin  has  disappeared  from  the 
thoroughly  washed  slide,  which  is  then  stood  on  end  and  allowed  to 
dry. 

A  drop  of  immersion  oil  is  placed  on  the  stained  film  and  the  specimen 
examined  with  a  one-twelfth-inch  immersion  lens.  If  it  be  desired  to  pre- 
serve the  specimen,  balsam  is  applied  to  the  dried  slide  and  a  cover-glass 
placed  on  it.  In  properly  prepared  films  the  cellular  elements  and  bacteria, 
other  than  the  tubercle  bacillus,  will  have  selected  the  blue  dye;  the  tubercle 
bacillus,  however,  -^-ill  appear  red  on  the  bluish  background. 

X-Ray. — A  valuable  aid  in  determining  the  presence  of  consolidation  of 
the  lung  in  tuberculosis  is  the  use  of  the  fluaroscope  or  x-ray  pJiotograph, 
for  such  a  lesion  often  reveals  a  very  distinct  opacity. 

Tuberculin. — In  the  diagnosis  of  pulmonary  tuberculosis  there  can  be  no 
doubt  that  tuberculin  when  properly  employed  is  a  valuable  agent,  although 
I  believe  that  in  the  majority  of  instances  it  should  not  be  used,  since  careful 
examination  of  the  patient  and  consideration  of  his  liistory  will  in  most 
instances  reveal  the  presence  of  tuberculosis,  or  point  to  its  presence  with 
such  a  degree  of  certainty  that  the  patient  should  certainly  be  sent  away 
for  his  health  on  the  ground  that  he  is  a  fair  mark  for  a  tuberculous  infec- 
tion, and  that  his  lun^  is  in  such  a  condition  that  he  is  at  all  times  liable  to 
the  rapid  development  of  a  true  tuberculous  process. 

Tuberculin,  which  is  used  hypodermically,  for  these  diagnostic  purposes 
is  usually  given  to  adults  in  the  dose  of  a  milligram,  and  if  tuberculosis 
is  present  it  causes  a  reaction  in  the  form  of  a  rise  in  temperature  of 
two  or  three  degrees  within  a  few  hours.  If  the  dose  is  larger  than  this, 
susceptible  persons  may  have  a  violent  reaction.  If  the  patient  fails  to 
react  to  the  smaller  doses,  before  deciding  that  the  tuberculin  test  has 
proved  him  free  from  tuberculosis,  doses  of  2  mg.  or  3  mg.  or  even  more 
should  be  given  at  intervals  of  three  or  four  days,  or  a  week. 

The  use  of  tuberculin  for  diagnostic  purposes  has  a  larger  field  in  cases 
of  suspected  renal  or  abdominal  tuberculosis  than  it  has  in  the  diagnosis 
of  pulmonary  lesions,  in  which  the  physical  signs  can  usually  be  demon- 
strated. 

It  is  to  be  remembered  that  the  tuberculin  reaction  sometimes  occurs  in 
persons  who  have  syphilis,  and  it  is  thought  by  some  that  the  reaction 
which  is  produced  may  actually  increase  the  rapidity  of  the  tuberculous 
process. 

In  order  that  a  careful  record  of  its  effects  may  be  obtained  the  tempera- 
ture of  the  patient  should  be  taken  after  the  injection  at  intervals  of  every 
two  hours  for  six  hours,  and  after  that  every  hour  for  twelve  hours.    Before 


TUBERCULOSIS  323 

the  test  is  made  it  must  be  determined  that  the  patient  is  afebrile  by  a  careful 
record  of  his  temperature  for  several  days,  as  otherwise  the  usual  fever  may 
be  mistaken  for  a  reaction. 

Tuberculin  may  be  used  in  hypodermic  tablets,  each  of  which  contains 
1  mg.,  or  in  the  form  of  the  tuberculin  (Koch),  which  is  a  liquid  prepa- 
ration. If  the  tablet  is  used  it  is  dissolved  in  water  as  is  an  ordinary 
hypodermic  tablet.  If  the  liquid  tuberculin  is  employed  the  bottle  con- 
taining it  is  uncorked  and  a  small  pipette,  which  is  graduated,  is  dipped 
into  the  contents  and  then  withdrawn,  with  the  finger-tip  over  the  outside 
end  to  hold  the  fluid  in  the  pipette,  as  in  testing  urine.  The  quantity  of  the 
fluid  as  expressed  in  milligrams  is  then  allowed  to  run  out  into  a  sterile 
porcelain  dish,  and  pure  water  is  drawn  up  in  the  pipette  to  wash  it  free 
of  any  residue  of  the  original  fluid.  This  wash-water  is  then  added  to  the 
contents  of  the  dish,  and,  after  mixing,  the  fluid  is  drawn  up  into  a  hypo- 
dermic syringe  and  given  to  the  patient  through  an  ordinary  hypodermic 
needle. 

It  has  been  urged  against  Tuberculin  R.  that  there  is  a  possibility  of  its  con- 
taining Hving  bacilli  which  may  infect  the  patient.  For  this  reason  many 
clinicians  employ  a  tuberculin  prepared  by  filtration  and  subsequent  con- 
centration of  sterilized  bouillon  cultures,  whereby  a  germ-free  product  is 
assured.     (See  Treatment.) 

Prognosis.— It  is  not  long  since  it  was  almost  universally  thought  that  sub- 
acute pulmonary  tuberculosis  was  an  utterly  hopeless  and  incurable  disease. 
At  present  we  know  that  it  is  in  many  instances  a  readily  curable  afl^ection, 
even  when  it  is  not  possible  to  obtain  the  very  best  conditions  for  cure. 
Further,  we  know  that  hundreds  of  persons  have  the  disease  and  get  well 
without  even  knowing  that  they  have  had  it.  It  is  manifest,  however,  that 
only  those  cases  can  recover  in  which  the  disease  is  not  far  advanced  and 
in  which  the  vital  resistance  of  the  individual  can  be  maintained  at  such  a 
level  that  the  protective  processes  of  combat  and  repair,  already  described 
may  be  carried  out  to  completion. 

The  degree  of  vital  resistance  of  the  patient  is  of  very  great  importance 
in  deciding  the  prognosis.  Often  the  most  powerfully  built  individual  falls 
a  victim  to  rapid  phthisis  while  his  comparatively  feeble  comrade  manifests 
the  most  remarkable  vitality.  Additional  factors  in  determining  the  outlook 
in  an  individual  case  are  the  maintenance  of  the  body  weight,  the  absence 
of  anaemia  (but  red  cheeks  do  not  necessarily  mean  good  blood),  and  the 
presence  of  a  good  digestion,  particularly  in  respect  to  starches  and  fats.  A 
good  family  history  is  not  as  important  a  factor  for  good  as  a  bad  history  is 
important  for  evil. 

A  large  number  of  statistics  as  to  the  curability  of  this  disease  by  climate 
and  feeding  and  by  out-door  life  are  now  obtainable,  and  some  statistics 
will  be  found  discussed  under  Treatment. 

F.  C.  Wood  believes  that  the  diazo  reaction  can  be  used  to  aid  in  deter- 
mining the  question  of  prognosis,  stating  that  if  no  reaction  occurs  and  the 
kidneys  are  intact  the  outlook  is  favorable,  but  that  if  the  urine  reveals  a 
strong  and  persistent  reaction  the  outlook  is  evil.  (For  the  diazo  test,  see 
article  on  Typhoid  Fever.) 


324  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

The  average  duration  of  life  in  a  case  of  pulmonary  phthisis  is  limited 
to  two  years. 

Marriage  should  be  forbidden  for  either  sex  if  suffering  from  tuberculosis, 
even  if  it  be  in  a  mild  form.  The  woman  who  is  tuberculous  may  survive 
her  first  pregnancy  only  to  pass  into  a  hurried  decline  after  the  birth  of  her 
child  or  during  lactation.  Several  pregnancies  almost  always  destroy  her. 
The  man  not  infrequently  loses  nervous  vigor  by  marriage,  and  this  is  the 
more  prone  to  occur,  as  it  is  notorious  that  tuberculous  men  are  cursed  with 
a  degree  of  sexual  desire  which  is  in  excess  of  that  of  health. 

The  prognosis  of  hsemoptysis  so  far  as  its  causing  immediate  death  is 
concerned  is  favorable.  Patients  rarely  die  during  the  hemorrhage  unless 
it  takes  place  in  those  who  are  already  very  feeble  and  anaemic.  Rarely 
the  hemorrhage  is  so  profuse  as  to  cause  death  by  suffocation.  West  gives 
the  proportion  of  deaths  from  this  cause  as  but  1  or  2  out  of  every  100 
cases  that  die  of  this  disease,  whereas  60  per  cent,  of  tuberculous  cases  are 
supposed  to  suffer  from  heemoptysis  at  some  period  of  the  malady. 

The  secondary  effects  of  hemorrhage  may,  however,  be  disastrous,  for  if 
the  neighboring  part  of  the  lung  is  inundated  with  blood  and  with  bacilli, 
the  bronchioles  in  that  part  become  filled  with  the  extravasation  and  a 
traumatic  tuberculous  pneumonia  speedily  ensues. 

Treatment  of  Pulmonary  Tuberculosis. — ^The  treatment  of  pulmonary 
tuberculosis  in  its  subacute  or  chronic  forms  may  be  considered  in  several 
parts. 

1.  Its  treatment  by  proper  diet,  proper  exercise,  and  rest. 

2.  Its  management  by  suitable  out-door  life,  and  particularly  by  climate. 

3.  The  employment  of  drugs  to  control  or  modify  symptoms  which  are 
severe  enough  to  demand  attention. 

4.  The  use  of  tuberculin  as  a  curative  remedy. 

5.  The  avoidance  of  the  use  of  drugs  with  the  idea  that  they  can  cure 
the  disease;  for  he  who  tries  to  cure  pulmonary  tuberculosis  by  drugs  does 
not  know  the  morbid  anatomy  of  the  malady. 

It  is  of  vital  importance  in  the  treatment  of  pulmonary  tuberculosis  that 
the  disease  be  recognized  at  the  earliest  possible  moment  and  that  curative 
measures  be  immediately  instituted.  The  possibility  of  cure  depends  solely 
upon  the  limitation  of  the  lesion,  and  this  is  difficult  to  accomplish  in  direct 
proportion  to  its  size  and  the  degree  to  which  degenerative  changes  have 
advanced. 

Diet. — There  can  be  no  doubt  that  the  proper  nourishment  of  the  patient 
is  the  most  important  matter  demanding  the  attention  of  the  physician; 
for  tuberculosis  is  not  only  a  disease  in  which  emaciation  progresses  rapidly, 
but  it  is  one  in  which  the  outlook  depends  entirely  upon  the  ability  of  the 
patient  to  carry  out  protective  processes  through  which  alone  he  can  hope 
to  recover  his  health.  Under  these  circumstances  it  is  evident  that  the 
physician  must  do  everything  in  his  power  to  keep  the  digestion  in  the  best 
possible  order,  to  administer  foods  which  are  easily  digested  and  readily 
absorbed,  and,  equally  important,  to  prescribe  no  drugs  or  foods  which  by 
disordering  the  stomach  will  interfere  with  the  function  of  this  important 
viscus.     It  must  also  be  remembered  that  the  digestion  of  food  requires 


TUBERCULOSIS  325 

nervous  energy  just  as  does  the  performance  of  any  other  vital  function, 
and  care  must  be  taken  that  food  is  not  ingested  at  a  time  when,  by  reason 
of  exercise  or  other  cause,  a  considerable  quantity  of  nervous  energy  has 
been  recently  expended.  The  physician  is,  therefore,  in  the  difficult  position 
of  knowing  that  the  patient  must  take  large  quantities  of  nutriment  if 
recovery  is  to  be  expected,  and  at  the  same  time  be  careful  that  the  digestion 
is  not  overburdened  by  the  too  frequent  administration,  or  too  free  employ- 
ment, of  nutritious  articles.  If  the  patient's  digestion  is  moderately  strong, 
he  may  follow  a  line  of  diet  about  as  follows: 

Before  getting  up  in  the  morning  he  should  receive  a  teacupful  of  hot 
milk,  which  should  be  sipped  and  not  gulped  down  in  one  or  two  large 
swallows.  After  taking  this,  he  should  rest  in  bed  for  fifteen  or  twenty 
minutes;  should  then  bathe,  or  be  bathed,  and  clothed,  and  for  his  breakfast 
have  wheaten-grits,  oatmeal,  or  some  of  the  more  modern  cereal  preparations 
which  are  known  to  possess  real  nutritive  value.  If  his  appetite  is  good 
he  may  also  have  at  this  time  a  tender  chop  or  a  small  piece  of  steak,  and 
if  accustomed  to  the  use  of  tea  or  coffee,  these  beverages  may  be  allowed 
unless  it  is  found  that  they  increase  nervous  irritability.  In  some  instances 
the  patient  may  desire  to  take  an  orange  or  some  other  fruit  with  his  break- 
fast, and  to  this  there  can  be  no  objection.  The  meal  should  be  adequate, 
but  not  large  enough  to  be  heavy. 

Half-way  between  his  breakfast  and  his  mid-day  meal  the  patient  should 
receive  some  light  luncheon,  consisting  of  a  cup  of  broth,  a  piece  of  toast, 
a  glass  of  koumyss,  or  a  sandwich  made  of  scraped  beef;  or,  if  he  tires  of 
this,  one  made  with  toast  and  anchovy  or  caviar.  Often  an  egg,  cooked 
or  raw,  may  be  taken  between  meals  with  advantage.  If  desired,  a  glass 
of  sherry  or  some  red  wine  may  also  be  taken  at  this  time ;  or,  in  its  place, 
Scotch  or  rye  whiskey  may  be  given. 

The  dinner  should  be  the  heaviest  meal  of  the  twenty-four  hours,  and  should 
be  taken  between  twelve  and  two  o'clock.  It  should  consist  of  a  nutritious 
and  somewhat  stimulating  soup  which  is  easily  digested  and  absorbed ;  one  of 
the  clear  soups  being  preferred  rather  than  a  puree,  unless  it  is  known  that 
the  patient  readily  digests  thickened  and  rich  soups.  This  may  be  followed 
by  a  small  piece  of  fresh  fish,  great  care  being  taken  that  the  fish  is  really 
fresh,  and  then  by  a  hearty  course  of  any  one  of  the  roast  or  broiled  meats, 
accompanied  by  two  or  three  wholesome  vegetables,  such  as  potatoes,  string 
beans,  asparagus,  spinach,  carrots,  macaroni,  and  similar  substances.  With 
this  meal  it  may  be  well  for  the  patient  to  take  a  little  sherry  wine  or  whiskey 
and  water,  particularly  if  he  is  accustomed  to  stimulants  with  his  meals. 
Some  plain,  nutritious  dessert  like  cornstarch  or  rice-pudding  may  also  be 
taken. 

During  the  afternoon  a  light  luncheon  should  be  given  him,  somewhat 
similar  to  that  which  has  been  taken  in  the  middle  of  the  forenoon,  two 
or  three  hours  after  his  dinner.  In  the  evening;  another  li^ht  meal  should 
be  taken,  which  should  consist  of  arrow-root  or  an  egg  cooked  in  some 
simple  form,  or  a  few  stewed  oysters  or  milk-toast  may  be  used,  and  again 
before  going  to  bed  at  night  a  cup  of  broth,  a  glass  of  koumyss,  a  cup  of 
hot  milk,  or  some  curds  and  whey  may  be  given. 


326  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

The  patient  who  is  able  to  take  the  quantity  of  food  which  has  just  been 
described  is,  of  course,  one  whose  digestion  is  in  fairly  good  condition.  But 
if  careful  attention  is  paid  to  the  digestive  tract  by  the  administration  of 
aids  to  digestion,  such  as  pepsin,  pancreatin,  and  taka-diastase,  if  the  bowels 
are  moved  regularly  by  the  use  of  proper  laxatives,  and  if,  above  all,  the 
patient  is  required  to  conserve  his  nervous  energy  in  order  to  expend  it  upon 
his  digestive  apparatus,  it  is  quite  remarkable  what  large  quantities  of  food 
may  be  taken,  even  by  the  consumptive  who  otherwise  seems  quite  feeble. 

The  actual  quantity  of  the  food  at  each  feeding  must  be  varied  from  day 
to  day  with  the  patient's  appetite  and  with  the  conditions  which  may  arise. 
If  the  patient  has  passed  a  restless  and  feverish  night,  the  quantity  of  food 
at  each  feeding  should  be  small;  whereas,  if  he  has  had  a  restful  night,  and 
therefore  has  been  able  to  gain  nervous  energy,  larger  quantities  may  be 
given.  So,  too,  limited  quantities  should  be  ordered  when  the  tongue  is  at 
all  foul,  and  larger  quantities  ordered  when  it  is  comparatively  clean.  It 
is  of  vital  importance  that  these  daily  variations  should  be  made  in  the  diet, 
for  the  digestive  apparatus  of  no  one  is  prepared  day  in  and  day  out  to 
take  exactly  the  same  quantity  of  food,  and  digest  it  satisfactorily.  Both 
the  physician  and  the  patient  must  remember  that  professional  advice  as 
to  food  and  digestion  is  much  more  important  for  the  patient  than  advice 
as  to  the  treatment  by  drugs. 

Exercise. — The  majority  of  cases  of  pulmonary  tuberculosis  do  not 
require  much  exercise  provided  they  are  supplied  with  sufBcient  fresh 
air.  Patients,  however,  differ  very  greatly  in  regard  to  this  matter.  Some 
of  them  seem  capable  of  taking  moderate  exercise  with  great  advan- 
tage, and  others  cannot  take  any  exercise  without  suffering  either  from  a 
disordered  digestion  or  from  a  restless  night  caused  by  inordinate  fatigue. 
In  many  instances  the  patient's  health  can  best  be  preserved  by  giving 
him  fresh  air,  and  supplanting  exercise  by  massage  and  gentle  Swedish 
movements.  Of  course,  these  remarks  do  not  hold  true  of  those  cases  in 
which  a  small  area  of  the  lung  is  involved,  with  almost  no  impairment  of 
the  general  health  and  muscular  strength.  These  patients  should  take 
healthy  exercise,  being  careful  to  avoid  excessive  fatigue,  and  they  should 
be  impressed  with  the  idea  that  exercise  in  sufficient  degree  to  approach 
exhaustion  is  not  only  bad  on  general  principles,  but  actually  diminishes 
their  ability  to  prevent  the  spread  of  the  infection  in  their  lungs.  The 
whole  question  of  exercise  must,  therefore,  be  gauged  in  each  case  by  the 
real  strength  of  the  indi\adual  rather  than  by  his  ambition  to  be  up  and  about. 

Climate  axd  Out-door  Life. — In  these  two  factors  we  have  our  greatest 
aid  in  the  treatment  of  pulmonary  tuberculosis,  although,  of  course,  these 
agents  must  be  prescribed  with  the  same  care  as  governs  our  employment 
of  ordinary  remedies.  There  can  be  no  doubt  whatever  that  an  out-door 
existence  is  capable  of  curing  pulmonary  tuberculosis  imder  certain  circum- 
stances, even  when  the  climate  is  by  no  means  theoretically  suitable  for 
pulmonary  cases.  This  is  a  matter  of  importance  when  it  is  remembered 
that  a  very  large  proportion  of  consumptives  find  it  impossible  to  travel 
great  distances  to  obtain  those  climatic  conditions  which  are  most  favorable 
to  them. 


TUBERCULOSIS  327 

At  every  modern  resort  for  consumptives  every  measure  is  taken  to  keep 
the  patients  for  many  hours  each  day  in  the  open  air,  the  essentials  being 
that  they  shall  be  exposed  to  sunlight,  and,  if  possible,  to  the  direct  rays  of 
the  sun,  and  protected  from  high  winds.  These  conditions  can  be  obtained 
by  the  erection  of  suitable  sheds  facing  the  sun,  and  providing  wind 
guards  which  will  place  the  patient  in  a  quiet  atmosphere.  Even  should 
the  patient  be  unable  to  go  to  the  country  for  fresh  air,  good  results  have 
been  found  to  follow  this  plan  of  treatment  while  he  remains  in  a  city  resi- 
dence, either  in  a  suitably  arranged  room  or  in  a  tent  or  shed  erected  upon 
the  roof  of  his  house. 

The  climate  to  which  the  patient  should  resort,  if  it  is  possible  for  him 
to  travel,  should,  in  the  great  majority  of  instances,  be  one  which  is  found 
at  an  altitude  varying  from  3000  to  6000  feet.  There  are  two  great  essentials 
in  such  a  climate:  first,  that  there  shall  be  an  unusual  number  of  hours 
of  sunshine  in  the  course  of  the  year,  and,  second,  that  the  atmosphere 
shall  be  dry.  A  third  point  of  importance,  but  by  no  means  an  essential 
one,  is  that  the  atmosphere  shall  be  quiet,  in  order  that  there  may  be  little 
dust.  The  temperature  is  of  comparatively  little  importance,  provided  it  is 
not  accompanied  by  humidity,  for  it  is  quite  remarkable  how  patients 
suffering  from  this  disease  often  thrive  in  temperatures  which  in  winter 
are  far  below  the  freezing  point,  and  in  summer  are  often  as  high  as  90°. 
At  those  altitudes  of  from  5000  to  6000  feet  which  are  suited  to  this  class  of 
patients  the  atmosphere  is  so  clear  that  the  sun's  rays  are  not  interfered 
with,  and  even  if  the  thermometer  shows  that  a  zero  temperature  is  present, 
the  patient,  if  properly  clad  and  protected  from  wind,  can  very  frequently 
lie  out-of-doors  all  day,  warmed  by  the  heat  of  the  sun.  This  is  beneficial 
to  an  extraordinary  degree. 

A  high  altitude  is  advantageous  for  the  tuberculous  patient,  not  only 
for  the  reasons  which  we  have  given,  but  also  because  the  rarity  of  the 
atmosphere  requires  that  he  use  all  possible  portions  of  the  lung  tissue, 
and,  this  being  the  case,  he  gradually  expands  and  calls  into  functional 
activity  all  those  parts  of  the  lung  in  the  neighborhood  of  the  tuberculous 
lesion  which  have  a  tendency  to  become  functionally  inactive.  This  develop- 
ment of  active  circulation  of  air  and  blood  does  much  toward  aiding  nature 
in  walling  off  the  tuberculous  focus  and  preventing  its  further  spread.  A 
high  altitude  is  also  advantageous  because  it  seems  to  increase  the  quantity 
of  haemoglobin  in  the  blood.  Whether  it  increases  the  number  of  red  blood 
cells  is  still  a  matter  of  debate,  some  asserting  that  the  increased  number 
of  corpuscles,  found  in  the  superficial  bloodvessels  after  a  patient  has  been 
some  weeks  at  a  high  altitude,  depends  more  upon  an  altered  distribution 
of  blood  than  upon  any  actual  increase. 

Of  the  high-altitude  resorts  which  are  most  popular  because  of  their 
excellent  climate  for  consumptives  may  be  mentioned  Colorado  Springs, 
Colorado,  certain  parts  of  Arizona  and  New  Mexico,  and  parts  adjacent  in 
America,  and  the  so-called  Engadine,  in  Switzerland,  of  which  the  most 
celebrated  places  are  Davos,  Pontresina,  and  San  Moritz. 

A  high,  dry  climate  is  contraindicated  in  tuberculous  patients  who  are 
suffering  from  tuberculous  laryngitis,  since  the  dry  air  increases  the  laryngeal 


328  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

irritation.  It  is  also  contraindicated  in  patients  who  have  dilatation  or 
degeneration  of  the  heart  muscle,  and  great  care  should  be  taken  to  deter- 
mine the  state  of  the  heart  in  all  tuberculous  patients  before  sending  them 
away  from  home.  A  persistently  high  pulse  rate  is  a  distinct  contraindication 
to  altitudes.  If  valvular  disease  exists,  and  there  is  a  tendency  to  failure 
of  compensation,  a  high  altitude  is  also  contraindicated;  but  where  com- 
pensation is  adequate,  the  mere  presence  of  a  murmur  does  not  necessarily 
contraindicate  resort  to  an  altitude,  provided  that  the  patient  is  cautious 
not  to  overexert  himself. 

Emphysema  associated  with  pulmonary  tuberculosis  usually  contrain- 
dicates  a  high  altitude. 

It  has  been  taught  by  some  that  a  tendency  to  haemoptysis  also  renders 
a  high  altitude  inadvisable,  but  very  eminent  phthisiologists,  on  the  con- 
trary, have  asserted  that  a  tendency  to  hemorrhage  does  not  contraindicate 
health  resorts  of  this  character.  My  own  personal  feeling  is  that  the 
patient  who  has  a  tendency  to  hsemoptysis  should  approach  a  high  altitude 
very  gradually  in  order  that  his  heart  and  lungs  may  become  accustomed 
to  the  altered  atmospheric  conditions,  and  certainly,  for  the  first  few  weeks 
after  his  arrival,  should  rest  constantly. 

Still  another  contraindication  to  such  an  altitude,  unless  perchance  the 
climate  is  very  mild  and  the  temperature  fairly  constant,  is  renal  disease 
of  any  kind,  or  tuberculosis  of  the  genito-urinary  tract.  Should  any  of  these 
contraindications  exist,  the  climate  of  choice  is  one  which  is  represented 
by  San  Diego,  California,  where  the  air  is  pure,  where  sudden  changes  of 
temperature  do  not  occur,  and  where  a  flood  of  sunshine  is  constantly 
obtainable. 

In  those  cases  which  have  a  great  deal  of  secretion,  excessive  cough,  and 
excessive  expectoration,  dry  climates,  such  as  are  found  near  Phoenix,  Ari- 
zona, and  Silver  City,  New  Mexico,  are  the  climates  of  election. 

For  those  who  are  unable  to  take  a  long  journey,  and  for  those  who  are  not 
thought  to  be  suitable  cases  for  high  altitudes,  the  Adirondacks  in  the  neigh- 
borhood of  Saranac  Lake,  New  York;  White  Haven,  Pennsylvania;  or 
Asheville,  North  Carolina,  can  be  recommended.  These  altitudes  are  in 
the  neighborhood  of  2500  feet.  Lower  altitudes  which  have  been  found 
advantageous  for  these  cases  exist  at  Thomasville,  Georgia,  and  Lake- 
wood,  New  Jersey,  where  the  curative  elements  are  the  sunshine  and 
pure  air. 

It  is  interesting  to  note,  in  regard  to  the  treatment  of  pulmonary 
tuberculosis  by  fresh  air,  proper  diet,  and  moderate  or  high  altitudes,  that  a 
large  percentage  of  cases  can  be  cured.  Thus,  Trudeau  reported,  at  the 
Adirondack  Cottage  Sanitarium,  where  the  altitude  is  less  than  2500  feet, 
for  the  years  1897,  1898,  and  1899,  cures  in  72  per  cent,  of  incipient  cases 
and  17.8  per  cent,  in  advanced  cases;  and  Clapp  and  Bowditch,  of  the 
sanatorium  at  Rutland,  report  for  the  year  ending  September  1,  1901, 
cures  in  72.5  per  cent,  of  incipient  cases  and  46.11  per  cent,  in  ad- 
vanced cases. 

Still  more  recently  Trudeau  has  presented  the  results  obtained  by  an  analysis 
and  study  of  all  the  cases  under  his  observation  in  the  last  seventeen  years. 


TUBERCULOSIS  329 

Of  the  1500  cases  under  consideration,  which  have  been  discharged  from 
two  to  seventeen  years,  434  could  not  be  traced,  leaving  1066  which  have 
been  traced.  Of  these  1066,  46.7  are  still  living,  31  per  cent,  are  known 
to  be  well  at  present,  in  6.5  per  cent,  the  disease  is  still  arrested,  4  per  cent, 
have  relapsed,  5.2  per  cent,  are  chronic  invalids,  and  53.3  per  cent,  are  dead. 
As  to  the  influence  of  the  stage  of  the  disease  on  the  permanency  of  the 
results  obtained,  he  found  66  per  cent,  of  the  258  incipient  cases  discharged 
are  well  at  present.  Of  the  563  advanced  cases  28.6  per  cent,  are  well, 
and  of  the  far-advanced  cases  2.5  per  cent,  only  remain  cured.  Thus  we 
learn  that  31  per  cent,  of  all  cases  discharged  from  two  to  seventeen  years 
ago  have  remained  well,  and  that  66  per  cent,  of  the  incipient  cases  dis- 
charged during  the  same  time  continue  well  at  present.  Surely  these  results 
are  encouraging  and  he  has  shown  us  the  way  in  a  great  work.  Thirty  years 
ago  physicians  were  of  the  opinion  that  cures  did  not  take  place  from  pul- 
monary tuberculosis  in  more  than  2  per  cent,  of  cases. 

Sea  voyages,  which  at  one  time  were  very  popular  in  the  treatment  of 
tuberculosis  of  the  lungs,  are  no  longer  regarded  with  much  favor.  The 
possibilities  of  seasickness,  bad  weather,  and  of  consequent  close  confine- 
ment are  naturally  not  looked  upon  with  favor,  when  we  consider  that  free 
feeding  and  fresh  air  are  absolutely  essential  for  these  patients.  Further 
than  this,  the  atmosphere  at  sea  is  never  dry,  but  always  more  or  less  damp. 
Again,  there  are  practically  no  comfortable  sailing  ships  at  the  present  time, 
and  steamers  make  such  rapid  voyages  that  the  patient  is  not  long  enough 
at  sea  to  be  materially  benefited. 

Before  the  physician  decides  to  send  his  patient  away  from  home  for  the 
climatic  treatment  of  his  disease,  he  should  determine  whether  such  treat- 
ment really  offers  fair  chance  of  benefit;  for  it  is  a  vital  mistake  to  exhaust 
the  strength  and  finances  of  the  individual  in  a  vain  endeavor  to  arrest 
an  inevitable  process.  If  it  is  decided  that  the  disease  has  advanced  so 
little  that  such  a  trip  can  promise  good,  the  next  question  which  arises  is 
as  to  whether  the  patient  is  strong  enough  to  stand  the  journey,  and,  again,  if 
he  can  stay  away  long  enough  to  be  benefited;  for  in  all  instances  it  is  useless 
for  a  patient  to  leave  home  with  any  expectation  of  returning  in  less  than 
six  months  or  a  year,  and  usually  he  had  better  give  up  the  hope  of  return- 
ing except  for  a  visit,  if  he  wishes  to  preserve  his  health  after  the  climate 
has  done  its  good  work.  It  is  also  a  grave  mistake  to  send  such  patients 
far  from  home  unless  they  can  be  accompanied  by  some  relative  or  friend, 
as  homesickness  exercises  a  deleterious  influence  upon  vitality. 

Drugs. — I  have  already  mentioned  the  use  of  the  various  digestants 
when  speaking  of  the  diet.  The  ever-present  anaemia  of  many  of  these 
patients  is  to  be  overcome  by  the  careful  administration  of  iron  and  arsenic. 
Arsenic  for  many  years  has  had  the  reputation  of  being  a  drug  of  great 
value  in  tuberculosis.  Iron  is  also  very  useful,  but  it  should  not  be  given 
in  the  large  doses  ordinarily  employed.  As  I  have  repeatedly  pointed  out, 
the  quantity  of  iron  in  the  body  is  exceedingly  small,  not  more  than  about 
10  grains,  and  therefore  the  administration  of  2  or  3  grains  of  reduced  iron 
two  or  three  times  a  day  provides  in  twenty-four  hours  far  more  iron  than 
can  possibly  be  utilized,  and  at  the  same  time  tends  to  produce  constipation 


330  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

and  so  disturb  digestion.    Most  cases  will  do  better  if  they  are  given  in  the 
neighborhood  of  ^^  to  ^  grain  of  reduced  iron  three  times  a  day. 

Strychnine  may  be  used  in  moderation  as  a  bitter  and  as  a  nervous  tonic, 
but  it  is  a  mistake  to  use  it  as  a  circulatory  stimulant,  as  it  is  only  an  irri- 
tant to  the  nervous  system,  and  produces  fictitious  strength.  Quinine 
cannot  be  given  in  doses  which  are  adequate  to  control  hectic  fever,  and 
if  any  attempt  of  this  kind  is  made  it  disorders  the  stomach  and  pro- 
duces headache;  2  or  3  grains,  twice  or  thrice  a  day  as  a  bitter  tonic,  are 
quite  sufficient  for  the  average  patient. 

The  syrups  of  the  hypophosphites  and  lactophosphates  have  been  popular 
with  the  profession  for  many  years.  In  many  instances  the  improvement 
which  follows  their  use  depends  upon  the  iron  or  strychnine  which  they 
contain,  and  too  frequently  these  syrupy  preparations  disorder  the  stomach 
and  spoil  the  appetite.  If  it  is  desired  to  administer  calcium,  potash, 
and  soda  to  such  patients,  it  is  better,  in  the  writer's  experience,  to  give 
an  elixir  of  the  glycerophosphates  in  the  dose  of  a  dessertspoonful  three 
times  a  day  to  an  adult. 

When  the  heart  is  weak,  particular  care  should  be  taken  in  regard  to 
rest,  and  digitalis  may  be  given,  but  it  should  be  used  in  small  doses  over  a 
long  period  of  time  rather  than  in  full  doses  for  a  short  period.  It  is  quite 
remarkable  what  good  results  follow  the  use  of  2  or  3  minims  of  a  physio- 
logically tested  tincture  of  digitalis  three  times  a  day.  These  doses,  main- 
tained for  some  time,  produce  a  true  improvement  in  the  heart  muscle  and 
do  not  disorder  the  stomach;  whereas,  larger  doses  soon  upset  the  cardiac 
balance,  and  almost  certainly  disturb  digestion,  and  even  produce  vomiting. 

For  the  control  of  night  sweats  no  remedy  equals  camphoric  acid  in  my 
experience,  given  in  the  dose  of  15  to  20  grains,  two  or  three  hours  before 
the  time  that  the  sweat  usually  comes  on.  The  best  way  to  administer  it 
is  in  cachet  or  capsule,  or  dissolved  in  a  little  brandy.  The  difficulty  of 
the  use  of  atropine  for  this  purpose  is  that  it  checks  other  secretions  and 
sometimes  by  so  doing  renders  the  cough  more  dry  and  annoying. 

Fever,  as  a  rule,  requires  treatment  only  if  it  becomes  excessive.  The 
patient  may  be  sponged  with  tepid  water  and  alcohol,  and  even  cool  water 
may  be  used.  But  care  must  be  taken  that  the  temperature  does  not  break 
rapidly  and  become  subnormal.  The  use  of  the  coal-tar  antipyretics  is 
entirely  inexcusable.  They  diminish  vital  resistance,  are  apt  to  produce 
profuse  sweats,  and  increase  cyanosis  and  dyspnoea  when  the  pulmonary 
lesions  are  well  developed. 

The  use  of  creosote  or  of  any  of  its  derivatives,  with  the  idea  that  they 
are  beneficial  for  pulmonary  tuberculosis,  is  based  upon  an  utterly  erroneous 
view  of  the  disease  and  of  the  action  of  these  drugs.  When  bronchitis  is 
present  as  a  complication  their  value  as  stimulating  expectorants  is  worthy 
of  consideration,  and  under  these  circumstances,  by  improving  the  con- 
dition of  the  bronchial  mucous  membrane  and  aiding  expectoration,  they 
may  eventually  help  the  patient,  but  they  certainly  do  not  exercise  any  influ- 
ence upon  the  tuberculous  process  itself.  Worse  than  this,  in  many  instances 
they  do  not  even  act  as  expectorants,  unless  given  in  doses  so  large  as  to 
disorder  the  stomach.     The  number  of  unfortunate  consumptives  whose 


TUBERCULOSIS  331 

struggle  with  their  disease  has  been  lost  through  disorder  of  the  digestion 
arising  from  the  administration  of  expectorants  is  not  comforting  to  con- 
template. 

Cough  is  to  be  controlled  by  the  use  of  such  cough  sedatives  as  heroin 
in  the  dose  of  -^V  to  yf  of  a  grain  three  or  four  times  in  twenty-four  hours. 
A  very  useful  plan  of  treatment  under  these  circumstances  is  the  adminis- 
tration of  the  elixir  of  terpin  hydrate  and  heroin  in  the  dose  of  a  teaspoonful 
every  four  hours.  In  some  instances  cannabis  indica  is  useful  as  a  cough 
sedative.  In  still  other  cases,  if  the  cough  seems  to  be  due  to  a  dry  and 
irritable  condition  of  the  bronchial  tubes,  quiet  and  sleep  is  obtainable  if 
there  is  disengaged  in  the  air  of  a  room,  from  a  bronchitis  kettle,  steam 
which  arises  from  water  into  which  is  poured  creosote,  oil  of  pine,  and 
oil  of  eucalyptus,  equal  parts,  to  the  extent  of  ^  to  1  drachm.  Care  should 
be  taken  that  the  patient  does  not  go  out-of-doors  into  the  cold  atmosphere 
after  inhaling  the  warm  steam-laden  atmosphere. 

When  a  laryngeal  tuberculosis  develops,  these  steam  inhalations  are  often 
exceedingly  valuable. 

Sometimes  an  excessive  cough  at  night  can  be  stopped  by  giving  the 
patient  a  drachm  of  Hoffmann's  anodyne,  or  a  little  spirit  of  camphor.  In 
other  instances  morphine  in  the  dose  of  -^-^  to  y^  of  a  grain  is  required, 
but  opiates  are  to  be  carefully  avoided  if  other  measures  of  relief  are 
sufficient. 

When  the  cough  depends  upon  the  accumulation  of  large  quantities 
of  material  in  the  bronchial  tubes  or  in  cavities,  it  is  of  vital  impor- 
tance that  it  should  not  be  arrested  by  the  administration  of  drugs; 
for  it  is  an  effort  on  the  part  of  nature  to  get  rid  of  materials  which,  if  they 
are  retained  in  the  lung,  will  greatly  increase  septic  poisoning.  This  is 
particularly  true  of  morning  cough,  which,  though  it  is  often  exceedingly 
annoying,  is  really  an  effort  to  empty  a  cavity  which  has  become  filled 
during  the  night.  Such  coughing  can  frequently  be  aided  by  placing  the 
patient  in  such  a  position  that  the  cavity  will  readily  drain  into  its  supply- 
ing bronchus. 

Whenever  the  physician  in  the  treatment  of  pulmonary  tuberculosis  is 
tempted  to  employ  a  drug,  the  question  of  its  influence  upon  the  stomach 
and  digestion  should  be  carefully  decided,  even  though  the  indications  for 
the  use  of  the  remedy  which  exist  in  other  portions  of  the  body  seem 
very  clear  and  conclusive.  Thus,  the  use  of  cod-liver  oil  in  the  treatment  of 
pulmonary  tuberculosis  is  undoubtedly  to  be  commended,  provided  that 
the  patient  can  digest  it,  and  at  the  same  time  take  ordinary  food.  Even 
a  healthy  person  cannot  exist  on  cod-liver  oil  alone,  and  it  is  a  vital  mistake 
to  impair  the  appetite  and  digestion  by  giving  full  doses  of  this  sometimes 
valuable  drug.  Any  sign  of  indigestion  of  the  oil,  as  in  eructations,  or  in 
the  passing  of  oily  stools,  should  be  the  signal  for  stopping  its  use  at  once. 
The  digestion  of  good  food  does  more  for  a  patient's  vitality  than  the  diges- 
tion of  good  oil. 

Serum  Therapy. — An  endeavor  has  been  made  to  treat  tuberculosis  by 
means  of  antitubercle  serum,  but  so  far  the  results  which  have  been 
obtained  have  not  been  sufl&ciently  encouraging    to  cause  the  plan  to  be 


332  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

very  popular,  although  in  the  early  stages  of  the  disease  the  use  of  this 
serum  may  act  as  an  aid  to  the  control  of  the  tuberculous  process. 

Antistreptococcic  serum  has  been  used  on  the  ground  that  nearly  all 
cases  of  tuberculous  cavity  are  infected  by  the  streptococcus  as  well  as  the 
tubercle  bacillus,  and  that  if  the  former  malign  organism  was  removed,  or 
its  toxins  antagonized,  the  patient  could  the  better  combat  the  original 
cause  of  the  illness.  If  streptococci  are  found  in  the  sputum  in  large  numbers 
it  may  be  used  to  aid  the  patient,  but  otherwise  its  use  is  futile. 

Tuberculin. — The  employment  of  tuberculin  as  a  specific  remedy  for 
pulmonary  tuberculosis  has  not  as  yet  received  general  professional  endorse- 
ment. It  is  true  that  a  very  large  number  of  physicians  who  are  especially 
engaged  in  the  treatment  of  tuberculous  patients  have  written  papers  in 
which  they  have  highly  praised  the  employment  of  this  substance,  and  that 
statistics  are  numerous  which  tend  to  show  that  it  produces  advantageous 
results.  It  must  be  admitted,  therefore,  that  at  times  it  does  good.  But, 
on  the  other  hand,  it  is  a  good  rule  in  practice  to  follow  the  majority  in  the 
use  of  new  remedies ;  for  new  remedies  which  really  are  advantageous  are 
taken  up  and  constantly  employed  by  everyone.  Probably  the  conclusions 
as  reached  by  Trudeau,  in  regard  to  tuberculin,  represent  the  real  facts  of 
the  case  when  he  says:  "My  experience  with  tuberculin  treatment  at  the 
Sanitarium  thus  far  has  led  me  to  believe  that  when  carefully  tried,  in 
suitable  cases,  it  has  proved  apparently  free  from  danger,  and  that  it  has 
seemed  to  have  some  favorable  influence  in  bringing  about  healing  of  the 
lesions,  probably  by  inciting  the  formation  of  fibrous  tissues." 

The  tuberculin  which  should  be  employed  is  that  which  is  prepared 
by  the  more  modern  methods.  It  is  now  made  by  a  number  of  reliable 
concerns,  and  it  can  be  obtained  both  in  this  country  and  abroad.  This 
remedy  is  not  one  which  is  suitable  to  all  cases  and  should  only  be  given 
by  an  expert  in  its  use. 

When  tuberculin  is  used  for  curative  purposes  the  so-called  "Tuberculin 
R. "  is  always  employed.  It  is  a  very  much  more  powerful  product  than 
ordinary  tuberculin.  This  preparation  bears  this  name  because  of  the  fol- 
lowing facts:  Tubercle  bacilli  are  coated  with  fatty  acid.  This  fatty  acid 
is  removed  by  triturating  them  in  a  mortar  and  washing  the  mass  with  dis- 
tilled water.  This  mixture  is  then  placed  in  a  centrifuge  and  it  is  found 
that  the  fluid  separates  into  two  layers.  The  upper  layer  contains  no  tuber- 
cle bacilli,  and  it  is  called  "Tuberculin  Oberst"  (T.  O.),  but  the  lower  layer, 
which  contains  bacilli,  is  called  "Tuberculin  Residuatum,"  or  T.  R.  This 
lower  layer  is  repeatedly  treated  by  triturating  and  centrifuging  until  all  the 
bacilli  are  removed.  The  advantage  of  this  product,  T.  R.,  is  that  it  does 
not  cause  suppuration,  but  does  cause  immunization.  By  care  in  grading 
the  dose  it  may  be  possible  to  produce  a  curative  effect  without  causing 
reaction. 

When  the  physician  desires  to  use  T.  R.  as  a  curative  agent  he  begins  by 
employing  -5-^  milligram  or  less  if  that  dose  produces  a  reaction.  This 
dose  is  prepared  by  adding  1  c.c.  of  Tuberculin  R.  to  500  c.c.  of  normal 
saline  solution  (O.A  per  cent.).  One  c.c,  therefore,  represents  one  dose 
of  -5-^  milligram.    As  the  solution  when  used  should  not   be    more   than 


TUBERCULOSIS  333 

twenty-four  hours  old,  this  method  necessarily  involves  v^asting  a  great  deal 
of  the  product. 

The  dose  is  injected  into  the  tissues  of  the  back  by  means  of  a  sterilized 
syringe  on  every  alternate  day.  It  is  desirable  to  avoid  reaction,  and  all 
febrile  movement  that  may  be  induced  by  one  injection  must  have  disap- 
peared before  another  dose  is  given.  After  repeated  doses  the  patient 
may  be  able  to  stand  very  large  doses  without  any  reaction  and  with  good 
effect. 

When  vomiting  complicates  pulmonary  tuberculosis,  its  cause  must  be 
discovered.  If  it  follows  excessive  cough,  the  cough  must  be  controlled  in  the 
manner  already  described.  If  it  arises  from  gastric  irritability,  2  to  5  grains  of 
subnitrate  of  bismuth  and  1  to  2  grains  of  oxalate  of  cerium  may  be  given 
an  hour  before  meals.  In  other  instances,  where  the  stomach  is  depressed 
rather  than  irritated,  1  or  2  drops  of  Fowler's  solution  before  meals  is 
advantageous. 

The  treatment  of  hoemoptysis  consists  in  the  administration  of  a  hypo- 
dermic injection  of  |-  of  a  grain  of  morphine  if  the  patient  shows  great 
mental  perturbation  because  of  the  hemorrhage.  It  does  not  have  any 
direct  influence  upon  the  flow  of  blood  by  producing  nervous  quiet,  but  it 
relieves  the  patient's  mind  and  so  quiets  the  circulation.  If  the  flow  of 
blood  is  profuse,  the  patient  should  be  allowed  to  occupy  that  position  in 
which  it  is  most  easy  for  him  to  rid  his  bronchial  tubes  of  fluid.  I  have 
seen  relief  produced  by  permitting  him  to  lie  flat  on  his  chest  with  his  head 
resting  on  the  edge  of  the  mattress  in  such  a  way  that  the  blood  readily 
flowed  from  his  mouth  without  violent  efforts  at  coughing. 

A  multitude  of  measures  have  been  recommended  for  the  control  of  the 
hemorrhage.  Manifestly,  none  of  them  can  exercise  much  power  for  good. 
No  one  would  think  of  attempting  to  control  the  hemorrhage  from  a  ruptured 
varicose  vein  in  the  leg,  or  from  a  small  artery  on  the  surface  of  the  body, 
by  the  internal  administration  of  any  drug  of  which  we  have  knowledge. 
Such  indirect  styptics  as  tannic  and  gallic  acid  are  useless.  When  the 
hemorrhage  ceases  after  the  administration  of  these,  or  other  styptics,  by 
the  stomach,  it  is  evident  that  the  arrest  must  be  due  to  the  natural  clotting 
of  the  blood  rather  than  to  any  effect  of  drugs.  That  this  is  the  correct 
view  of  the  case  is  still  further  emphasized  by  the  fact  that  the  pulmonary 
bloodvessels  are  very  poorly  supplied  with  vasomotor  nerves  and  with 
muscular  fibres,  and  therefore  drugs  which  act  by  contracting  bloodvessels 
cannot  exercise  any  powerful  influence  in  this  area.  Finally,  absorption  is 
so  slow  from  the  stomach  that  it  is  incredible  that  styptics  can  exercise  a 
material  effect  before  the  hemorrhage  destroys  the  patient  or  is  stopped 
by  clotting.  If  the  circulation  is  bounding,  a  dose  of  chloral  or  aconite  may 
be  given  as  a  circulatory  sedative.     Nitroglycerin  is  also  of  value. 

The  use  of  adrenalin  by  the  stomach  is  of  doubtful  value,  first,  because, 
as  just  pointed  out,  the  pulmonary  bloodves:;els  are  poorly  supplied  with 
muscular  fibres  upon  which  the  adrenalin  can  act,  and,  second,  because  it 
is  very  doubtful  whether  when  adrenaUn  is  placed  in  the  stomach  it  is  not 
decomposed,  or  at  least  largely  prevented  from  exercising  its  constricting 


334  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

influence  upon  bloodvessels  at  distant  parts.  The  use  of  astringent  sub- 
stances in  atomizers  is  equally  futile.  All  of  the  fluid  strikes  against  the 
pharyngeal  wall,  and  may  run  down  into  the  stomach,  but  it  does  not  reach 
the  lungs.  Only  fluid  which  can  be  used  in  a  vaporizer,  such  as  that  which 
is  driven  by  a  cylinder  of  compressed  air,  can  by  any  possibility  reach  the 
bleeding  spot. 

Some  practitioners  have  recommended  the  application  of  ice  upon  the 
perineum  in  cases  of  haemoptysis,  believing  that  in  some  reflex  manner  it 
diminishes  hemorrhage  from  the  lungs,  and  others  have  applied  a  small 
ice-bag  over  the  cavity  from  which  the  hemorrhage  takes  place.  There 
is  much  more  danger  of  these  measures  adding  to  shock  by  chilling 
the  patient  than  there  is  chance  of  their  doing  good.  As  already  stated, 
haemoptysis  rarely  produces  death  as  the  immediate  result  of  the  loss  of 
blood,  and  remedies  which  receive  credit  for  arresting  the  flow  are  probably 
unworthy  of  the  confidence  imposed  in  them. 

Tuberculosis  of  the  Alimentary  Canal. — ^Tuberculosis  of  the  alimentary 
canal  may  occur  in  any  of  its  parts  from  the  tonsils  to  the  anus,  and,  while 
its  development  is  a  comparatively  rare  primary  form  of  the  infection,  it  is 
nevertheless  met  within  sufficient  frequency  to  make  it  of  importance.  In 
an  analysis  of  5142  autopsies  William  Hunter,  the  Government  Bacteriolo- 
gist of  Hong  Kong,  found  that  this  condition  was  rarely  present  in  children 
under  five  years,  notwithstanding  the  very  great  prevalence  of  tuberculosis 
among  the  Chinese. 

Tuberculosis  of  the  Tonsils. — The  tonsils  may  contain  tubercle  bacilli,  on 
their  way  to  the  infection  of  neighboring  lymphatic  glands,  or  they  may 
be  actually  tuberculous  themselves,  containing  in  their  substance  mihary 
tubercles  or  caseous  foci.  These  lesions  are  more  frequently  met  with  in 
children  than  in  adults,  and  may  depend  upon  autoinfection — that  is,  the 
tonsils  may  be  infected  by  tuberculous  sputum  which  is  expectorated 
(secondary) ,  or  they  may  become  infected  by  the  entrance  of  tubercle  bacilli 
in  dust  by  the  nose  or  mouth  or  perhaps  in  the  milk  of  tuberculous  cows 
(primary).  Koplik  has  recently  made  an  interesting  report  on  this  subject 
in  the  American  Journal  of  the  Medical  Sciences. 

Even  more  important  than  tuberculosis  of  the  tonsils  is  tuberculosis  of 
the  so-called  third  or  pharyngeal  tonsil,  constituting  the  "  postnasal  adenoid." 
As  is  well  known,  these  growths  are  not  rarely  tuberculous  in  origin. 
From  these  adenoids  the  bacifli  may  pass  through  the  lymphatics  and 
so  cause  tuberculosis  of  the  mediastinal  and  bronchial  lymph  nodes. 

Tuberculosis  of  the  Pharynx  and  (Esophagus. — The  pharyngeal  wall  is  not 
uncommonly  the  site  of  mihary  tubercles,  in  the  course  of  chronic  pulmonary 
tuberculosis,  and  even  more  commonly  tuberculous  ulceration  extends  from 
the  larynx  and  epiglottis  to  the  pharynx  and  adds  greatly  to  the  discomfort 
of  the  patient.  Tuberculosis  of  the  oesophagus  is  exceedingly  rare,  but  some 
cases  have  been  recorded.  It  may  comphcate  general  miliary  tuberculosis, 
being  a  part  of  the  systemic  infection,  or  it  may  arise  from  the  swallowing 
of  tuberculous  sputum,  or,  again,  from  the  extension  of  the  disease  from 
a  tuberculous  lymph  node  or  vertebra.  The  ulceration  may  lead  to 
perforation  from  within  or  the  reverse. 


TUBERCULOSIS  335 

Tuberculosis  of  the  Stomach. — ^Tuberculosis  of  the  stomach  rarely  occurs, 
probably  because  its  juices  protect  it  from  infection.  When  it  does  occur, 
it  appears  as  a  miliary  tuberculosis  due  to  circulatory  infection,  or  as  single 
or  multiple  tuberculous  ulcers  involving  the  mucous  membrane.  These 
ulcers  are  usually  the  result  of  a  process  starting  from  an  ulcerating  gland 
which  becomes  attached  to  the  stomach  and  so  causes  disease  by  the  exten- 
sion of  the  inflammatory  process.  Van  Wart  has  recently  reported  an 
instance  of  solitary  tubercle  in  the  muscular  layer  of  the  stomach  which  is 
believed  to  be  unique. 

Tuberculosis  of  the  Intestines. — Tuberculosis  of  the  intestines  is  a  much 
more  common  condition,  and  in  the  great  majority  of  instances  is  secondary 
to  infection  elsewhere.  Primary  intestinal  tuberculosis  occurs  usually  in 
children,  and  as  the  result  of  the  ingestion  of  milk  which  is  infected  by  the 
specific  bacillus.  This  primary  form  has  been  denied  an  existence  by  such 
excellent  men  as  Leube  and  others,  but  so  many  other  pathologists,  of 
whom  BoUinger  may  be  taken  as  a  leader,  have  observed  it  that  its  existence 
is  proved. 

The  secondary  or  common  type  of  intestinal  tuberculosis  is  usually  the 
result  of  pulmonary  tuberculosis,  and  arises  from  the  swallowing  of  tuber- 
culous sputum.  When  the  pulmonary  lesions  have  lasted  for  a  long  time 
intestinal  infection  will  be  found  at  autopsy  in  a  large  proportion  of  cases, 
about  25  per  cent.  Statistics  have  been  published  by  certain  pathologists 
giving  over  50  per  cent.  The  lesions  are  found  chiefly  in  the  ileum  (80 
per  cent,  of  the  intestinal  cases)  just  before  it  joins  the  caecum,  or  in  the 
ileum  and  colon  45  per  cent.,  in  the  colon  alone  3  per  cent.,  and  in  the 
rectum  7  per  cent.,  according  to  Frerichs.  These  statistics  as  to  the  relative 
frequency  of  the  various  lesions  hold  true  of  the  disease,  as  it  appears  in 
children  as  well,  even  when  the  malady  appears  as  a  primary  affection. 

Tuberculous  infection  of  the  intestine  primarily  involves  the  lymph  nodes 
of  the  bowel,  causing  them  to  become  swollen  by  reason  of  the  characteristic 
cell  proliferation  which  the  tubercle  bacillus  always  produces.  The  solitary 
glands  project  markedly  above  the  surface  as  yellowish-white  masses  which 
finally  undergo  caseation  and  softening,  and  then  the  mucous  membrane 
covering  them  breaks  down,  forming  an  ulcer  which  is  surrounded  by 
somewhat  overhanging  edges.  The  ulcers  are  not  very  numerous;  at  times 
only  one  node  may  be  involved.  If  the  agminated  glands,  or  Peyer's  patches, 
are  infected,  separate  caseous  masses  develop,  several  ulcers  form,  and 
finally  coalesce,  forming  a  large  necrotic  surface  of  very  irregular  outline. 
It  is  interesting  to  note  that  this  condition  is  quite  different  from  the  process 
in  enteric  fever,  in  which  disease  the  glands  are  affected  generally  and  the 
individual  agminated  mass  is  uniformly  infiltrated.  Tuberculous  ulcers  of 
the  agminated  glands  usually  extend  transversely  across  the  gut,  whereas 
the  lesion  of  enteric  fever  extends  longitudinally. 

The  overlying  serosa  is  commonly  thickened,  it  may  contain  distinct  tuber- 
cles, and  at  operation  the  diagnosis  of  tuberculous  ulcer  may  be  made 
without  opening  the  bowel.  Fibrosis  and  thickening  with  associated  con- 
traction may  cause  stricture  and  symptoms  of  obstruction;  perforation  is 
not  common  and  is  usually  overlooked. 


336  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

Tuberculosis  of  the  CEecum  in  the  neighborhood  of  the  appendix  may 
give  rise  to  the  beUef  that  appendicitis  or  tumor  of  the  bowel  is  present. 
(See  Symptoms.) 

When  the  rectum  is  affected  the  ulceration  is  preceded  by  infiltration 
and  caseation  in  the  submucosa,  it  often  encircles  the  bowel,  and  the  tissues 
near  the  seat  of  the  ulcer  are  frequently  dotted  with  small,  yellowish  or 
whitish  tubercles,  which  add  to  the  area  of  the  ulcer  as  they  undergo  degen- 
erative change.  They  also  give  rise  to  tuberculous  infection  of  the  perito- 
neum and  perirectal  tissues  and  to  tuberculous  abscesses  and  fistulse. 

With  the  distinct  and  specific  lesions  just  described  tuberculous  disease 
of  the  bowel  presents  an  associated  condition  of  acute  and  chronic  catarrh 
or,  in  other  words,  a  true  enterocolitis. 

Of  recent  years  much  has  been  written  of  chronic  hyperplastic  tuberculosis 
of  the  intestine.  In  this  form  the  intestinal  wall  is  greatly  thickened,  the 
lumen  commonly  narrowed  and  sausage-Kke.  Distinct  cylindrical  seg- 
ments of  the  involved  tissue  may  be  recognized  through  the  thin  abdom- 
inal walls.  Neoplastic  masses  which  may  attain  the  size  of  a  fetal  head 
occasionally  develop,  and  polypoid  growths  may  occur  on  the  interior  of 
the  bowel.  The  condition  is  most  common  in  the  ileocsecal  region,  and 
is  rarely  restricted  to  the  small  intestine,  but  may  involve  one  or  more  parts 
or  the  whole  of  the  colon,  causing  strictures  with  interposed  dilated  areas, 
although  actual  dilatation  is  rare.  The  stenosis  may  be  almost  complete. 
Histologically  there  is  marked  hyperplasia  of  the  connective  tissue  of  the 
intestinal  wall,  and  the  great  thickening,  sometimes  attaining  5  cm.,  is  due 
largely  to  this  cause.  Caseous  areas  and  even  typical  tubercles  may  be 
absent.    The  newly  formed  tissue  is  often  but  scantily  supplied  with  bacilli. 

Symptoms  of  Intestinal  Tuberculosis. — The  symptoms  of  intestinal 
tuberculosis  consist  chiefly  in  the  manifestations  met  with  in  most  cases  of 
enterocolitis.  The  patient  complains  of  looseness  of  the  bowels,  or  diarrhoea, 
and  a  considerable  amount  of  colicky  pain.  With  these  signs  there  is  wasting 
and  decrease  in  strength.  The  tongue  may  be  coated,  but  it  is  often  un- 
duly clean  and  the  normal  roughness  of  its  mucous  membrane  is  replaced  by 
a  raw-beef  appearance.  Palpation  of  the  abdomen  may  reveal  tenderness 
at  certain  points,  which  is  not,  however,  very  well  marked,  and  auscultation 
will  show  an  excessive  amount  of  peristaltic  movement  and  rumbling.  At 
times  the  appetite  may  be  excessive  owing  to  the  fact  that  the  diarrhoea 
causes  starvation  of  the  tissues,  which  is  recognized  by  the  system  and  shown 
in  a  desire  for  more  food.  At  such  times,  in  particular,  the  stools  may 
contain  undigested  particles  of  food.  There  are,  however,  no  symptoms 
in  this  early  stage  that  can  be  considered  typical,  and  the  presence  of 
tuberculosis  elsewhere  may  be  the  chief  reason  for  beUeving  that  the 
alimentary  canal  is  involved. 

^^^len  ulceration  occurs  the  presence  of  mucopus,  blood,  and,  more  im- 
portant, the  discovery  that  tubercle  bacilli  are  in  the  stools  make  it  possible 
for  us  to  state  positively  the  cause  of  the  disease.  If  the  disease  develops 
farther,  as  it  is  prone  to  do  if  life  is  prolonged  a  sufficient  length  of  time, 
the  peritoneal  coat  of  the  intestine  is  involved  and  gradually  a  general 
adhesive  peritonitis,  such  as  was  described  in  the  article  on  peritoneal 


TUBERCULOSIS  337 

tuberculosis,  is  produced,  with  its  characteristic  thickening  of  the  peritoneum 
and  cicatricial  contraction  of  the  omentum  and  mesentery.  This  produces 
constrictions  in  the  intestine,  which  may  be  due  to  the  peritonitis  or  to  the 
ulcerative  process  inside  the  bowel. 

In  some  cases  the  inflammatory  process  produced  by  tuberculosis  of  the 
caput  coli  is  so  intense  that  pain  in  the  region  of  the  appendix  may  give 
rise  to  the  belief  that  an  acute  appendicitis  or  appendicular  abscess  is 
present.  In  a  case  known  to  be  tuberculous  the  possibihty  of  this  condition 
is  manifest,  but  in  one  which  has  a  small  and  unrecognized  tuberculous 
focus  elsewhere,  as  in  the  hmgs,  operative  procedures  for  appendicitis  may 
be  hurriedly  resorted  to  when  no  necessity  for  them  exists. 

So,  too,  the  finding  of  a  mass  in  this  region,  without  sharp  pain,  may  mislead 
the  physician  into  a  diagnosis  of  malignant  growth  if  the  rest  of  the  body  be  not 
well  investigated  for  a  tuberculous  focus.  Such  a  mass  may  be  difi^erentiated 
from  carcinoma  by  the  fact  that  there  is  a  focus  of  tuberculosis  elsewhere. 
If  the  growth  be  slow  it  is  probably  tuberculous;  whereas  if  rapid  it  is  probably 
cancerous,  for  cacal  tuberculosis  may  last  two  years  and  csecal  cancer 
rarely  lasts  longer  than  eight  months.  Further  than  this,  if  the  patient  is 
below  thirty  years  of  age  tuberculosis  is  more  likely  than  cancer;  whereas 
after  forty  years  the  reverse  is  true.  The  tumor  when  outlined  by  palpation 
in  tuberculosis  is  elongated  and  the  thickened  intestine  can  be  felt,  whereas 
in  cancer  it  is  usually  sharply  circumscribed  and  the  rest  of  the  bowel 
cannot  be  outhned.  Fever  is  usually  present  in  tuberculosis  and  absent  in 
cancer.  The  presence  of  tubercle  bacilh  in  the  stools  will,  of  course,  decide 
the  diagnosis,  and  even  if  they  cannot  be  found,  the  presence  of  a  tuberculous 
focus  elsewhere,  in  a  person  below  forty  years,  should  be  considered  as  point- 
ing strongly  to  this  bacillus  as  the  cause  of  the  growth. 

At  times  the  tumor  found  at  the  ileocsecal  region  results  in  obstruction 
of  the  ileocsecal  valve,  and  the  colon  becomes  greatly  distended  with  gas, 
appearing  as  a  large  mass  in  the  sides  and  in  the  epigastrium.  In  other 
cases  the  colon  undergoes  atrophy,  and  can  be  felt  through  the  emaciated 
belly  wall  as  a  narrow,  thickened  band.  I  have  seen  the  entire  colon  in 
a  case  of  this  character  shrunken  to  such  an  extent  that  it  was  smaller  than 
the  ileum.  In  doubtful  cases  resort  may  be  had  to  tubercuhn  to  determine 
the  true  nature  of  the  mass. 

Prognosis  in  Intestinal  Tuberculosis.— The  prognosis  in  intestinal 
tuberculosis  is  not  as  grave  as  in  pulmonary  tuberculosis,  as  far  as  early 
death  is  concerned.  In  the  majority  of  instances  the  patient  dies  of  the 
primary  focus  before  the  state  of  the  bowel  is  grave  enough  to  cause  death. 
Such  cases  often  last  for  several  years  and  have  periods  of  improvement 
followed  by  relapse,  and  characterized  by  gradual  loss  of  vitality.  If  death 
is  caused  by  the  intestinal  state  it  comes  as  a  direct  result  of  profound 
feebleness  and  exhaustion. 

Treatment  of  Intestinal  Tuberculosis. — The  treatment  of  intestinal 
tuberculosis,  as  in  tuberculosis  of  the  lungs,  consists  to  a  great  extent  in  the 
maintenance  of  the  greatest  degree  of  nutrition  and  vitality  that  is  possible, 
and  this  can  only  be  accomplished  by  an  out-door  life,  plenty  of  sunshine, 
the  avoidance  of  fatigue,  and  the  use  of  such  foods  as  are  easily  digested  in  the 
22 


338  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

stomach  or  in  the  duodenum,  so  that  the  greater  part  of  the  nourishment  will 
be  absorbed  before  the  lower  part  of  the  ileum  is  reached.  In  those  cases  in 
which  excessive  peristalsis  rapidly  carries  the  contents  of  the  small  intestine 
to  the  large  bowel  before  absorption  can  occur,  it  is  needful  to  insist  on  small 
quantities  of  food  being  taken  at  a  time,  and  to  order  that  no  water  be  taken 
at  meals.  It  is  also  essential  that  the  patient  shall  immediately  after  taking 
food  lie  down  and  rest  in  order  to  apply  all  the  nervous  energy  possible  to 
the  process  of  digestion  and  to  prevent  stimulation  of  the  bowel  to  active 
movement.  For  the  purpose  of  arresting  peristalsis  and  diarrhoea  the 
salicylate  of  bismuth  in  the  dose  of  10  to  15  grains  three  or  four  times  a  day 
may  be  given,  or  salol  and  the  subnitrate  of  bismuth  may  be  used.  Another 
valuable  drug  is  eudoxine  in  the  dose  of  10  to  20  grains  three  times  a 
day  in  capsule,  or  bismuth  subgallate  may  be  given  in  the  same  dose.  In 
some  instances  iodoform  given  in  keratin-coated  pills  in  the  dose  of  5  grains 
four  times  a  day  to  exercise  the  influence  of  this  substance  on  the  tuberculous 
lesions;  or  if  the  disease  is  in  the  rectum  or  colon,  20  grains  may  be  injected 
dissolved  in  4  ounces  of  olive  oil,  or  5  to  10  grains  may  be  given  in  suppository. 
Some  relief  and  comfort  can  also  be  obtained  by  the  use  of  a  hot-water 
bag  over  the  abdomen  and  by  painting  the  belly  wall  every  few  days  with 
tincture  of  iodine. 

Tuberculosis  of  the  Liver. — Tuberculosis  of  the  liver  occurs  as  part  of  a 
general  miliary  tuberculosis,  as  a  form  characterized  by  the  formation  of 
fairly  large  aggregations  of  tubercles  in  which  the  nodules  may  be  as  large 
as  a  walnut.  Tuberculosis  of  this  organ  is  practically  always  secondary 
to  disease  elsewhere.     (See  Tuberculosis  of  the  Peritoneum.) 

The  miUary  form  is  characterized  by  the  formation  of  miliary  tubercles 
which  are  intralobular  or  interlobular  in  position.  They  may  even  be  in 
the  walls  of  the  biliary  ducts,  and  vary  in  size  from  those  so  small  that  they 
cannot  be  seen  with  the  naked  eye  to  others  which  are  several  miUimetres 
in  diameter.  When  the  tubercles  are  massed  together  so  that  they  form 
small  nodules,  the  cells  of  the  liver  are  of  course  destroyed,  the  surrounding 
cells  suffer  coagulation  necrosis  and  infiltration  with  spheroidal  cells,  and 
tubercle  bacilli  may  be  found  in  large  numbers  in  the  cheesy  masses. 

Tuberculosis  of  the  Genito-urinary  System. — Tuberculosis  may  involve 
any  part  of  the  genito-urinary  tract,  and  is  by  no  means  rarely  met  with  in 
the  testicle,  the  Fallopian  tube,  the  bladder,  and  the  kidneys. 

Tuberculosis  of  the  Testicle. — "When  tuberculosis  appears  in  the  testicle 
it  develops  in  one  or  two  forms.  In  one  of  these  the  onset  is  abrupt  and 
accompanied  by  acute  inflammation,  and  in  the  other  type  the  disease 
develops  slowly,  with  no  inflammation  and  without  pain.  When  the  acute 
inflammation  of  the  first  type  disappears  the  testicle  presents  irregular 
nodules,  which  also  develop  in  the  chronic  form.  In  a  large  proportion  of 
cases  the  disease  is  secondary  to  lesions  elsewhere,  but  it  may  be  primary, 
particularly  if  it  begins  in  the  epididymis.  Verneuil  believes  with  others 
that  infection  may  occur  during  coitus  if  tuberculous  disease  of  the  uterus 
exists,  but  that  state  is  very  uncommon.  Bab^s  has  found  tubercle  bacilli 
in  the  vagina. 

In  nearly  all  cases,  whether  the  disease  be  primary  or  secondary,  the 


TUBERCULOSIS  339 

lesion  begins  in  the  head  of  the  epididymis,  forming  nodides  which  undergo 
caseous  changes.  The  infection  spreads  to  the  vas,  which  becomes  thickened 
and  nodular,  and  to  the  testicle,  the  vaginal  tunic  of  which  is  infected.  In 
more  than  three-fourths  of  the  cases  this  secondary  infection  of  the  testicle 
takes  place. 

When  primary  infection  of  the  testicle  occurs  the  tubercles  also  produce 
nodules,  which  soften  and  may  form  a  sac  of  cheesy  matter.  Sinuses  may 
form  after  adhesion  to  the  scrotum  has  taken  place  and  discharge  exter- 
nally. 

Symptoms  of  Tuberculosis  of  the  Testicle.^Iu  the  form  of  the 
disease  characterized  by  sudden  onset  the  symptoms  closely  resemble  those 
caused  by  gonorrhceal  orchitis,  for  sickening  pain  and  swelling  are  present. 
Instead  of  subsiding  in  the  course  of  a  week  or  ten  days,  the  swelling 
persists,  although  the  pain  disappears;  but  before  many  days  have  passed 
softening  occurs  and  the  so-called  abscess  is  formed  escaping  by  one  or  more 
sinuses.  The  swelling  is  often  bilateral,  and  in  some  instances  massive 
caseation  does  not  take  place,  but  hydrocele  develops.  In  the  chronic 
painless  form  there  is  gradual  enlargement,  usually  of  one  testicle,  with  the 
development  of  one  or  more  nodules  and  a  sense  of  weight.  In  place  of 
caseation  a  fibroid  process  may  develop. 

Diagnosis. — The  diagnosis  of  acute  tuberculosis  of  the  testicle  can  be 
made  only  after  care  has  been  exercised  to  exclude  the  possibility  of  injury, 
metastasis  in  mumps,  gonorrhoea,  syphilis,  and  the  orchitis  of  some  of  the 
acute  infectious  diseases  such  as  typhoid  fever.  A  previous  history  of 
gonorrhceal  orchitis  is,  however,  of  importance,  for  this  condition  predis- 
poses to  tuberculosis  of  this  part.  The  absence  of  any  of  these  causes,  the 
presence  of  tuberculous  lesions  elsewhere,  as  in  the  seminal  vesicles  or  pros- 
tate, or  in  organs  farther  removed,  and  the  fact  that  the  patient  is  in  young 
adult  life,  all  favor  the  diagnosis  of  this  disease  being  present.  The  develop- 
ment of  suppuration  and  the  finding  of  the  bacilli  in  the  cheesy  pus  will,  of 
course,  decide  the  diagnosis. 

The  chronic  type  must  be  separated  from  sarcoma  and  from  the  thicken- 
ing following  gonorrhceal  orchitis.  The  absence  of  any  recent  history  of 
gonorrhoea,  or  of  urethral  discharge,  and  the  presence  of  an  irregular  tumor 
which  increases  in  size,  all  point  to  tuberculosis  as  the  cause.  The  finding  of 
the  bacilli  proves  tuberculosis,  but  the  presence  of  the  gonococcus  does 
not  prove  the  absence  of  tuberculosis,  for  obvious  reasons.  If  hydrocele 
is  present  the  injection  of  some  of  the  fluid  into  the  peritoneal  cavity  of 
a  guinea-pig  may  decide  the  diagnosis  by  producing  tuberculosis  in  that 
animal. 

Treatment. — In  most  cases  it  is  far  safer  to  remove  the  gland.  The 
palliative  treatment  consists  in  the  ordinary  hygienic  measures  used  in 
tuberculosis  and,  if  the  disease  is  localized,  in  incision  and  drainage  with 
iodoform  gauze;  or  in  other  cases,  after  the  abscess  is  evacuated,  the  cavity 
may  be  injected  with  iodoform  in  glycerin  or  in  olive  oil  to  the  extent  of 
15  drops.  In  other  cases  a  few  drops  of  this  mixture  may  be  injected  into 
the  gland  at  different  points  every  three  or  four  days,  care  being  taken 
that  antisepsis  is  preserved. 


340  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

Tuberculosis  of  the  Bladder. — This  condition  may  be  either  primary  or 
secondary,  and  when  secondary  it  may  be  due  to  infection  through  the 
bloodvessels  from  a  distant  point,  or  by  direct  extension  from  the  prostatic 
urethra,  which  is  diseased  through  infection  of  the  prostate  gland,  which 
is  affected  in  97  per  cent,  of  cases  of  genito-urinary  tuberculosis  according 
to  Kazywicki.  In  other  instances  the  tuberculous  lesions  are  transferred 
from  the  kidney  by  the  ureter  to  the  bladder.  In  still  other  instances  the 
infection  passes  from  the  vas  deferens  or  epididymis  or  seminal  vesicles  to 
this  viscus.  Primary  vesical  tuberculosis  is  quite  rare,  and  when  it  occurs 
is  due  to  infection  from  tuberculous  female  genitals  (Fournier).  In  many 
instances  a  case  of  tuberculosis  of  the  bladder  which  is  seemingly  primary 
is  really  secondary  to  an  unrecognized  infection  of  the  kidney.  This  renal 
condition  in  other  instances  may  be  known  to  exist  during  life,  but  it  may 
develop  so  synchronously  with  the  vesical  lesions  that  it  is  difficult  to  tell 
which  organs  were  first  affected.  In  many  other  cases  the  primary  lesion 
may  really  exist  in  the  prostate  or  in  the  seminal  vesicles. 

The  bladder,  when  affected  by  tuberculosis,  develops  grayish  miliary 
tubercles  in  its  epithelial  lining,  which  can  rarely  be  seen  through  the  cysto- 
scope  as  small  gray  spots,  which,  like  all  other  tuberculous  growths  of  small 
size,  tend  to  amalgamate  and  form  patches  which  in  turn  may  ulcerate, 
and  so  destroy  the  mucous  membrane.  The  ulcers  may  be  single  or  mul- 
tiple, and,  like  tuberculous  ulcers  of  the  bowel,  may  have  irregular  outlines 
with  the  base  covered  by  greenish  or  grayish  pus.  Sometimes  they  are  deep, 
at  others  superficial,  and  in  the  severe  cases  they  may  penetrate  the  walls  of 
the  bladder  and  cause  abscesses,  which  in  turn  may  perforate  the  rectum, 
the  vagina,  or  even  the  tissues  in  the  suprapubic  area.  The  chief  lesions 
are  usually  in  the  area  of  the  trigonum.  Tubercle  bacilli  may  be  found  in 
the  pus  in  the  urine. 

Symptoms. — The  symptoms  of  tuberculosis  of  the  bladder  are  usually 
not  well  marked  in  the  early  stages,  and  the  onset  of  the  malady  may  be  so 
gradual  that  the  disease  is  well  developed  before  it  is  recognized.  At  first 
nothing  more  than  a  little  vesical  irritability  may  appear,  and  the  urine 
remains  clear  and  normal  in  appearance.  The  microscope  may,  however, 
reveal  a  few  red  blood  cells,  and  later  distinct  hcematuria  develops,  which  is 
characterized  by  the  appearance  of  a  few  drops  of  clear  blood  at  the  end  of 
urination.  As  soon  as  the  mucous  membrane  of  the  bladder  becomes 
eroded  infection  is  prone  to  occur  and  cystitis  develops,  and  with  the  appear- 
ance of  cystitis  pain  comes  to  be  a  prominent  symptom,  associated  with 
tenesmus  and  a  constant  desire  to  urinate,  which  exhausts  the  patient  and 
prevents  sleep.  The  earliness  with  which  these  symptoms  develop  depends 
upon  the  seat  of  the  disease.  If  it  be  in  the  trigonum,  they  arise  promptly; 
if  elsewhere,  they  may  be  postponed  for  months.  Retention  of  urine  may 
follow  ulceration,  or  in  other  cases  as  the  neck  of  the  bladder  ulcerates 
incontinence  is  produced. 

Diagnosis.— The  diagnosis  of  vesical  tuberculosis  depends  upon  the  pres- 
ence of  these  symptoms  and  the  finding  of  the  bacillus  in  the  urine,  or  by 
inoculation  of  a  rabbit  or  guinea-pig  with  the  urine,  with  the  subsequent 
development  of  the  disease  in  that  animal  ;  but  the  failure  of  either  of  these 


TUBERCULOSIS  341 

tests  does  not  exclude  tuberculosis.  If  gonorrhoea,  stone  in  the  bladder, 
stricture  of  the  urethra,  or  a  history  of  the  use  of  irritating  drugs  can  be 
excluded,  and  if  no  spinal  disease  exists  to  cause  secondary  bladder  trouble, 
tuberculosis  should  be  suspected.  The  presence  of  tuberculosis  elsewhere, 
of  course,  suggests  that  this  disease  is  the  cause  of  the  bladder  trouble. 

Treatment. — For  the  general  plan  of  treatment  in  these  cases  reference 
must  be  made  to  treatises  on  genito-urinary  disease.  The  bladder  must  be 
soothed  by  alkaline  diuretics  if  the  urine  is  acid,  hyoscyamus  may  be  given 
for  vesical  irritability,  and  if  the  disease  is  active  iodoform  in  olive  oil  may 
be  injected  into  the  bladder  every  day,  using  a  10  per  cent,  solution.  The 
bladder  should  be  carefully  emptied  before  the  iodoform  is  injected.  In 
other  cases  corrosive  sublimate  1 :  5000  may  be  employed  by  injection.  In 
severe  cases  perineal  drainage  is  to  be  resorted  to. 

Tuberculosis  of  the  Kidneys. — With  regard  to  the  pathway  by  which  -the 
bacillus  reaches  the  kidney  two  views  have  generally  been  held.  Hsema- 
togenous  infection  is  admitted.  Until  recently  an  ascending  infection  has 
been  thought  not  uncommon,  but  there  is  at  present  a  decided  tendency  to 
doubt  that  infection  travels  from  below  upward;  it  has  been  shown  by  many 
observers  that  tubercle  bacilli  are  occasionally  present  in  the  urine  of  tuber- 
culous patients,  even  when  subsequent  examination  at  autopsy  discloses  no 
tuberculosis  of  the  genito-urinary  organs,  and  hence  it  is  not  necessary  to 
invoke  ascending  infection  to  explain  renal  lesions  secondary  to  tuberculosis 
elsewhere. 

Tuberculosis  of  the  kidneys  appears  in  an  acute  and  chronic  form.  The 
former  is  of  the  miliary  type  and  is  associated  with  the  signs  of  tuberculous 
infection  elsewhere,  and  cannot  be  treated  separately  from  the  general  state. 
The  chronic  form  may  arise  as  a  primary  lesion,  or,  far  more  commonly, 
as  a  secondary  process  due  to  disease  of  the  lower  genital  tract.  When  the 
disease  is  primary  the  bacillus  probably  gains  access  to  the  kidney  through 
the  blood;  this  type  is  that  usually  met  with  in  children.  But  the  form 
ascending  from  the  genitals  is  that  met  with  in  adults,  as  a  rule.  Males 
are  more  frequently  affected  than  females.  The  disease  is  most  frequent 
between  twenty-five  and  forty  years  of  age,  but  it  has  occurred  in  an  infant 
at  the  breast  and  in  very  old  men.     The  lesions  are  often  bilateral. 

The  pathological  process  in  primary  and  secondary  renal  tuberculosis 
is  quite  different.  In  the  primary  form,  in  which  the  infection  comes  by 
the  blood,  the  bacilli,  resting  in  the  vessels  of  the  tufts  and  tubules,  form 
small  tubercles,  which  gradually  undergo  necrosis  and  so  cause  a  spread  of 
the  disease  to  other  parts  of  the  kidney,  particularly  the  callces  and  the 
pelvis.  The  necrosis  of  tuberculous  nodes  gives  rise  to  areas  of  softening 
or  abscess  cavities,  and  these  are  filled  with  cheesy  material  which  rarely 
contains  blood  and  urine,  although  lime  salts  are  frequently  present  in  the 
dead  tissue.  Not  only  tubercle  bacilh  but  pyogenic  and  other  micro- 
organisms are  often  present.  The  capsule  of  the  kidney  is  thickened  and 
may  show  scattered  tubercles.  The  size  of  the  organ  is  considerably 
increased  by  the  growth  of  the  tubercles  and  the  associated  inflamma- 
tion, forming  the  so-called  massive  tuberculosis  of  the  kidney.  Finally,  the 
kidney  may  be  shrunken. 


342  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

As  the  tuberculous  process  in  the  pelvis  of  the  kidney  increases  the  ureter 
is  usually  infected,  and  as  a  result  is  often  partly  occluded.  This  produces 
a  retention  of  urine  in  the  kidney  and  so  a  secondary  hydronephrosis 
develops,  or  it  may  be  a  pyonephrosis.  Sometimes  in  the  early,  and  much 
more  frequently  in  the  later,  stages  of  the  affection  the  tissues  surrounding 
the  kidney  become  more  or  less  affected  and  a  perinephritic  tuberculosis  may 
appear  from  rupture  of  a  softened  area  through  the  capsule  of  the  kidney. 

When  that  form  of  renal  tuberculosis  which  is  secondary  to  tuberculosis 
in  the  lower  genito-urinary  tract  develops,  the  ureter  is  first  involved,  and 
thence  the  pelvis  of  the  Iddney.  The  disease  then  attacks  the  tips  of  the 
pyramids  and  so  gradually  the  entire  gland  is  involved,  but  to  a  less  degree 
than  in  the  form  first  described.  Pyonephrosis  is  very  common  in  these 
cases,  and  obstruction  in  the  flow  of  urine  is  usual. 

Symptoms. — Often  no  symptoms  appear  until  the  pelvis  of  the  kidney  is 
diseased,  when  pain  becomes  a  marked  symptom.  This  pain  may  be  dull 
or  acute,  as  if  due  to  a  renal  calculus,  with  the  characteristic  radiation  of 
the  pain  to  the  penis  and  inner  side  of  the  thigh.  The  urinary  symptoms 
are  frequent  urination,  slight  incontinence,  and,  later,  distinct  signs  of 
cystitis  develop.  Before  the  pelvis  of  the  kidney  is  affected  the  urine  may 
be  normal,  but  afterward  it  contains  pus  and  blood,  the  pus  coming  from 
this  area  or  from  the  necrotic  ulcerating  tubercle.  Attacks  of  violent  pain, 
arising  from  acute  hydronephrosis  due  to  blocking  of  the  ureter  by  cheesy 
masses,  may  occur,  followed  by  a  free  flow  of  purulent  urine  as  the  obstruc- 
tion gives  way.  Tubercle  bacilli  can  usually  be  found  in  the  urine,  but  care 
must  be  taken  that  the  smegma  bacillus  is  not  mistaken  for  the  specific 
bacillus,  and,  as  indicated  above,  the  demonstration  of  the  tubercle  bacillus 
does  not  prove  that  the  infection  is  in  the  genito-urinary  organs. 

The  associated  symptoms  are  those  of  anaemia,  debility,  and  loss  of  flesh. 
A  lumbar  tumor  may  also  appear. 

When  the  case  is  grave  the  question  of  operation  must  be  considered, 
and  it  is  important  to  discover  if  the  disease  is  bilateral  or  unilateral  before 
operating.    This  may  be  done  by  unilateral  catheterization. 

Tuberculosis  of  the  Fallopian  Tubes,  Ovaries,  and  Uterus.— The  fre- 
quency of  tuberculosis  of  the  Fallopian  tubes  is  notable.  It  forms  the 
largest  part  of  all  statistics  involving  the  female  genitalia,  for,  as  stated 
below,  the  ovary  and  uterus  are  rarely  affected.  Tuberculosis  of  these 
parts  was  recognized  and  reported  as  early  as  1744  by  Morgagni.  In 
1888  Hegar  published  an  important  paper  on  this  subject  which  marked 
an  epoch  in  its  study.  To  illustrate  the  great  frequency  of  tuberculosis  of 
the  female  genital  tract  the  statistics  of  eight  European  pathologists  may 
be  cited.  In  8627  cases  of  tuberculosis  in  females,  this  disease  had  infected 
the  genitals  208  times.     These  relative  proportions  are  probably  too  small. 

Unlike  tuberculous  disease  elsewhere,  tuberculosis  is  quite  frequently  a 
primary  lesion  in  these  parts,  the  infection  being  received  in  some  cases  from 
the  male  during  coitus  (Verneuil,  Cohnheim),  but  in  the  majority  of  instances 
taking  place  through  the  blood  or  lymphatics.  According  to  the  statistics 
of  Schramm,  Spaeth,  Hosier,  and  Frerichs,  genital  tuberculosis  is  found 
to  be  primary  in  about  18  per  cent,  of  cases  of  genital  tuberculous  disease. 


TUBERCULOSIS  343 

Genital  tuberculosis  is  most  common  during  the  period  of  sexual  life. 
Pathologically  the  condition  under  these  circumstances  is  like  that  of  an  ordi- 
nary salpingitis,  the  tubes  being  thickened  and  filled  with  cheesy  material. 
Because  of  the  inflammation  associated  with  the  tuberculous  process  the  fim- 
briated extremity  of  the  tubes  becomes  adherent  to  the  ovaries  and  the  uterus 
may  become  infected.  This  condition  may  develop  in  children  as  well  as  in 
adults,  and  it  is  usually  bilateral.  True  abscess  of  the  tube  may  arise  from 
this  cause  and  a  tuberculous  parametritis  and  peritonitis  often  start  from 
this  nidus.    In  some  cases  a  miliary  tuberculosis  of  the  tube  develops. 

The  ovary  is  rarely  involved,  but  when  this  occurs  it  is  always  a  secondary 
infection  from  an  infected  tube  or  other  adjacent  parts  or  from  the  blood. 
The  uterus  is  affected  only  in  very  rare  instances. 

Prognosis. — The  prognosis  in  tuberculosis  of  the  female  genitalia  is  more 
favorable  than  would  be  imagined,  provided  an  early  diagnosis  is  made  and 
operative  treatment  resorted  to.  It  is,  of  course,  more  favorable  in  these 
instances  if  the  lesion  be  a  primary  one,  for  if  severe  disease  is  present  else- 
where, operation  may  be  contraindicated  and  general  recovery  impossible. 

Treatment. — The  treatment  is  entirely  surgical. 

Tuberculosis  of  the  Heart. — Ferrend  and  Rathery  have  reported  a  case 
of  tuberculous  vegetative  endocarditis  following  primary  tuberculosis  of 
the  spleen.  Tubercle  baciUi  were  found  in  these  vegetations  and  in  the 
clotted  heart  blood. 

Tuberculosis  of  the  myocardium  is  very  rare.  In  1902  Anders  collected 
71  cases  of  tuberculosis  of  the  myocardium,  and  reported  one  of  his  own, 
which  were  all  he  could  find  in  literature.  Out  of  3999  autopsies  reported 
by  Valentin  and  Sangelli  this  condition  was  found  in  only  9  instances. 
Weigert,  however,  states  that  he  has  found  minute  tubercles  in  different 
portions  of  the  heart  in  nearly  all  his  autopsies  on  patients  who  died  from 
acute  miliary  tuberculosis. 

Tuberculosis  of  the  Thyroid  Gland. — Fraenkel  and  Chiari  in  480 
autopsies  on  tuberculous  subjects  found  the  thyroid  gland  affected  13  times. 

Tuberculosis  of  the  Brain  and  Cord. — Tuberculosis  of  the  meninges 
of  the  brain  and  cord  has  already  been  mentioned  when  discussing  the  tuber- 
culous infection  of  the  serous  membranes.  The  tissues  of  the  brain  and 
cord  are,  comparatively  speaking,  very  rarely  affected.  When  tuberculous 
lesions  occur-  in  these  parts  they  are  practically  always  secondary  to  tuber- 
culous lesions  elsewhere,  but  there  are  a  few  exceptions  to  this  rule.  Thus, 
Demme  has  recorded  a  unique  case  of  tuberculous  tumor  of  the  cerebellum 
in  a  child  of  twenty-three  days,  and  he  has  also  had  a  case  in  which  infection 
seemingly  took  place  through  the  nose. 

When  tuberculous  tumors  develop  in  these  parts  of  the  nervous  system 
they  appear  as  solid  or  caseous,  rounded  masses,  which  resemble  the  ordinary 
tuberculous  growth  as  it  is  seen  elsewhere.  They  vary  in  size  from  a 
millet-seed  to  an  orange.  When  incised  they  are  caseous,  fibrocaseous,  or 
hyaline  and  calcareous,  or  all  of  these  changes  may  be  found  associated. 
The  surface  of  the  growth  is  sometimes  soft  and  translucent,  and  the  adjacent 
brain-tissue  may  be  filled  with  miliary  tubercles,  which,  coalescing  with  the 
main  growth,  in  this  way  increase  its  size.     The  growth  does  not  undergo 


344  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

the  rapid  changes  usually  met  with  elsewhere.  Sometimes  these  nodules 
become  encapsulated  by  fibrous  tissue  just  as  does  the  ordinary  tuberculous 
growth  in  the  lung,  or  rapid  softening  in  the  surrounding  tissues  develops 
and  suppuration  takes  place. 

These  tuberculous  growths  do  not  tend  to  infiltrate  the  surrounding  tissues. 
They  generally  occur  in  the  brain  tissue  itself,  and  while  it  has  been  asserted 
that  they  always  spring  from  the  pia  mater,  this  view  is  of  doubtful  value.  As 
they  often  project  above  the  surface,  the  cerebrospinal  fluid  is  readily  infected. 
One-third  of  these  tuberculous  growths  occur  in  the  cerebellum,  in  one  of  its 
hemispheres  or  in  the  middle  lobe.  After  the  cerebellum,  the  cerebrum 
is  the  most  common  site,  and  after  this  Gowers  gives  the  following  order: 
the  pons,  the  cerebral  ganglia,  the  quadrigeminal  bodies.  As  a  rule,  more 
than  1  growth  exists;  but  sometimes  2  and  sometimes  as  many  as  10  or  12 
are  present.  Thus,  Trevelyan  found  them  multiple  in  17  out  of  33  cases, 
which  is  a  smaller  proportion  than  is  usual,  and  the  largest  number  in  any 
one  case  was  4.  In  a  case  reported  by  Middleton  there  were  20,  and 
in  a  case  reported  by  Homen  there  were  12.  West  and  Henoch  have 
each  reported  a  case  in  which  there  were  12  tuberculous  tumors.  There 
are  a  few  cases  recorded  in  which  recovery  has  taken  place  notwithstanding 
the  presence  of  a  tuberculous  tumor  in  the  brain,  and  without  operation. 
(For  literature  see  Trevelyan's  article  in  the  Lancet  for  November  7,  1903.) 
The  symptoms  and  treatment  of  tubercle  of  the  brain  are  discussed  under 
Brain  Tumor. 

LEPROSY. 

Definition. — Leprosy  is  a  chronic  infectious  disease  caused  by  a  specific 
bacillus,  and  is  characterized  by  the  occurrence  of  granulomatous  new- 
growths  in  the  skin,  mucous  membrane,  peripheral  nerves,  and  viscera.  The 
lesions  are  partly  ansesthetic  and  there  is  a  marked  tendency  to  destructive 
ulceration  and  trophic  lesions. 

History. — The  history  of  leprosy  is  as  old  as  the  written  history  of  the 
human  race.  The  earliest  known  records  are  in  two  Eg}^tian  papyri  of 
4260  B.C.  and  2400  B.C.  The  detailed  description  of  leprosy  in  the  third 
book  of  Moses  is  familiar  to  all.  In  India  and  China  the  earliest  writings 
that  unmistakably  describe  leprosy  appeared  about  700  B.C.  The  disease 
appears  much  later  in  European  history.  It  was  not  mentioned  by  Hippoc- 
rates, and  we  may  assume  that  it  was  unknown  in  his  time.  It  appeared 
in  Greece  before  375  B.C.  and  gradually  spread  over  all  Europe,  its  exten- 
sions being  generally  along  the  track  of  conquering  armies.  Its  extensive 
distribution  in  the  ^liddle  Ages  finally  brought  about  stringent  restrictive 
regulations  which,  beginning  in  the  thirteenth  century,  served  to  gradually 
decrease  the  disease  until  now  it  occurs  only  in  isolated  centres  of  infection. 

Distribution. — At  present  the  distribution  of  leprosy  is  very  extensive, 
principally  in  tropical  and  subtropical  countries.  It  is  a  mistake  to  con- 
sider that  leprosy  is  essentially  a  disease  of  warm  climates.  In  Europe 
it  appears  only  in  small,  scattered  centres  or  in  isolated  cases.  It  prevails  in 
greatest  numbers  in  Finland,  Sweden,  Iceland,  and  Norway,  particularly 


LEPROSY  345 

the  latter.  In  Russia  it  is  found  in  forty-nine  provinces,  most  frequently  in 
the  Baltic  provinces  of  Lifu  with  60S  and  Kurland  with  201  cases.  Isolated 
cases  occur  in  England,  Germany,  Brittany,  and  Italy.  The  total  number 
of  cases  in  Western  Europe  at  present  is  estimated  at  3000.  The  disease 
is  found  all  over  tropical  Asia.  In  British  India  the  number  of  lepers  is 
estimated  at  105,000,  or  one  in  every  two  thousand  of  population.  It  is 
believed  that  leprosy  prevails  in  the  southern  provinces  of  China  more 
than  anywhere  else,  although  no  accurate  figures  are  available.  It  is 
very  common  in  Japan,  the  number  of  cases  being  estimated  at  23,660 
(Souton),  and  in  Ceylon,  Persia,  Arabia,  and  the  Malayan  country.  In 
the  Philippines  there  are  probably  15,000  lepers.  The  disease  is  widely 
distributed  in  Africa,  particularly  along  the  upper  Nile  and  the  countries 
bordering  along  the  Red  Sea  and  the  Mediterranean.  Leprosy  was  intro- 
duced into  the  Sandwich  Islands  in  1859,  and  in  1891  one  in  thirty  of  the 
population  was  affected. 

Much  has  been  said  of  the  early  existence  of  leprosy  in  America.  There 
is  no  evidence  to  show  that  the  disease  existed  prior  to  the  Spanish  discovery. 
The  so-called  evidence  of  pre-Columbian  leprosy  in  America  is  entirely  too 
vague  to  justify  any  deductions.  In  point  of  fact  it  suggests  syphilis  or 
sacrificial  mutilation  more  strongly  than  leprosy.  At  present  lepers  are 
found  in  large  numbers  in  Mexico  and  many  countries  of  South  America. 
In  Colombia  there  are  said  to  be  seven  in  every  one  thousand  in  the  popula- 
tion. There  are  some  cases  in  New  Brunswick  and  British  Columbia.  Cuba 
and  the  Antilles  are  severely  infected ;  the  latest  figures  give  1297  lepers  in 
Cuba.  In  the  United  States  the  disease  is  generally  distributed.  A  recent 
official  report  shows  that  nearly  every  large  city  has  at  least  one  case,  the 
aggregate  number  for  the  United  States  reaching  over  900.  The  disease 
occurs  in  three  main  foci,  namely,  one  in  Louisiana,  which  has  existed  since 
1785,  and  has  lately  been  estimated  as  containing  about  500  cases;  another 
in  California,  the  infection  having  been  brought  in  by  the  Chinese,  and  a 
third  in  Minnesota,  where  it  is  estimated  that  there  are  170  lepers,  the  num- 
ber being  almost  entirely  made  up  of  emigrants  from  the  infected  districts  in 
Norway,  from  which  region  infected  persons  also  carried  the  disease  into  the 
Mormon  settlements  of  Utah.  These  settlements  in  Utah  have  also  been 
infected  from  Hawaii. 

Etiology. — The  specific  cause  of  leprosy  is  the  Bacillus  lepra;,  discovered 
by  Hansen  in  1871.  This  bacillus  is  about  the  same  size  and  has  the  same 
morphology  as  the  tubercle  bacillus.  Like  it  it  is  also  acid  fast;  that  is  to 
say,  when  stained  with  an  aniline  dye  it  does  not  decolorize  readily  in  the 
presence  of  mineral  acid.  It  stains  a  little  more  easily  than  the  tubercle 
bacillus  and  decolorizes  more  rapidly.  It  has  not  been  grown  successfully 
on  artificial  culture  media.  It  is  found  packed  in  very  great  numbers 
inside  the  leprosy  cells,  but  it  does  not  invade  the  nucleus.  It  is  also  found 
in  zooglea  masses  in  the  lymph  spaces,  in  the  granulomatous  lesions,  and 
in  the  infiltrated  nerve  tissues.  A  number  of  cases  have  been  reported  in 
which  the  bacillus  has  been  found  in  the  circulating  blood. 

Manner  of  Infection. — There  is  one  case  of  experimental  inoculation  on 
record  in  the  person  of  a  Hawaiian  convict  reported  by  Arning.    Four  weeks 


346  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

after  inoculation  the  disease  began  to  develop  with  acute  pain  and  thicken- 
ing of  the  nerve  trunks,  and  a  little  while  after  a  typical  leprous  nodule 
appeared  at  site  of  inoculation.  The  patient  died  of  the  disease  in  six  years. 
Unfortunately  this  experiment  was  made  in  a  leprosy  country  and  the  man 
had  a  leprous  family  history,  so  that  the  evidence  derived  from  it  cannot 
be  regarded  as  absolutely  conclusive.  There  can  be  no  doubt  that  in  a  large 
number  of  instances  the  bacillus  gains  admission  through  abrasions  of  the 
skin  and  mucous  membrane,  and  possibly  also  from  the  friction  of  infected 
clothing. 

Corroboration  of  the  idea  that  the  bacilli  gain  entrance  through  local 
lesions  is  found  in  the  fact  that  where  people  go  habitually  without  shoes, 
as  in  tropical  countries,  the  disease  first  appears  in  the  feet  in  a  large 
proportion  of  cases.  Ehler  states  that  in  Iceland  the  face  and  hands  are 
most  frequently  attacked  because  the  remainder  of  the  body  is  so  fully  pro- 
tected by  clothing.  Boinet,  in  Hanoi,  considered  infected  earth  to  be  the 
probable  carrier  of  the  disease  to  the  feet  of  the  natives.  He  found  the  earth 
saturated  with  sputa,  crusts,  and  discharges  of  the  lepers.  He  was  able 
to  demonstrate  that  the  soil  of  the  cemetery  at  Hanoi  was  highly  charged 
with  bacilli,  but  this  evidence  is  of  little  value,  as  acid-fast  bacilli  are 
widely  distributed.  Carasaquilla  believes  that  leprosy  may  be  conveyed 
by  the  bite  of  fleas,  and  infection  by  the  mosquito  must  also  be  borne 
in  mind,  since  the  bacilli  are  sometimes  found  in  the  blood  and  have  also 
been  demonstrated  in  mosquitoes.  Scabies  may  transfer  the  infection. 
A  large  proportion  of  cases  are  undoubtedly  infected  in  sexual  intercourse. 
The  contagion  of  leprosy  is,  however,  feeble. 

The  immunity  of  physicians  and  nurses  is  proverbial,  although  several 
striking  instances,  as  that  of  Father  Damien,  are  on  record  in  which 
attendants  on  lepers  have  fallen  victims  to  the  disease.  It  would  seem 
that  long  intimate  contact  were  necessary  to  contract  it.  Hutchinson  sug- 
gests that  leprosy  may  be  conveyed  from  person  to  person  by  commensal 
contagion;  that  is  to  say,  by  eating  food  prepared  by  the  sore  hands  of  a 
leper,  and  by  eating  out  of  infected  dishes  and  utensils.  Von  Bergmann,  in 
a  study  of  106  cases  of  leprosy  in  Riga,  found  that  60  per  cent,  occurred  in 
people  who  had  lived  in  intimate  contact  with  lepers.  In  the  workhouse 
at  Riga  there  were  23  cases:  4  who  entered  with  it,  19  who  contracted  it  in 
the  house;  9  cases  developed  in  women  whose  neighbors  in  the  next  beds 
had  leprosy. 

Great  significance  was  formerly  attached  to  the  factor  of  heredity  in 
leprosy,  but  recent  studies  of  the  epidemiology  of  the  disease  have  disproved 
its  importance.  Boinet  cites  a  case  in  which  grandfather  and  grandmother 
were  lepers,  while  the  father  and  five  children  escaped  although  living  in  a 
leprous  community.  Children  of  lepers  removed  soon  after  birth  from 
the  infected  districts  do  not  develop  leprosy,  while  their  brothers  and  sisters 
who  continue  to  live  in  the  leper  community  may  contract  it.  None  of  the 
children  of  Norwegian  lepers  who  have  emigrated  to  the  United  States 
have  developed  the  disease.  Tonkin,  in  a  careful  study  of  lepers  in  Algeria, 
found  that  only  10  per  cent,  of  the  cases  had  any  leprous  taint  in  their  ances- 
try; so  that  90  per  cent,  at  least  must  have  derived  the  disease  from  other 


LEPROSY  347 

sources.  He  found,  further,  that  less  than  10  per  cent,  of  the  children  of 
lepers  developed  the  disease,  which  is  certainly  a  low  percentage  of  con- 
tagion for  persons  living  in  close  intercourse  with  lepers,  even  disregarding 
the  question  of  heredity.  There  is  nowhere  a  record  of  a  leprous  foetus, 
although  one  or  two  cases  of  infants  born  with  leprosy  has  been  reported. 

The  disease  is  exceedingly  rare  under  one  year;  and,  in  fact,  before  the 
fifth  or  sixth  year.  It  must  be  recognized  as  very  feebly  contagious, 
therefore,  when  close  and  prolonged  contact  is  eliminated.  Of  the  various 
types  the  tuberculous  is  far  more  contagious  than  the  anaesthetic. 

Many  writers  have  maintained  that  defective  nutrition  and  diet  play  an 
important  role  in  this  disease.  Hutchinson  is  at  present  the  foremost  ex- 
ponent of  the  theory  that  the  disease  is  conveyed  by  food  and  that  the  germs 
gain  entrance  to  the  body  through  the  stomach.  He  believes  that  tainted 
fish  carry  the  infection,  although  leper  bacilli  have  never  been  found  in  them. 
This  idea  of  fish  serving  as  the  medium  for  the  infection  of  leprosy  is  not  a 
new  one.  They  have  been  suspected  in  all  ages,  and  it  is  true  that  leprosy 
occurs  chiefly  in  countries  where  fish  forms  a  staple  article  of  food,  and  where 
a  large  proportion  of  the  inhabitants  are  engaged  in  fishing.  There  is  noth- 
ing inherently  improbable  in  the  theory  that  fish  may  carry  the  infection, 
or  that  a  fish  diet  may  represent  a  common  additional  factor  in  the  develop- 
ment of  the  disease.  As  against  this  theory,  Hansen  maintains  that  it  is 
necessary  to  demonstrate  the  bacilli  in  fish.  He  states  that  the  people  of 
Norway  are  using  more  fish  than  ever  at  present,  but  nevertheless  leprosy 
is  constantly  decreasing. 

Morbid  Anatomy. — In  tuberculous  leprosy  the  lesions  consist  in  granulo- 
matous growths  or  diffuse  infiltration  of  the  skin  and  mucous  membrane. 
The  granulomatous  growths  are  built  up  of  small  round  and  fusiform  cells 
and  large  vacuolated  cells,  called  by  Virchow  leprosy  cells.  These  cells 
are  probably  of  endothelial  origin  and  are  packed  full  of  bacilli.  They 
frequently  develop  into  giant  cells.  The  bloodvessels  are  increased.  In 
diffuse  leprous  infiltration  the  same  histological  elements  are  observed.  The 
new-growth  invades  the  bloodvessels,  hair  follicles,  and  sweat  glands.  The 
bacilli  are  found  everywhere,  but  in  greatest  numbers  in  the  giant  and 
leprosy  cells. 

In  the  macular  lesions  there  is  a  larger  proportion  of  connective  tissue, 
the  bacilli  are  fewer,  and  none  of  the  large  types  of  cells  are  seen.  In  the 
anaesthetic  type,  diffuse  or  nodular  infiltrations  are  found  in  the  nerve 
trunks.  The  nerves  are  firmer  than  normal  and  darker  in  color.  The 
interstitial  connective  tissue  is  markedly  increased  and  the  axis  cylinders 
are  atrophied. 

Leprous  nodules  and  infiltrations  are  found  in  the  liver,  spleen,  testicle, 
intestines,  and  kidneys.  In  the  bones  osteomyelitis,  necrosis,  and  atrophy 
are  observed,  the  bone  being  replaced  in  many  instances  of  leprous  mutila- 
tions by  connective  tissue.  In  the  larger  joints  changes  occasionally  are 
observed  that  are  very  similar  to  the  trophic  joint  changes  of  tabes. 

Symptoms  and  Clinical  Forms. — Leprosy  shows  itself  under  an  extreme 
variety  of  forms.  Its  beginning  is  very  insidious  and  at  first  the  progress 
is  very  slow.    Even  after  a  number  of  years  the  lesions  may  be  very  insig- 


348  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

riificant  and  not  at  all  conclusive  to  the  casual  observer.  The  incubation 
period  is  uncertain,  and  is  usually  accepted  as  very  long.  The  average 
incubation  is  assumed  to  be  between  two  and  three  years,  although  cases 
are  reported  in  which  it  is  supposed  to  have  lasted  from  ten  to  twenty-seven 
years;  these  prolonged  instances  must  be  viewed  with  suspicion  as  to  their 
accuracy.  In  many  other  cases  periods  as  brief  as  from  three  or  four  weeks 
to  three  or  four  months  are  given.  It  will  be  recalled  that  the  incubation 
of  the  Hawaiian  inoculation  case  was  four  weeks. 

Another  disputed  point  in  the  symptomatology  of  leprosy  is  the  existence 
of  the  primary  sore  or  the  leprous  chancre,  as  it  has  been  called.  It  has 
been  shown  that  all  evidence  points  to  direct  inoculation  as  the  source  of 
leprosy,  and  it  is  not  unreasonable  to  assume  a  primary  sore  at  the  point 
of  inoculation  of  the  germ.  Many  observers  hold  that  such  a  sore  does 
occur,  and  that  in  a  large  majority  of  cases  it  is  located  on  the  nasal  septum. 
Thus,  Stickler  was  able  to  demonstrate  ulceration  of  the  septum  in  128 
out  of  153  early  cases. 

Leprosy  begins  with  marked  prodromata,  of  which  fever  is  the  most 
common.  It  comes  in  crises  of  several  days'  duration  and  is  usually  mistaken 
for  malaria.  It  is  entirely  analogous  to  the  pre-eruptive  fever  of  syphilis. 
Head  and  joint  pains  are  common  as  well  as  general  malaise,  with  frequent 
drenching  and  exhausting  sweats  unassociated  with  fever.  Epistaxis  is  a 
common  and  early  symptom  and  corroborates  Stickler's  observation  of  the 
existence  of  a  primary  ulcer  in  the  nose.  After  lasting  from  a  few  months 
to  two  years,  an  unusually  severe  attack  of  fever  ushers  in  the  primary 
eruption  or  macidar  stage  of  leprosy. 

Macular  eruptions  consist  in  erythematous  patches,  smooth,  shiny,  and 
slightly  elevated.  They  occur  all  over  the  body,  but  are  more  profuse  on 
the  face,  the  backs  of  the  hands,  and  forearm.  The  supraorbital  ridges 
and  malar  prominences  are  commonly  affected.  The  hairy  scalp  is  not 
invaded.  The  patches  come  and  go,  although  the  later  crops  show  a  tendency 
to  persist  and  for  the  skin  to  become  slightly  thickened.  When  the  macules 
invade  the  hairy  portion  of  the  body,  the  hair  is  lost  or  becomes  white  and 
downy.  The  macules  are  anaesthetic,  particularly  in  the  centre  of  the 
patches. 

Next  follows  the  stage  of  development  of  the  leprous  nodules  or  the 
deposit  of  specific  leprous  infiltration.  Here  the  disease  may  be  broadly 
divided  into  three  clinical  types:  first,  tuberculous  or  nodular  leprosy,  in 
which  the  skin  and  mucous  membrane  are  invaded  by  the  specific  new- 
growth;  second,  the  anaesthetic  or  nerve  leprosy,  where  the  leprous  deposits 
take  place  in  the  nerve  trunk;  third,  the  mixed  type  of  leprosy,  which 
combines  both  of  the  foregoing  and  to  which  class  all  cases  ultimately  tend. 

Tuberculous  or  nodular  leprosy  may  begin  with  or  without  the  mac- 
ular stage.  The  leprous  nodules  appear  under  the  skin,  particularly  about 
the  face  and  ears;  the  nodules  are  palpable  as  distinct,  tough,  flattened  masses 
under  the  skin.  They  have  a  peculiar,  rubbery  consistence,  are  painless, 
and  freely  movable.  Diffuse  infiltration  of  the  skin  takes  place,  and  large, 
flat,  leprous  patches  are  formed.  The  leprous  lesions  grow  steadily  larger, 
until  on  the  face  large  folds  and  masses  of  tissue  are  formed,  producing  the 


LEPROSY  349 

condition  known  as  Leontiasis,  or  the  lion-like  face  of  le'prosy.  New  nodules 
appear  and  other  portions  of  the  body  are  invaded  until  practically  the 
leprous  lesions  cover  the  entire  skin  surface.  In  the  early  stages  the  nodules 
occasionally  diminish  in  size  or  may  be  entirely  absorbed.  Later  they 
break  down  and  extensive  ulceration  occurs.  At  this  stage  the  mucous 
membrane  becomes  extensively  involved.  The  cartilaginous  structures  of 
the  nose  are  completely  lost,  and  leprous  ulcerations  of  the  larynx  occur, 
with  loss  of  voice  and  ultimately  cicatricial  stenosis,  which  may  cause  intense 
dyspnoea.  Extension  of  the  leprous  ulceration  into  the  corneal  structures 
may  cause  blindness.  The  ulcerations  produce  horrible  and  characteristic 
deformity. 

Death  takes  place  from  exhaustion  or  intercurrent  infection. 

Anesthetic  Leprosy. — Anaesthetic  leprosy  shows  a  very  different  picture 
from  the  foregoing.  The  macular  stage  continues  and  is  marked  by  increased 
'pigmentation  and  complete  anoesthesia  of  the  macule.  Gradually  extensive 
neuritis  is  developed  in  the  trunks  of  various  nerves,  causing  pain,  severe 
and  neuralgic  in  character,  and  later  large  areas  of  anaesthesia  or  numbness. 
The  superficial  nerve  trunks,  the  posterior  auricular,  and  the  ulnar  where 
it  winds  about  the  internal  condyle,  are  palpably  thickened.  Bullous  erup- 
tions occur  on  the  hands,  feet,  and  elbows,  and  along  the  course  of  the 
nerves  breaking  down  and  leaving  extensive  spreading  and  destructive  trophic 
ulcers.  As  a  further  result  of  these  trophic  disturbances  extensive  con- 
tractures develop,  and  fingers  and  toes  slough  away.  In  the  older  cases  the 
areas  in  the  distribution  of  the  affected  nerves,  which  at  the  beginning  of 
the  disease  were  painful  or  numb,  become  completely  anaesthetic  and  the 
muscles  become  extensively  atrophied.  When  this  condition  occurs  in  the 
hand,  a  typical  claw-like  hand  of  leprosy  is  produced.  The  atrophied  skin 
is  particularly  prone  to  injuries  and  to  extensive  ulceration.  The  course 
of  this  type  of  leprosy  is  excessively  chronic. 

The  mixed  leprosy  presents  a  combination  of  the  features  of  tuberculous 
and  anaesthetic  leprosy.  In  all  cases  of  extensive  tuberculous  leprosy  the 
nerve  trunks  eventually  become  involved,  and  the  evidences  of  neuritis  and 
trophic  disturbances  are  added  to  the  clinical  picture. 

Diagnosis. — In  advanced  cases  leprosy  could  hardly  be  mistaken  for  any 
other  disease.  The  lesions  are  too  striking  and  distinctive.  Difficulties  in 
diagnosis  arise  in  early  undeveloped  cases,  particularly  in  the  macular  and 
anaesthetic  types.  Here,  as  Manson  says,  the  touchstone  of  diagnosis  is  the 
anaesthesia.  It  should  be  sought  for  in  the  centre  of  macular  areas,  and  in  the 
centre  of  recent  nodules,  if  any  exist.  Advantage  may  also  be  taken  of 
the  fact  that  leprous  areas  do  not  perspire.  Baelz  uses  an  ingenious  plan  not 
only  for  diagnosis,  but  also  for  mapping  out  the  involved  areas.  Aniline 
is  rubbed  on  the  skin  and  pilocarpine  is  administered  hypodermically.  The 
leprous  areas  do  not  sweat  and  consequently  remain  unstained. 

The  most  satisfactory  diagnosis  consists  in  identification  of  the  bacilli.  For 
this  purpose  a  leprous  nodule  may  be  clamped,  punctured  with  a  needle, 
and  the  exuding  drop  of  fluid  properly  stained  and  examined.  Even  in  the 
very  earliest  cases,  long  before  other  symptoms  appear,  leprous  thickening 
can  be  demonstrated  in  the  ulnar  or  posterior  auricular  nerves.    In  doubtful 


350  DISEASES  DUE   TO   A    SPECIFIC  INFECTION 

cases  the  minute  fragment  of  one  of  these  nerves  should  be  excised  and 
stained  for  the  baciUi. 

Morrow  calls  attention  to  the  fact  that  leprosy  and  nasal  catarrh  go  hand 
in  hand,  and  that  in  the  large  proportion  of  cases  bacilli  can  be  demon- 
strated in  the  nasal  secretion.  It  has  also  been  shown  that  where  nasal 
secretion  is  scanty  a  few  doses  of  potassium  iodide  will  cause  a  sharp 
catarrhal  flow,  in  which  the  bacilli  may  be  demonstrated. 

Prognosis, — In  the  vast  majority  of  cases  leprosy  slowly  tends  to  a  fatal 
ending  from  exhaustion  or  intercurrent  infection.  Isolated  cases,  however, 
occur  in  which  the  disease  is  arrested  or  cured.  These  instances  of  arrest 
are  more  common  in  anaesthetic  leprosy  than  in  the  tuberculous  type.  Many 
of  these  cases  survive  twenty  or  thirty  years,  and  in  a  large  proportion  of 
these  the  specific  process  is  probably  ended,  although  the  extensive  damage 
by  nerve  involvement  and  trophic  lesions  remain.  Even  tuberculous  leprosy 
has  been  known  to  disappear. 

Many  cases  are  arrested,  and,  after  a  long  period  of  years,  death  occurs 
from  some  other  disease  not  associated  with  the  leprosy.  These  reported 
cures  must,  however,  be  accepted  with  extreme  caution.  It  is  probably 
more  fair  to  speak  of  them  as  arrests.  Mention  must  also  be  made  of 
the  marked  amelioration  that  occasionally  follows  the  removal  of  a  leper 
from  the  country  in  which  he  has  developed  the  disease. 

Treatment. — The  treatment  of  leprosy  comprises  careful  attention  to 
cleanliness,  provision  of  good  hygienic  surroundings,  abundance  of  nourish- 
ing food,  proper  clothing,  hygienic  dwellings,  and  light  occupation.  As 
special  remedies  gurgun  oil  and  chaulmoogra  oil  have  been  extensively 
used.  The  former  has  been  abandoned.  Chaulmoogra  oil  (oleum  gyno- 
cardii)  may  be  administered  by  the  mouth  in  doses  of  2  drachms,  or  by  the 
rectum,  in  an  emulsion  with  hot  milk,  when  it  is  badly  borne  by  the  stomach. 
In  some  cases  this  drug  seems  to  have  almost  a  specific  action.  In  a  few 
cases  apparent  cures  and  in  a  great  many  cases  very  marked  improvement 
is  observed.    The  oil  may  also  be  administered  hypodermically. 

Unna  advises  the  internal  use  of  massive  doses  of  ichthyol  combined  with 
inunction  of  pyrogaUic  and  chrysophanic  acid  externally.  The  treatment 
is  supplemented  by  hot  baths.  Several  cures  have  been  reported  following 
this  plan.  Crocker  reports  improvement  from  subcutaneous  injection  of  the 
bichloride  of  mercury,  and  De  Luca  from  intravenous  injections  of  mercury 
according  to  Bacelli's  method.  Raynaud  reports  marked  improvement  fol- 
lowing the  administration  of  sodium  cacodylate.  Roussel  reports  an  apparent 
cure  following  the  administration  of  potassium  chlorate,  and  Manson  a  case 
of  nerve  leprosy  apparently  cured  by  thyroidin.  Tuberculin,  antivenene, 
and  the  iodides  have  been  used  and  do  more  harm  than  good.  Danielsen 
recommends  salicylate  of  soda  in  ascending  doses  combined  with  tonics. 
He  believes  that  it  cures  leprosy  if  administered  early.  Baelz  uses  salicylic 
acid  locally.  He  treats  about  one  square  foot  of  skin  at  a  time  by  rubbing 
the  diseased  area  with  pummice  stone  until  blood  appears.  Salicylic  acid 
is  then  applied  in  a  20  per  cent,  ointment  with  lanolin  and  vaselin.  This 
treatment  is  combined  with  the  oil  of  gynocardium  internally  and  hot 
baths. 


FEBRICULA  351 

Nerve  stretching  has  been  recommended  and  practised  for  the  rehef  of  the 
painful  comphcations  and  trophic  disturbances  of  nerve  leprosy. 

Prophylaxis. — The  only  means  of  limiting  leprosy  is  by  isolation.  While 
absolute  segregation  is  the  ideal  and  proper  measure,  it  meets  with  so 
much  opposition,  and  so  many  cases  are  concealed,  that  in  the  long  run  a 
better  purpose  is  served  by  adopting  a  reasonable  compromise  similar  to 
that  followed  in  Norway.  This  includes  caring  for  indigent  lepers  in  an 
asylum  and  allowing  those  whose  people  are  able  to  take  care  of  them  to 
do  so  at  their  homes  under  proper  restrictions.  The  Russian  laws  only 
isolate  the  tuberculous  and  mixed  cases.  Although  it  is  true  that  the  nerve 
cases  are  much  less  contagious,  this  regulation  must  be  regarded  as  a 
mistake. 

FEBRICULA. 

Definition. — Febricula,  sometimes  called  ephemeral  fever,  is  a  condition 
usually  met  with  in  children,  and  is  undoubtedly  a  disturbance  of  the  heat 
mechanism  of  the  body  produced  by  the  action  not  of  one  but  of  several 
agents;  that  is  to  say,  many  different  causes  are  responsible  for  it  rather 
than  one  specific  cause. 

Etiology. — The  causes  of  febricula  are  very  numerous.  In  some  instances 
it  is  probably  the  result  of  some  infection  which  is  overcome  by  the  pro- 
tective process  of  the  body  before  it  can  develop  into  a  full-fledged  disease, 
such,  for  example,  as  an  aborted  influenza,  or  even  one  of  the  specific 
eruptive  fevers,  or  some  infection  entering  by  the  tonsils.  Some  years  ago 
physicians  believed  that  infectious  diseases  could  be  aborted  in  their  early 
stages  by  proper  measures  designed  to  aid  nature.  This  view  fell  into 
disrepute,  but  our  knowledge  of  protective  processes  and  of  antitoxic  bodies 
makes  it  probably  true.  In  children  an  ephemeral  fever  is  often  due  to 
gastrointestinal  catarrh.  Sometimes  it  is  due  to  gastrointestinal  intox- 
ication. 

Symptoms. — The  patient  after  a  feeling  of  wretchedness,  rarely  lasting 
more  than  a  few  hours,  is  found  to  be  mildly  febrile,  the  temperature  being 
about  102°  to  103°  at  the  most.  There  may  be  flushing  of  the  face  and 
even  delirium  in  young  neurotic  children.  The  jpulse  and  respirations  are 
quickened.  The  fever  usually,  but  not  always,  ends  by  lysis  in  about  three 
days  to  a  week. 

Diagnosis. — The  diagnosis  of  febricula  is  made  in  most  instances  after  the 
patient  is  well,  for  until  then  no  one  can  tell  that  the  symptoms  are  not  the 
early  signs  of  one  of  the  acute  infectious  fevers.  The  important  point  is, 
not  to  be  content  with  a  diagnosis  of  febricula,  which  is  but  another  way 
of  saying  that  the  condition  is  uncertain,  but  to  search  carefully  for  the 
real  cause. 

Treatment. — This  consists  in  rest  in  bed,  the  use  of  a  little  calomel  followed 
by  a  saline,  and  the  employment  of  a  mixture  of  citrate  of  potassium  and 
sweet  spirit  of  nitre  to  keep  the  kidneys  active. 


352  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 


MILK  SICKNESS. 

Definition. — Milk  sickness  is  a  disease  which  is  usually  communicated  to 
man  by  the  milk,  or  by  the  butter  or  cheese  made  from  the  milk  of  cows 
ill  of  a  malady  called,  when  it  affects  cattle,  "trembles,"  or  "slows." 
When  man  is  infected  it  is  given  this  name  and  the  additional  one  of  "  puking 
fever."  The  malady  is  one  which  exists  in  the  Southwestern  United  States, 
and  apparently  does  not  affect  animals  on  the  Atlantic  seaboard.  It  is  said 
that  the  flesh  of  affected  animals,  if  not  cooked,  may  convey  the  infection. 
It  is  important  to  know  that  the  infection  may  be  transmitted  from  a 
seemingly  healthy  cow  some  time  before  it  develops  symptoms  of  the 
disease. 

Symptoms. — The  symptoms  in  the  cow  consist  in  refusal  to  eat,  redness 
of  the  conjunctiva,  staggering  gait,  and  muscular  tremors,  whence  the  name 
"trembles."  In  man,  after  a  day  or  two  of  ill-health,  the  patient  is  seized 
with  epigastric  distress,  followed  by  vomiting  and  consti'pation,  fever,  and 
thirst.  Muscular  tremors  also  appear.  The  breath  is  peculiarly  foul  and 
offensive  and  the  tongue  swollen.  If  the  disease  is  severe  the  patient  may 
develop  typhoid  symptoms,  and  even  become  delirious,  comatose,  or  con- 
vulsed. In  fatal  cases  death  may  come  as  early  as  the  fourth  day,  or  be 
deferred  for  two  or  three  weeks.  The  more  severe  the  cerebral  symptoms, 
the  more  grave  the  prognosis. 

Treatment. — The  treatment  is  purely  symptomatic  and  consists  in  the 
use  of  stimulants  or  sedatives  as  they  may  be  needed. 

WEIL'S  DISEASE. 

Weil's  disease  is  a  very  rare  infectious  malady,  first  described  by  Weil 
in  1886,  which  for  some  unknown  reason  seems  particularly  prone  to  attack 
butchers.  It  is  characterized  by  the  development  of  fever  and  acute  jaundice, 
and  appears  usually  in  the  warm  months  of  the  year.  The  victims  of  its 
onset  are  usually  young  and  middle-aged  adults,  and  the  symptoms  are 
severe  headache,  lumbar  pain,  and  cramp-like  sensations  in  the  legs  and 
arms.  The  masseter  muscles  also  suffer  from  severe  pains.  Jaundice 
develops  as  an  early  symptom,  and  the  liver  and  spleen  are  found  swollen 
and  tender  on  deep  palpation.  The  stools  may  be  putty-colored,  as  if  from 
obstruction  of  the  gall-ducts.  The  fever  may  last  two  weeks,  often  rises 
to  103°  or  104°,  and  is  characterized  by  sharp  remissions,  as  in  sepsis. 
Albuminuria  may  occur,  and  even  coma  may  develop.  Recovery  usually 
takes  place,  but  convalescence  is  slow. 

Weil's  disease  must  be  separated  from  bilious  remittent  fever,  catarrhal 
jaundice,  and  phosphorus  poisoning.  This  separation  is  readily  accom- 
plished if  the  characteristic  symptoms  just  described  are  compared  to  those 
presented  in  the  course  of  these  conditions.  Remittent  fever,  which  is  the 
malady  most  closely  resembling  Weil's  disease,  is  differentiated  by  finding 
the  sestivo-autumnal  parasite  in  the  blood,  and  phosphorus  poisoning 
by  the  history  of  the  case  and  the  phosphorescent  character  of  the  vomit, 


GLANDULAR  FEVER  353 

which  can  be  noted  if  it  is  examined  in  the  dark.     Treatment  is  entirely 
symptomatic. 

GLANDULAR  FEVER. 

Definition. — Glandular  fever  is  an  acute  infectious  disease  characterized 
by  a  moderate  febrile  movement  and  a  painful  enlargement  of  the  cervical 
lymphatic  glands. 

History. — The  first  accurate  account  of  this  disease  was  published  in  1889 
by  Pfeiffer,  although  it  is  probable  that  the  condition  described  some  years 
before  by  Filatow,  of  Moscow,  under  the  name  of  idiopathic  inflammation 
of  the  cervical  glands,  was  in  reality  glandular  fever. 

Cases  have  been  reported  from  different  countries  on  the  Continent,  and 
from  England  and  the  United  States.  J.  Park  West,  of  Bellaire,  Ohio,  has 
reported  an  epidemic  in  which  ninety-six  children  were  attacked,  this  being 
the  most  extensive  epidemic  on  record. 

Etiology. — The  specific  micro-organism  of  this  disease,  if  there  be  one, 
has  not  been  discovered,  but  that  the  disease  is  infectious  in  nature  is  shown 
by  the  fact  of  its  occurrence,  as  a  rule,  in  small  epidemics  involving  several 
members  of  a  family.  The  disease  generally  occurs  before  puberty,  although 
Galvagni  and  A.  E.  Roussel  have  observed  it  in  adults. 

Symptoms. — The  onset  is  sudden  and  is  characterized  by  moderately  high 
jever,  restlessness,  headache,  pain  in  the  limbs,  and  soreness  and  pain  in 
the  neck,  which  is  increased  by  turning  the  head  or  by  swallowing.  The 
temperature  ranges  from  101°  to  103°  and  may  even  go  as  high  as  104°. 
The  bowels  are  usually  constipated,  although  in  some  of  the  severe  cases 
observed  by  West  copious  discharges  of  thin,  green  feces  mixed  with  mucus 
took  place  shortly  before  the  beginning  of  convalescence.  Abdominal  pain 
is  a  common  symptom,  and  pressure  over  the  lower  part  of  the  abdomen, 
particularly  in  the  midline  between  the  umbilicus  and  the  symphysis  pubis, 
often  elicits  pronounced  tenderness.  The  swelling  of  the  anterior  cervical 
glands,  which  usually  begins  on  the  left  side  and  then  extends  to  the  right, 
attains  its  maximum  between  the  second  and  fourth  days.  The  glands  are 
hard,  easily  distinguishable  from  one  another  by  palpation,  and  are  very 
sensitive  to  pressure.  Suppuration  rarely  occurs.  Examination  of  the 
pharynx  reveals  either  a  normal  condition  or  a  slight  hypersemia.  The 
liver  is  always  enlarged,  and  not  uncommonly  there  is  considerable  swelling 
of  the  spleen.  Acute  nephritis  is  the  most  frequent  and  most  serious  compli- 
cation. The  duration  of  glandular  fever  is  variable.  European  physicians 
have  described  a  mild  or  abortive  form  in  which  the  temperature  falls  to 
normal  on  the  second  or  third  day,  although  the  cervical  glands  remain 
swollen  several  days  longer.  The  average  febrile  period,  however,  is  from 
seven  to  ten  days.  In  West's  ninety-six  cases  the  average  duration  of  the 
disease  from  its  onset  until  the  complete  disappearance  of  glandular  swelling 
was  sixteen  days. 

Diagnosis. — The  occurrence  of  a  sudden  febrile  attack  accompanied  by 
an  early,  painful  enlargement  of  the  anterior  cervical  lymph  glands,  without 
any  inflammatory  involvement  of  the  pharynx,  makes  recognition  of  the 
disease  easy. 
23 


354  DISEASES  DUE   TO  A   SPECIFIC  INFECTION 

Prognosis. — Prognosis  is  always  favorable.  Convalescence  is  rapid,  as  a 
rule,  although  in  some  instances  it  is  retarded  by  a  considerable  degree  of 
depression  and  anaemia. 

Treatment. — Experience  has  demonstrated  that  there  is  no  drug  which 
will  influence  the  duration  or  course  of  this  disease.  The  patient  should 
be  confined  to  bed  and  a  mild  aperient  given  to  overcome  constipation 


MOUNTAIN  FEVER. 

So-called  mountain  fever  really  does  not  exist  as  a  separate  entity.  It 
has  been  proved  to  be  an  aberrant  form  of  typhoid  fever  infection  in  a 
number  of  instances,  particularly  by  the  United  States  Army  surgeons  or 
those  attached  to  the  United  States  Health  and  Marine  Hospital  Service. 
In  some  cases  the  infection  may  be  paratyphoid.  (See  Paratyphoid  Fever.) 
In  still  other  instances  the  fever  may  be  due  to  an  anaemia  depending  upon 
intestinal  parasites  such  as  the  Anchylostomum  duodenale.  Some  cases 
may  be  "tick  fever."     (See  below.) 


TICK  FEVER. 

Definition. — Under  the  name  of  "tick"  or  "spotted  fever,"  a  febrile 
malady  has  been  carefully  described  within  the  last  few  years.  It  is 
prevalent  in  Western  Montana,  particularly  among  the  eastern  foothills  of 
the  Bitter  Root  Mountains.  Curiously  enough,  it  is  chiefly  limited  to  the 
western  side  of  the  Bitter  Root  Valley,  in  an  area  from  four  to  ten  miles  wide 
and  fifty  miles  long.  Fewer  and  milder  cases  occur  in  Idaho,  Wyoming, 
Nevada,  and  Oregon,  at  a  level  of  from  3000  to  4000  feet.  Its  occurrence 
is  limited  to  the  period  of  from  the  middle  of  March  until  the  middle  of 
July.    Herders  and  ranchmen  are  usually  the  persons  affected. 

This  form  of  so-called  spotted  fever  is  not  to  be  confused  with  cerebro- 
spinal meningitis. 

Etiology. — According  to  the  studies  of  Wilson  and  Chowning,  and  of 
Anderson,  this  disease  is  due  to  a  parasite  which  is  conveyed  to  man  by 
the  bite  of  the  tick.  To  this  parasite  they  gave  the  name  Pyroplasma 
hominis,  and  therefore  suggested  that  tick  fever  be  called  pyroplasmosis 
hominis.  According  to  these  observers  this  parasite  in  its  smallest  form 
slightly  resembles  the  small  hyaline  bodies  of  malarial  fever,  but  it  is  at 
no  time  pigmented.  Stained  with  Laveran's  or  Nocard's  stain  chromatin 
masses  are  seen,  as  a  rule,  near  one  end  of  the  parasite.  It  appears  free 
in  the  blood  or  in  the  body  of  a  red  corpuscle.  Often  two  parasites  are 
present  in  one  blood  cell,  but  rarely  more  than  this.  They  may  be  joined 
together  by  their  lesser  extremities,  either  when  in  the  corpuscle  or  when 
floating  free  in  the  blood.  Sometimes  the  so-called  parasite  seems  to  change 
its  position  in  a  blood  cell,  but  no  amoeboid  movement  has  been  seen. 

In  the  second  phase  of  its  development  the  organism  in  the  red  blood 
corpuscle  appears  to  be  solitary  and  distinctly  larger  than  in  the  first  phase 


TICK  FEVER  355 

just  described.  During  this  stage  of  its  development  they  claim  that  it  also 
presents  active  amoeboid  movements. 

The  red  cells  of  the  general  circulation  are  not  infected  in  great  numbers, 
but  if  the  blood  in  the  capillaries  of  congested  tissues  is  examined,  it  is 
found  that  a  large  number  of  the  red  cells  have  become  infected.  The 
greatest  degree  of  corpuscular  infection  is  said  to  be  met  with  in  the  spleen, 
liver,  lungs,  and  kidneys. 

Since  these  observations  of  Wilson  and  Chowning,  Stiles  and  Craig 
claim  to  have  proved  the  non-existence  of  these  so-called  parasites,  the 
former  asserting  his  inability  to  discover  any  structures  which  lead  him 
to  a  belief  in  the  presence  of  a  protozoon  as  a  cause  of  the  malady.  Craig 
believes  that  the  changes  seen  by  Anderson  in  the  red  blood  cells  are  not 
due  to  a  parasite,  but  dependent  upon  certain  alterations  chiefly  taking 
place  in  the  haemoglobin,  such  as  are  often  seen  during  the  course  of 
epidemic  influenza,  typhoid  fever,  measles,  variola,  and  other  acute  infec- 
tions. The  cause  of  this  disease,  if  indeed  it  ultimately  proves  to  be  a 
separate  entity,  is,  therefore,  at  present  of  uncertain  character,  the  more 
so  as  there  is  reason  to  believe  that  the  Pyroplasma  higeminum,  which  is 
the  organism  of  Texas  cattle  fever,  is  incapable  of  infecting  man. 

Symptoms. — The  disease  makes  its  appearance  in  from  three  to  ten  days 
after  the  bite,  with  chilly  sensations,  malaise,  nausea,  headache,  and  muscular 
soreness.  The  bowels  are  constipated,  the  conjunctiva  congested,  the  urine 
scanty  and  albuminous,  and  slight  bronchitis  occurs.  Epistaxis  is  a  constant 
symptom.  The  fever  rises  sharply  after  the  chill,  but  has  morning  remissions 
like  typhoid  fever.  The  rapidity  of  the  pulse  is  out  of  proportion  to  the 
fever,  often  amounting  to  110  or  140  per  minute,  and  there  is  a  very  moderate 
leukocytosis.     Respiration  is  rapid. 

Its  acme  is  reached  by  the  twelfth  day,  when  it  gradually  falls  by  lysis  for 
four  days  more,  and  so  convalescence  begins.  In  fatal  cases  the  fever  remains 
high,  about  104°  or  105°,  or  even  106°.  The  pulse  is  usually  very  rapid  and 
thready,  and  the  blood  rapidly  becomes  ancemic. 

The  rash  usually  develops  about  the  third  day  on  the  wrists,  arms,  legs, 
and  forehead,  and  later  on  the  back,  chest,  and  abdomen.  This  rash, 
except  on  the  abdomen,  is  often  exceedingly  profuse. 

The  skin  presents  an  eruption  of  bright-red  macules,  varying  from  a 
pinhead  to  a  split  pea  in  size,  and  in  severe  cases  they  become  petechial  in 
character.  They  fade  as  the  fever  falls,  and  the  skin  may  desquamate. 
Sometimes  in  the  later  stage  of  the  eruption  they  appear  like  the  marks  on 
a  turkey's  egg.  Anderson  states  that  slight  gangrene  of  the  fingers,  toes, 
and  scrotum  may  occur.    Albuminuria  is  a  constant  symptom. 

Diagnosis, — The  section  of  the  country  in  which  the  disease  occurs,  the 
history  of  tick  bites,  and  the  finding  of  the  changes  in  the  blood  are  the 
factors  which  make  the  diagnosis  positive.  From  ordinary  purpura  the  dis- 
ease is  separated  by  the  lack  of  sore  throat  and  the  absence  of  arthritis. 
From  typhoid  fever  the  diagnosis  may  be  quite  difficult.  In  that  disease, 
however,  the  rose  rash  appears  first  on  the  belly  on  the  ninth  to  the  twelfth 
day,  whereas  in  tick  fever  it  appears  as  early  as  the  third  day,  and  on  the 
wrists.     The  discovery  of  a  positive  Widal  test  in  the  blood  will  settle  the 


356  DISEASES  DUE   TO   A    SPECIFIC  INFECTION 

diagnosis.  Typhus  fever  is  conveyed  from  man  to  man;  tick  fever  is  not 
directly  transferred.  Typhus  fever  breaks  out  in  groups  of  persons.  Tick 
fever  always  appears  sporadically. 

Prognosis. — The  disease  is  a  very  grave  one,  for  out  of  126  cases  88  died, 
a  mortality  of  about  70  per  cent.  Sometimes  the  mortality  is  as  high  as 
90  per  cent.  Death  usually  ensues  about  the  sixth  to  the  twelfth  day  of 
the  illness,  but  it  may  occur  as  early  as  the  fourth  day.  Experience  with 
cases  which  have  occurred  in  Idaho,  Wyoming,  and  Nevada  shows  that 
the  mortality  is  far  less  in  those  States  than  in  Montana.     ^ 

Treatment. — So  far  as  is  known  quinine  seems  to  act  as  a  specific  in  this 
disease.  Anderson  thinks  it  should  be  given  in  the  dose  of  15  grains  every 
six  hours,  hypodermically,  and  its  use  continued  into  convalescence.  The 
heart  must  be  supported  by  stimulants  if  it  is  feeble,  and  the  kidneys  flushed 
by  copious  draughts  of  water.  The  tick,  if  found,  should  be  removed  from 
the  skin  and  the  part  cauterized  with  95  per  cent,  carbolic  acid  to  prevent 
infection,  if  possible. 


FOOT-AND-MOUTH  DISEASE. 

Definition. — This  is  an  acute  infectious  disease  of  herbivorous  animals, 
which  sometimes  attacks  omnivora  and  which  spreads  in  epidemic  form 
over  large  territories,  causing  great  mortality  in  the  animals  affected.  When 
the  disease  attacks  the  cow  the  animal  becomes  feverish,  suffers  from  swell- 
ing of  the  mucous  membranes  of  the  mouth,  and  develops  blisters  on  the 
edges  of  the  tongue  and  on  the  lips.  These  blisters  become  discolored  and 
rupture,  leaving  ulcers.  At  times  similar  lesions  appear  on  the  teats.  The 
milk  of  such  animals  is  discolored  and  seems  to  be  thickened  as  if  by  mucus. 

The  disease  is  rarely  met  with  in  England  and  America,  and  only  possesses 
interest  to  us,  because  it  is  capable  of  being  conveyed  to  man.  This  convey- 
ance occurs  in  the  case  of  children  by  the  use  of  the  milk  of  the  diseased  cows, 
and  in  adults,  as  a  rule,  by  this  means  or  by  cheese  or  butter. 

The  symptoms  in  man  are  like  those  of  severe  stomatitis,  associated  with 
fever.  Recovery  in  man  usually  occurs,  but  a  mortality  of  about  10  per  cent, 
is  recorded. 

The  cause  of  the  disease  has  not  been  isolated.  Even  a  porcelain  filter 
does  not  arrest  the  organism,  if  organism  it  be,  that  causes  the  malady. 


MILIARY  FEVER. 

Definition. — Miliary  fever,  sometimes  called  "the  sweating  sickness,"  is 
an  acute  epidemic  disease  characterized  by  fever,  profuse  sweating,  an  erup- 
tion, and  a  peculiar  sense  of  constriction  in  the  epigastrium. 

History. — The  disease  was  far  more  prevalent  in  the  seventeenth  century 
than  it  has  been  since  that  time,  but  it  still  appears  in  certain  parts  of  the 
world.  Almost  every  country  in  Europe,  including  England,  has  suffered 
from  its  presence,  but  it  has  not,  so  far  as  I  have  been  able  to  discover,  ever 


JAPANESE  RIVER  FEVER  357 

appeared  in  the  United  States.     The  most  recent  epidemics  have  been  in 
Austria  in  1892  and  in  Styria  in  1893. 

Etiology. — The  cause  of  the  disease  is  unknown,  but  it  is  an  acute  infection, 
apparently  resembUng  influenza  in  the  manner  of  its  spread,  aUhough  it 
does  not,  as  a  rule,  attack  large  numbers  of  people  throughout  a  wide  area, 
as  does  that  disease.  On  the  contrary,  it  is  very  often  limited  to  the  popula- 
tion of  a  single  town  or  district. 

Symptoms. — The  symptoms  of  miliary  fever  are  ushered  in,  as  they  are  in 
all  the  infectious  diseases,  by  lassitude,  headache,  and  anorexia.  This  pro- 
dromal stage  may  last  a  day  or  two  or  be  so  brief  as  not  to  be  recognized. 
The  patients  go  to  bed  well,  and  wake  in  the  morning  to  find  themselves 
ill  and  suffering  from  a  drenching  sweat,  which  persists  throughout  the 
illness.  The  bowels  are  usually  confined,  the  tongue  coated,  and  the  pulse 
but  little  altered  in  character  for  the  first  few  days  of  the  illness.  A  symptom 
complained  of  by  the  patient  is  one  of  oppression,  as  if  the  air  of  the  room 
were  hot  and  vitiated.  The  fever  is  usually  high,  rising  to  104°  to  105°,  and 
in  fatal  cases  to  107°.  On  the  third  day  there  appears  on  the  skin  an  out- 
break of  red  miliary  papules,  which  often  develop  a  white  tip  before  they 
disappear,  and  between  these  are  scattered  large  numbers  of  pearly  vesicles, 
like  sudamina,  which  seem  filled  with  clear  fluid.  Prior  to  the  appearance 
of  this  eruption  a  peculiar  pricking  or  tingling  sensation  is  felt  in  the  skin. 
When  the  eruption  has  faded,  desquamation  sometimes  occurs.  The  entire 
progress  of  the  malady  is  usually  completed  in  nine  or  ten  days. 

The  following  facts  are  also  noteworthy,  viz.:  The  sweating  is  constant, 
but  is  characterized  by  paroxysms,  in  which  it  becomes  still  more  profuse. 
The  rash  appears  on  the  mucous  membrane  of  the  palate  and  cheeks.  The 
sudamina,  or  pearly  miliary  vesicles,  although  they  give  the  name  to  the  dis- 
ease, are  not  a  constant  symptom  in  all  cases. 

Abortion  nearly  always  occurs  if  a  pregnant  woman  is  attacked. 

Miliary  fever  causes  rapid  emaciation. 

It  is  very  prone  to  be  followed  by  a  relapse,  but  the  relapse  is  rarely  fatal. 

Prognosis. — Recovery  usually  occurs.  In  severe  cases,  in  which  the  onset 
is  fulminating,  death  may  occur  as  early  as  the  eighth  hour  after  the  attack 
begins.  These  cases  have  marked  nervous  symptoms,  consisting  of  convul- 
sions, delirium,  and  coma.  Evidently  the  patient  is  overwhelmed  by  tox- 
aemia. The  mortality  rate  in  various  epidemics  has  varied  from  5  to  25  per 
cent.    The  outlook  in  children  is  usuafly  good. 

Treatment.— This  consists  of  cold  sponging  to  control  excessive  fever,  the 
use  of  copious  draughts  of  water  to  compensate  for  the  loss  of  water  by  the 
skin,  and  for  the  purpose  of  flushing  the  kidneys,  and  in  the  administration 
of  stimulants,  if  they  are  needed,  to  support  the  heart. 


JAPANESE  RIVER  FEVER. 

Definition. — Japanese  river,  or  flood  fever,  is  an  acute,  infectious  disease, 
occurring  in  a  very  limited  area  in  the  island  of  Nippon,  beginning  with  a 
necrotic  ulcer,  attended  by  an  exanthem  and  continued  fever. 


358  DISEASES  DUE  TO  A  SPECIFIC  IX  FECI  ION 

The  disease  occurs  in  laborers  who  cukivate  the  inundated  bottom  lands 
of  several  rivers  on  the  west  coast  of  the  island  of  Nippon. 

Etiology. — The  etiology  is  obscure.  The  infection  is  evidently  carried  in 
the  corn  and  hemp  grown  in  these  sections,  and  the  primary  eschar  probably 
marks  its  point  of  entrance.  The  Japanese  ascribe  the  disease  to  the  bite  of 
a  small  acarus.  Baelz  denies  this.  Given  equal  exposure,  neither  age  nor 
sex  shows  any  difference  in  susceptibility  to  the  disease. 

Symptoms. — After  several  days  of  vialaise  and  repeated  rigors,  the  disease 
begins  with  the  breaking  out  of  a  small,  round  eschar  in  the  groin,  axilla, 
or  neck.  The  neighboring  lymphatic  trunks  and  glands  become  swollen, 
hard,  and  painful.  A  continued  fever  ranging  between  103°  and  104° 
develops,  with  bronchial  cough  and  marked  conjunctivitis.  About  the  sixth 
day  a  coarse,  red,  papular  eruption  appears  on  the  face,  forearms,  legs,  and 
trunk.  This  eruption  fades  away  in  from  one  to  seven  days.  The  fever 
lasts  a  week  longer,  when  it  falls  rather  rapidly,  and  convalescence  begins 
with  a  separation  of  the  eschar  from  the  primary  sore.  The  mortality  varies 
between  15  and  70  per  cent,  in  different  epidemics.  No  definite  postmortem 
changes  are  found,  beyond  congestion  of  the  bronchi,  occasional  hypostatic 
pneumonia,  marked  enlargement  of  the  spleen,  and  swelling  of  the  mesen- 
teric glands. 

Treatment. — Treatment  is  symptomatic.  Baelz  advises  ciuinine  and  sali- 
cylates as  antip}Tetics  to  be  used  with  caution. 


FRAMBESIA  (FRAME (ESIA  TROPICA,  YAWS). 

Definition. — Frambesia,  or  yaws,  is  a  chronic  contagious  and  infectious 
disease,  characterized  by  the  appearance  of  a  diffuse  granulomatous  erup- 
tion on  the  skin. 

History. — The  history  of  yaws  begins  with  the  historians  of  the  Spanish 
conquest  of  America.  It  is  a  disease  very  closely  confined  to  tropical  coun- 
tries and  very  widely  distributed  in  xAfrica,  in  the  coast  countries  of  trop- 
ical Asia,  and  in  many  of  the  Pacific  islands.  It  also  occurs  in  Central  and 
tropical  South  America  and  the  Antilles.  The  disease  was  exceedingly  com- 
mon in  Cuba  and  the  southern  United  States  during  the  first  half  of  the 
nineteenth  century,  having  been  brought  there  during  the  slave-trading  days. 
At  one  time  it  caused  such  a  degree  of  disability  among  the  negroes  that  the 
planters  were  forced  to  adopt  stringent  rules  for  its  limitation.  ^Nlost  of  the 
large  plantations  maintained  isolation  barracks,  or  "yaw  houses,"  for  these 
cases.  The  disease  still  lingers  in  Cuba  and  the  rest  of  the  Antilles.  It  has 
all  but  disappeared  from  the  United  States. 

Etiology. — ]Many  bacterial  forms  have  been  isolated  from  yaw  lesions,  but 
as  yet  the  specific  cause  has  not  been  determined.  The  disease  can  be,  and 
frequently  is,  conveyed  by  direct  inoculation,  intentional  or  accidental.  Such 
inoculation  may  take  place  in  wounds,  abrasions,  and  other  injuries  of  the 
skin.  In  some  yaw  countries,  notably  in  Fiji,  it  is  a  common  practice  for 
mothers  to  inoculate  their  children,  under  the  same  idea  which  prevails 
among  our  lower  classes,  who  frequently  expose  their  children  to  pertussis  and 


FRAMBESIA  359 

eruptive  diseases,  on  the  theory  that  the  illness  must  be  gone  through  with 
some  time,  and  the  earlier  the  better.  Heredity  has  no  bearing  on  the  etiology 
of  yaws.  Neither  does  a  pregnant  or  nursing  woman  wath  yaws  necessarily 
infect  her  child.  Outside  of  direct  inoculation  the  disease  is  conveyed  by 
food,  particularly  by  cooking  utensils.  In  persons  particularly  susceptible, 
infection  may  take  place  by  sleeping  in  a  yaw  house.  All  ages  are  attacked, 
but  the  majority  of  cases  are  seen  in  children.  The  black,  yellow,  and  white 
races  are  susceptible  in  the  order  named.  As  a  rule,  one  attack  confers  com- 
plete immunity.    Frambesia  is  also  seen  in  domestic  fowls. 

Symptoms. — The  incubation  period  of  yaws  is  very  variable.  Generally 
speaking,  in  inoculation  cases,  it  varies  between  fifteen  and  twenty  days.  In 
cases  ordinarily  acquired,  the  incubation  is  longer,  ranging  from  fourteen  to 
sixty  days.  In  a  small  proportion  of  cases  prodromal  symptoms,  languor, 
malaise,  headache,  and  rheumatic  fains  are  observed.  This  condition  is 
followed  by  what  is  known  as  the  primary  eruption  or  the  primary  sore,  con- 
cerning which  there  is  some  dispute  among  tropical  practitioners.  In  experi- 
mental inoculation  cases  the  primary  sore  is  constant  and  occurs  at  the  point 
of  inoculation.  It  begins  as  a  small  papule,  which,  in  the  course  of  a  week, 
is  converted  into  a  shallow  ulcer.  In  another  week  the  ulcer  heals,  leaving  a 
slight,  thickened  scar.  In  ordinary  infection  by  yaws  it  is  sometimes  present 
and  sometimes  absent. 

The  generalized  eruption,  the  so-called  secondary  eruption,  begins  with 
the  primary  sore  in  exceptional  cases,  but,  as  a  rule,  is  delayed  for  several 
weeks.  Occasionally,  in  the  period  between  the  eruption  of  the  primary  and 
secondary  lesions,  a  dry,  scaly  affection  of  the  skin  is  seen. 

The  secondary  eruption  begins  as  small  papules ,  which  itch  intensely.  They 
are  scattered  all  over  the  body,  but  are  most  commonly  seen,  in  order,  on 
the  face,  neck,  limbs,  genitals,  and  trunk.  The  hairy  scalp  is  not  commonly 
invaded;  the  axilla  very  rarely.  The  lesions  are  particularly  numerous  at 
the  mucocutaneous  borders,  the  mouth,  nose,  anus,  and  vulva.  The  erup- 
tion is  roughly  symmetrical.  The  papules,  at  first  the  size  of  a  pinhead  and 
slightly  prominent  imder  the  skin,  gradually  increase  in  size  till  they  are  as 
large  as  a  pea  or  a  hazelnut.  Small,  yellow  spots  of  pustulation  appear  on 
the  summit  of  the  lesions;  the  skin  cracks;  a  sticky,  yellow,  seropurulent  fluid 
exudes,  which  hardens  and  forms  rupia-like  crusts  or  caps  over  the  summit 
of  the  growths.  The  cap  is  tough  and  adherent.  When  it  is  pulled  off  it 
reveals  a  shiny,  red  papilloma  underneath.  This  warty  growth,  the  true 
yaw,  resembles  a  berry  in  appearance,  hence  the  name  yaw,  i.e.,  a  straw- 
berry; frambesia  from  framboise,  a  raspberry.  Indeed,  most  of  the  local 
native  names  for  the  disease  are  words  which  mean  berry  in  their  dialect. 

The  growths  resemble  syphilitic  condylomata  in  their  appearance.  They 
spring  from  the  papillary  layer  of  the  skin,  and  the  warty-like  lobulations 
represent  the  greatly  hypertrophied  papillae.  The  uncovered  yaw  freely 
exudes  the  sticky,  yellow  pus,  already  mentioned,  and  in  a  little  while  the  cap 
is  reproduced.  As  a  rule,  the  lesions  are  painless,  excepting  where  they  occur 
under  thick,  dense  skin,  as  in  the  palms  and  the  soles,  where  tension  may 
cause  great  pain.  Itching  is,  however,  very  persistent  and  annoying.  After 
persisting  weeks  and  months,  sometimes  passing  through  recrudescences  and 


360  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

successive  crops,  the  lesions  gradually  grow  smaller,  the  papillomata  dis- 
appear, and  a  dry  eschar  is  left,  which  falls  off,  leaving  a  patch  of  thickened 
skin,  bleached  in  the  negro  and  pigmented  in  the  light-skinned  races. 

In  old,  long-standing,  and  neglected  cases,  severe  hone  and  joijit  fains 
develop,  and  occasionally  extensive  periostitis  and  caries  occur.  These  are 
the  so-called  tertiary  lesions  of  frambesia.  They  are  not  constant;  indeed, 
they  never  appear  in  properly  treated  cases. 

Diagnosis. — There  are  only  two  diseases  with  which  typical  yaws  can  be 
confused,  syphilis  and  verruga.  Hutchinson  believes  yaws  and  syphilis,  if 
not  the  same  disease,  are  descendents  of  the  same  parent  stock;  that  originally 
they  were  identical  and  have  become  differentiated  by  thriving  for  long 
periods  on  different  soils.  Yaws  undoubtedly  suggests  syphilis  very  strongly, 
but  there  can  be  no  question  of  the  duality  of  the  diseases.  Syphilis  and 
yaws  have  frequently  been  observed  in  the  same  individual;  syphilitics  have 
been  successfully  inoculated  with  yaws,  and  vice  versa.  Finally,  the  histolog- 
ical differences  are  marked.  No  giant  cells  are  seen  in  yaws  and  no  thick- 
ened bloodvessels. 

Scheube  believes  yaws  and  verruga  to  be  identical,  but  Glogner  has 
recently  drawn  a  careful  distinction  between  the  histology  of  the  two 
diseases,  and  has  clearly  shown  that  they  are  not  identical. 

Prognosis. — The  prognosis  is  uniformly  good. 

In  patients  reduced  by  disease  and  in  infants  the  prognosis  of  yaws  is 
not  so  favorable. 

Treatment. — Iodide  of  potash  is  the  remedy  for  frambesia.  Mercury  not 
only  does  not  do  these  patients  good,  but  actually  seems  to  do  them  harm. 
Stomatitis  occurs  with  the  greatest  facility  and  is  very  severe.  When  the 
general  condition  is  low,  arsenic,  iron,  and  the  bitter  tonics  are  indicated. 
Most  tropical  practitioners  advise  local  treatment  of  the  lesions.  This 
includes  antiseptic  and  stimulating  applications  and  removal  of  old  lesions 
with  the  curette.  The  prophylaxis  of  yaws  consists  in  cleanliness  and  isola- 
tion of  the  infected.  Great  care  must  be  taken  of  abrasions  and  cuts,  and 
infected  dwellings  should  be  avoided. 


VERRUGA  (VERRUGA  PERUVIANA). 

Definition.  Verruga  (a  wart)  is  a  chronic,  infectious,  and  inoculable  dis- 
ease, characterized  by  initial  fever,  rheumatic  pains,  anaemia,  and  the  devel- 
opment of  granulomatous  lesions  (warts)  on  the  skin,  mucous  membranes, 
and  internal  organs. 

Distribution. — Verruga  is  limited  to  certain  high  valleys  of  Peru,  on  the 
Pacific  slopes  of  the  Andes.  At  present  it  is  principally  observed  in  the 
valleys  of  Huarochiri,  Tanyos,  Rimac,  and  Canta,  at  elevations  varying 
from  3000  to  8000  feet  above  the  sea.  It  is  not  observed  at  lower  levels. 
Cases  are  also  reported  from  the  mountain  districts  of  Ecuador,  Bolivia, 
and  Chile.  The  disease  has  existed  since  remote  times  in  Peru,  possibly  in 
wider  extension  than  at  present.  It  occurred  among  the  soldiers  of  Pizzaro's 
expedition,  and  is  first  mentioned  by  Zarate  in  his  History  of  Peru  (1543). 


VERRUGA  361 

Etiology. — Verruga  occurs  in  small  epidemics,  but  is  not  contagious.  Car- 
rion, a  medical  student,  in  1885,  proved  its  inoculability  on  himself  and  died 
of  the  infection.  As  a  rule,  one  attack  of  the  disease  confers  immunity.  The 
specific  cause  of  verruga  has  not  been  established.  The  belief  is  prevalent 
among  the  population  that  the  waters  of  certain  springs  are  the  cause  of  the 
disease.  Moisture,  heat,  and  elevation  above  the  sea  seem  to  be  necessary 
factors.  Malaria  is  apparently  closely  associated  with  the  development  of 
verruga;  a  particularly  pernicious  type,  locally  known  as  "  Oroya  Fever," 
being  commonly  observed  with  it.  All  ages  and  both  sexes  are  equally  liable. 
Natives  of  the  verruga  zone  seem  to  suffer  less  severely  than  strangers  com- 
ing to  the  valley.  For  a  time  this  disease  was  believed  to  be  a  form  of  yaws, 
or  frambesia,  and,  like  it,  was  interpreted  as  a  form  of  syphilis.  Yaws, 
however,  is  not  observed  in  the  internal  organs.  Furthermore,  verruga  is 
observed  in  the  domestic  animals,  including  fowls,  an  observation  contrary 
to  any  known  manifestation  of  syphilis. 

Symptoms. — The  incubation  period  is  given  as  ten  days  to  a  year.  Fifteen 
to  forty  days  (according  to  Odriozola)  seems  a  more  reasonable  figure.  In 
the  inoculation  case  of  Carrion  the  incubation  was  twenty-three  days.  Clin- 
ically, two  stages  present  themselves,  the  stage  of  invasion  and  the  stage 
of  eruption.  The  stage  of  invasion  begins  with  prodromal  symptoms. 
Lassitude,  restlessness,  and  weariness  of  the  legs,  lasting  for  a  few  days, 
are  followed  by  an  evening  fever. 

The  fever  gradually  increases  in  severity,  with  marked  rigors,  and  may 
be  remittent  or  intermittent.  In  a  few  days  joint  pains  develop.  The  joints 
invaded  are  the  smaller  articulations  of  the  hands  and  feet,  the  knees,  and 
the  spine.  The  pain  is  severe,  is  worse  at  night,  and  is  fugitive,  passing 
rapidly  from  one  joint  to  another.  Painful  contractions  of  particular  muscle 
groups  occur,  most  frequently  in  the  calf-muscles  and  sternomastoids.  Some- 
times large  muscle  groups  are  affected,  so  that  in  extreme  cases  opisthotonos 
may  develop.  As  the  disease  progresses,  ancemia  and  emaciation  occur. 
The  skin  becomes  pale  and  icteric;  the  liver  and  spleen  become  enlarged. 
Soft  bruits  are  heard  over  the  prsecordium.  The  fever  persists  from  three  to 
five  weeks,  when  it  gradually  declines,  and,  with  its  disappearance,  begins 
the  stage  of  eruption.  The  eruption  usually  develops  after  twenty  days,  or 
it  may  be  delayed  as  long  as  six  or  eight  weeks.  In  rare  instances  it  is 
observed  at  the  very  beginning  of  the  disease. 

With  the  breaking  out  of  the  eruption,  all  the  general  symptoms  are 
remarkably  ameliorated.  Beginning  first  as  small,  pinkish  papides,  the 
lesions  become  dark  blue  in  color,  and  finally  develop  into  warty  excrescences. 
They  appear  on  the  face,  particularly  around  the  eyelids  and  nose,  on  the 
limbs,  about  the  joints,  and  rarely  on  the  trunk.  The  palms,  soles,  and 
hairy  parts  of  the  body  are  also  attacked.  In  size  the  lesions  vary  from  a 
millet-seed  to  growths  as  large  as  an  apple.  They  may  be  few  or  many 
hundreds  in  number.  These  warty  growths  are  exceedingly  vascular  and 
bleed  freely,  thus  increasing  the  anaemia  of  the  patient.  When  they  develop 
on  the  mucous  membranes  and  internal  organs,  dysphagia  becomes  a  very 
common  symptom,  and  hemorrhages  occur  from  the  various  organs  that  are 
the  seat  of  the  lesions;  haematemesis,  haemoptysis,  hsematuria,  metrorrhagia. 


362  DISEASES  DUE  TO  A  SPECIFIC  INFECTION 

etc.  After  persisting  from  four  to  six  months,  perhaps  passing  through 
various  recrudescences,  the  lesions  subside  by  invohition  and  desiccation 
or  desquamation,  or  they  may  ulcerate,  or  the  larger  lesions  may  suppu- 
rate. 

Prognosis.— The  prognosis  is  always  grave,  particularly  so  in  white  people, 
in  whom  60  to  70  per  cent,  of  all  cases  die.  In  natives  the  mortality  is  about 
10  to  15  per  cent.  The  early  and  complete  establishment  of  the  eruption  is 
a  very  favorable  sign.  In  delayed  or  partial  eruptions  the  prognosis  is  grave. 
Excessive  anaemia  is  also  an  unfavorable  sign. 

Treatment. — Treatment  is  symptomatic.  On  account  of  the  very  general 
association  of  this  disease  with  malaria,  quinine  should  always  be  freely 
administered.  Sudorifics  and  hot  drinks  are  usually  employed  with  the  idea 
of  hastening  or  completing  the  eruption.  Descent  to  lower  altitudes  not  only 
diminishes  the  pain  and  abbreviates  the  disease,  but  also  lessens  the  ten- 
dency to  hemorrhages  from  the  lesions.  Odriozola  recommends  the  removal 
of  all  ulcerated  verrugas. 

EUBISAGARI. 

This  disease  occurs  endemically  in  certain  districts  of  northern  Japan. 
It  is  very  closely  related  to  the  endemic  paralytic  vertigo  of  Switzerland 
(Gerlier's  disease).  Kubisagari  manifests  itself  by  attacks  characterized 
by  dimness  of  vision,  diplopia,  and  ptosis,  associated  with  marked  weakness 
of  certain  muscle  groups. 

With  respect  to  the  etiology  of  the  disease,  very  little  is  known.  Like 
Gerlier's  disease,  it  is  observed  among  people  who  live  under  the  same  roof 
with  their  cattle.  Miura  attributes  the  disease  to  the  effluvium  from  the 
cattle  and  notes  that  the  endemic  section  is  also  particularly  badly  infected 
with  cattle  plague. 

Kubisagari  is  a  disease  of  all  ages  and  both  sexes,  and  occurs  principally 
in  the  warm  months. 

The  course  of  the  disease  is  very  chronic.  The  attacks  come  on  at  inter- 
vals of  a  few  hours  to  several  days  and  last  from  a  few  minutes  to  two  to 
three  hours.  They  are  brought  on  by  hunger,  indigestion,  muscular  fatigue, 
and  eye-strain.  Ptosis  and  diplopia  are  constant  symptoms.  Paresis  occurs 
in  various  muscle  groups,  most  commonly  in  the  posterior  muscles  of  the 
neck,  the  head  dropping  forward  in  consequence  (hence  the  name  "  kubisa- 
gari," i.  e.,  one  who  hangs  his  head).  Paresis  of  the  muscles  of  mastication, 
deglutition,  and  locomotion  may  render  chewing,  swallowing,  or  walking 
difficult  or  impossible.  Between  attacks  these  symptoms  all  disappear, 
excepting  the  ptosis  and  head-hanging,  which  may  be  permanent.  The 
superficial  and  deep  reflexes  are  increased.  The  eye-grounds  show  conges- 
tion of  the  optic  disk. 

The  prognosis  is  favorable.  Kubisagari  never  tends  of  itself  to  a  fatal 
issue. 

Treatment. — Bromide  of  potassium  has  some  effect  in  controlling  the  fre- 
quency of  the  attack.  Miura  reports  the  favorable  action  of  the  iodides  and 
arsenic  in  some  cases. 


DISEASES  OE  THE  EESPIEATOEY  SYSTEM. 


DISEASES  OF  THE  NOSE. 

ACUTE  CORYZA. 

Definition. — Acute  coryza  is  an  inflammation  of  the  nasal  mucous  mem- 
brane, characterized  in  its  early  stages  by  hypersemia,  redness,  and  swelling, 
and  followed  by  free  secretion  of  mucus  and  serum. 

Etiology. — Without  any  doubt  acute  coryza  is  an  infectious  malady, 
although  it  usually  follows  exposure  to  cold  or  wet.  The  exposure  produces 
a  condition  favorable  to  the  growth  of  the  micro-organisms  which  cause  the 
disease.  No  single  organism  has  been  isolated,  and  in  some  cases  several 
are  probably  active  at  once.  Coryza  is  a  conspicuous  symptom  of  certain 
forms  of  influenza  and  may  be  produced  by  a  number  of  micro-organisms, 
among  which  the  pneumococcus  should  be  mentioned.  Hajek  claims  to 
have  isolated  an  organism  called  the  Diplococcus  coryzce,  which  he  believes 
is  responsible  for  the  malady. 

The  disease  can  be  transmitted  from  one  person  to  another,  probably  by 
droplets  of  infected  discharge,  the  susceptibility  of  an  individual  depending 
upon  both  a  local  and  general  lowering  of  vital  resistance.  The  breathing 
of  vitiated  air,  as  in  badly  ventilated  theatres  and  steam  cars,  and  of  dust- 
laden  atmospheres,  as  in  certain  industries,  is  a  frequent  predisposing  cause. 
The  possibility  of  a  diphtheritic  origin  in  certain  cases  should  not  be  over- 
looked. Damp  cold,  even  if  of  moderate  degree,  is  more  provocative  of  the 
disease  than  dry  cold. 

Pathology  and  Morbid  Anatomy. — The  pathology  of  acute  coryza  is  that  of 
an  ordinary  catarrhal  inflammatory  process  affecting  a  mucous  membrane. 
The  bloodvessels  of  the  submucosa  become  hypersemic,  congested,  and 
engorged,  and  from  them  an  extravasation  of  white  blood  cells  and  red 
corpuscles  takes  place,  accompanied  by  a  transudation  of  serum,  which 
increases  the  swelling,  and  finally  escapes  upon  the  surface  of  the  mucous 
membrane,  to  be  thrown  off  with  the  desquamated  epithelium.  The  mucous 
glands  secrete  an  excess  of  mucus  laden  with  dead  epithelial  cells  and  leuko- 
cytes or  pus  corpuscles.  As  recovery  takes  place,  the  inflammatory  exudate 
in  the  submucosa  is  absorbed,  the  dead  epithelial  cells  are  replaced  by  young 
cells,  and  in  this  manner  the  process  of  repair  is  completed. 

Symptoms.— The  symptoms  of  acute  coryza  consist  in  primary  chilliness 
and  some  restlessness  and  in  a  sensation  of  dryness  of  the  nasal  mucous  mem- 

(  36.S  ) 


364  DISEASES  OF  THE  NOSE 

hrane  of  the  part  affected.  This  is  accompanied  by  a  loss  of  the  sense  of  smell 
and  by  a  dull  frontal  headache,  probably  due  to  congestion  in  the  frontal  sinus. 
There  is  frequently  severe  sneezing,  due  to  the  irritation  of  the  nasal  nerves 
by  the  inflammation  and  to  the  trickling  of  the  serum  over  the  angry  mucous 
membrane.  The  voice  sounds  as  if  the  nose  was  "stopped  up."  As,  the 
disease  progresses,  large  amounts  of  mucopurulent  material  are  discharged 
from  the  nostrils  and  find  their  way  back  into  the  nasopharynx.  The  consti- 
tutional symptoms  are  often  quite  severe,  and  consist  in  chilliness  and  flushes 
of  heat,  followed  by  relaxation  of  the  capillaries  of  the  skin  and  more  or  less 
perspiration.  Aching  in  the  head,  in  the  muscles,  and  the  small  of  the  back 
are  prominent  symptoms,  indicating  that  the  local  nasal  process  is  not  the 
only  part  disordered,  but  that  other  parts  are  indirectly  affected.  Without 
doubt,  the  two  chief  causes  of  these  symptoms  are  the  loss  of  large  amounts 
of  liquids  by  the  nose,  something  like  1^  to  2  pints  a  day  in  some  cases,  and 
the  absorption  of  toxic  materials  due  to  the  infection. 

Diagnosis. — The  acute  rhinitis  due  to  an  oncoming  attack  of  measles,  or 
that  due  to  an  attack  of  hay  fever,  are  the  two  states  that  most  closely  resem- 
ble true  coryza.  In  infants  the  possibility  of  the  attack  being  due  to  syphilis, 
"syphilitic  snuffles,"  must  be  considered. 

Treatment. — The  treatment  of  acute  coryza  consists,  if  the  patient  is  seen 
in  the  stage  of  onset,  of  the  use  of  a  saline  purgative  to  deplete  the  system 
and  unload  the  bowels,  and  in  the  internal  use  of  full  doses,  20  to  30  grains 
every  hour  for  five  doses,  of  bicarbonate  of  sodium  in  water.  At  the  same 
time  the  well-known  combination  called  "  rhinitis  tablets  "  may  be  given. 
These  consist  of — 

R — Quininse  sulph.       .         .         .         .         .         .         .  gr.  j. 

CamphorsB      .  .  .  .  .  .  .  .  gr.  i. 

Ext.  belladonnse     .......  gr  y^g. — M 

Sig. — One  or  two  every  thirty  minutes  till  six  are  taken. 

The  nasal  mucous  membrane  should  be  washed  by  a  gentle  spray  of 
normal  salt  solution,  followed  by  a  spray  of — 

R — Cocainse  hydrochloratis  .  .  .  .  .  .     gr   'v 

Chloretone      .  .  .  .  .  .  .  .     gr.  ij. 

Aqufe  destillat.        .  .  .  .  .  q.  s.  ad  f^j.- — M 

Sig. — Apply  as  a  spray. 

Followed  by  a  spray  of — 

R — Antipyrini      ........     gr.  xv. 

Cocainse  hydrochloratis  .  .  .  .  .  .     gr.  j. 

Aqu£e  camphoree     .         .         .         .         .         .         .  f^iij. 

AquEB  destillat.       .         .         .         .         .       q.  s.  ad  ig]. — M. 

This,  in  turn,  should  be  followed  by  a  spray  of  menthol  in  the  proportion 
of  6  grains  to  the  ounce  of  liquid  albolene. 

In  many  instances  a  hot  foot-bath  and  a  dose  of  5  to  10  grains  of  Dover's 
powder  may  be  used  to  abort  an  attack. 

After  the  disease  is  well  on  its  way,  it  is  bound  to  run  its  course.    We  can 


CHRONIC  NASAL   CATARRH  365 

only  give  relief  by  using  a  typp  of  nasal  treatment  like  that  just  suggested 
and  in  cleansing  the  nasal  chambers  of  mucus. 

When  the  attack  has  run  its  course  the  consequent  debility  is  best  con- 
trolled by  the  use  of  fresh  air,  arsenic,  ammonium  benzoate,  and  bitter  tonics. 


CHRONIC  NASAL  CATARRH. 

Definition. — Chronic  nasal  catarrh,  as  its  name  implies,  is  a  chronic  inflam- 
matory state  of  the  nasal  mucous  membranes,  frequently  due  to  repeated 
attacks  of  the  acute  variety,  or  occasionally  coming  on  more  insidiously. 
When  it  is  well  developed  the  tissues  of  the  nasal  chambers  are  relaxed  and 
somewhat  oedematous,  the  secretion  is  abnormal  in  character  and  in  quantity, 
and  this  pathological  condition  is  often  subject  to  acute  exacerbations  due 
to  exposure  to  the  usual  causes  of  coryza. 

Etiology. — ^The  causes  of  chronic  nasal  catarrh  are,  as  just  stated,  repeated 
attacks  of  acute  coryza  and  continued  exposure  to  the  action  of  irritating 
dust  or  of  cold,  moist  air,  laden  with  infectious  materials.  The  condition  may 
be  of  syphilitic  origin  or  arise  from  depleted  vitality  from  constitutional  dis- 
orders," such  as  Bright's  disease.  Foreign  bodies  should  be  searched  for, 
particularly  if  the  patient  is  a  child,  and  nasal  growths  may  be  found  as  a 
cause,  although,  as  a  rule,  the  catarrh  causes  the  formation  of  growths. 

Pathology. — An  examination  of  the  nasal  mucous  membrane  in  cases  of 
this  disease  shows  that  the  bloodvessels  are  distended  and  have  lost  their 
normal  elasticity.  They  are  unable  to  drive  out  any  additional  blood  which 
may  be  sent  to  them  because  of  the  other  parts  being  chilled.  Exudation 
into  the  connective  tissues  takes  place, and  so  this  structure  becomes  thickened 
and  enlarged.  At  this  stage  the  condition  is  sometimes  called  hypertrophic 
rhinitis. 

Repeated  or  protracted  irritation  induces  hyperplasia  of  the  connective 
tissue  of  the  submucosa,  continued  epithehal  exfoliation,  glandular  atrophy, 
and  sclerotic  changes  in  all  the  layers  of  the  mucous  membrane.  In  the 
earlier  stages  these  changes  are  those  already  mentioned  when  discussing 
acute  coryza;  later  cell  proliferation  and  leukocytic  accumulation  in  the 
nasopharyngeal  submucosa  greatly  thicken  the  membrane,  particularly 
over  the  turbinates  and  the  septum  (hypertrophic  rhinitis),  while  organiza- 
tion (fibroid  change)  increases  the  fibrous  tissue  in  the  areas  involved,  fol- 
lowed by  contraction  with  atrophy  of  erectile,  glandular,  and  even  nerve 
tissues  (atrophic  rhinitis).  This  lessens  secretion,  which  tends  to  inspissate, 
form  scabs,  and  decompose,  causing  the  fetid  emanations  to  which  the  name 
"ozgena"  has  been  given. 

Extension  to  one  or  more  of  the  facial  sinuses,  necrosis  of  bone,  or 
involvement  of  the  Eustachian  orifice  or  tube  are  possibilities  constantly  to 
be  remembered. 

Symptoms. — ^The  symptoms  of  this  stage  of  the  disease  consist  in  a  con- 
stant secretion  in  excess  of  nasal  mucus,  which  passes  in  large  part  into  the 
postnasal  and  nasopharyngeal  spaces.  This  secretion  may  be  thin  and 
liquid  or  thick  and  mucopurulent,  and  is  apt  to  vary  in  quantity  with  exposure 


366  DISEASES  OF  THE  NOSE 

to  cold  or  dust.  The  secretion  is  so  thick  that  it  readily  becomes  inspissated 
and  partly  blocks  the  nasal  passages,  and,  furthermore,  becomes  loaded  with 
bacteria,  so  that  it  may  be  somewhat  fetid. 

Treatment. — The  treatment  consists  in  maintaining  nasal  cleanliness  by 
an  ordinary  nasal  douche-cup,  to  be  used  night  and  morning,  employing  in 
it  normal  salt  solution  or  Dobell's  solution  warmed  to  the  temperature  of  the 
body.  The  physician  should  also  cleanse  the  parts,  when  the  patient  visits 
him,  by  a  mild  alkaline  wash,  and  when  no  acute  exacerbation  is  present  the 
hypertrophied  mucous  membrane  over  the  middle  turbinate  should  be 
cocainized  and  then  lightly  touched  with  a  small  electrocautery,  a  piece  of 
oiled  cotton  being  placed  between  the  spot  cauterized  and  the  nasal  septum, 
to  prevent  adhesions  from  forming  during  the  period  of  acute  swelling 
which  follows  the  operation.  Care  should  be  taken  to  keep  the  parts  clean 
for  several  days  to  prevent  infection,  if  the  patient  is  primarily  anaemic  or 
debilitated.  This  treatment  should  not  be  resorted  to  before  the  general 
health  is  improved  by  tonics. 


ATROPHIC  NASAL  CATARRH. 

Definition. — In  this  condition  the  nasal  mucous  membrane  and  the  under- 
lying tissue  undergo  atrophy  and  contraction,  with  the  result  that  the  blood- 
vessels of  the  part  are  occluded  or  destroyed. 

Etiology. — Atrophic  nasal  catarrh  follows  the  chronic  type  of  ordinary 
nasal  catarrh  as  a  late  condition.  At  times  it  seems  to  be  due  to  some  con- 
genital defect  in  the  shape  of  the  nasal  chambers,  and  in  some  cases  it  begins 
to  develop  as  the  result  of  one  of  the  acute  infectious  diseases. 

Pathology. — The  chief  change  is  an  atrophy  of  the  cells  of  the  nasal  mucous 
membrane  and  an  overgrowth  of  the  submucous  connective  tissue,  which  is 
prone  to  undergo  contractile  changes.  This  cuts  off  blood  supply  and 
increases  the  atrophic  process. 

Symptoms. — These  consist  in  the  formation  of  scabs,  or  crusts  of  thickened, 
tenacious  mucus,  which  are  usually  infected  by  many  pathogenic  germs. 
Some  ulceration  of  the  nasal  septum  may  appear,  and  the  patient  may  com- 
plain of  a  constant  feeling  of  dryness  and  irritation,  or  occlusion  of  the  nasal 
passages. 

The  nasopharyngeal  mucous  membrane  is  often  dry  and  shiny  in  appear- 
ance. When  the  condition  is  far  advanced  a  state  of  ]etid  ozaena  develops, 
in  which  the  breath  of  the  patient  becomes  fetid  beyond  the  power  of  words 
to  describe  it.  Nothing  equals  it,  except  the  breath  in  a  case  of  pulmonary 
gangrene. 

The  sense  of  smell  is  practically  destroyed  by  the  process,  and  the  patient 
is  often  ignorant  of  how  disagreeable  his  breath  has  become. 

Prognosis. — The  outlook  for  a  cure  of  this  condition  is  unfavorable.  The 
bad  odor  can  usually  be  reheved. 

Treatment. — The  patient  should  be  told  to  use  a  nasal  douche-cup  with 
warm  Dobell's  solution  twice  a  day.  Kyle  recommends  1  drop  of  ordinary 
poal  oil  dropped  into  each  nostril  after  this.    The  physician  should  see  the 


HAY  FEVER  367 

patient  every  few  days,  cleanse  the  nasal  chambers,  and  apply  a  1:2000 
solution  of  trichloracetic  acid  on  an  applicator  to  the  nasal  passages,  or 
1 :  500  solution  of  formaldehyde  may  be  used. 


HAY  FEVER. 

Definition. — Hay  fever  is  an  inflammation  of  the  nasal  mucous  membrane 
which  occurs  periodically  and  usually  at  a  time  of  the  year  when  certain 
plants  are  in  a  certain  stage  of  growth.  Associated  with  the  localized  inflam- 
mation, there  is  often  present  an  asthmatic  condition,  in  which  a  sense  of 
oppression  is  well  developed.  In  other  instances  true  asthmatic  attacks 
ensue.  Hay  fever  is  often  called  "  autumnal  catarrh,"  "  rose  cold,"  "  rag- 
weed fever,"  or  "  periodic  rhinitis." 

Distribution, — The  prevalence  of  hay  fever  depends  largely  upon  the  pres- 
ence in  the  air  of  the  pollen  of  certain  plants,  and  in  those  parts  of  the  country 
where  these  plants  do  not  grow  the  disease  is  unknown.  It  is  more  rare  in 
England  than  in  America,  but  much  more  common  in  these  countries  than 
elsewhere,  being  comparatively  rare  in  France  and  Germany.  Negroes  and 
Indians  are  apparently  immune,  and  the  lower  classes  very  frequently  escape, 
the  disease  being  chiefly  a  malady  of  the  so-called  upper  classes.  The  dis- 
ease is  rare  after  the  fortieth  year  and  affects  males  oftener  than  it  affects 
females. 

Etiology. — There  are  two  chief  factors  in  the  development  of  hay  fever, 
namely,  an  idiosyncratic  state  of  the  patient  and  the  presence  of  an  exciting 
cause  in  the  atmosphere.  Much  discussion  has  taken  place  as  to  what  the 
condition  is  that  renders  the  patient  pecuharly  hable  to  this  affection.  In 
some  cases  it  seems  to  be  a  neurosis  of  the  nasal  cavities  or  a  local  disease; 
in  others  it  is  said  to  depend  upon  a  "hthajmic  state,"  whatever  that  may  be. 
In  every  case,  however,  there  is  a  condition  of  nasal  hypersesthesia  which 
renders  the  nasal  mucous  membrane  extremely  sensitive  to  irritants.  Many 
sufferers  from  hay  fever  present  irregularities  in  the  nasal  chambers  which 
may  aid  in  predisposing  them  to  attacks  of  the  malady. 

The  second  cause  of  hay  fever  in  the  great  majority  of  cases  is  the  presence 
in  the  air  of  pollen  from  some  plant,  chiefly  "ragweed."  Pollen  is  not  the 
only  cause,  however,  for  typical  attacks  occur  in  certain  persons  at  seasons 
of  the  year  when  no  pollen  is  present,  the  condition  being  induced  by  some 
irritating  dust  or  vapor  which  in  no  way  influences  the  ordinary  individual. 

Pathology  and  Morbid  Anatomy. — In  the  state  of  the  nasal  mucous  mem- 
brane there  is  nothing  peculiar  to  hay  fever,  which  presents  on  examination 
the  evidences  of  an  acute  catarrhal  inflammation  with  swelling  and  hyper- 
semia  of  the  parts  involved. 

Symptoms.^ — The  symptoms  of  "hay  cold"  are  usually  sudden  in  onset 
and  often  appear  on  a  certain  day  which  the  patient  can  foretell,  and  nearly 
always  at  a  definite  period  in  the  year,  for  the  reason  already  given.  An 
acute  rhinitis  develops  with  irritation  of  the  nasal  mucous  membrane,  and 
the  running  of  salty  fluid  from  the  nostrils  irritates  the  nares  and  the  upper 
lip.     The  conjunctival  mucous  membrane  is  irritated  and  inflamed,  and 


368  DISEASES  OF  THE  NOSE 

the  eyes  are  tearful,  partly  because  of  this  condition  and  partly  because 
the  tear  ducts  to  the  nose  are  stopped  by  the  swelling  of  the  mucous  mem- 
brane. Photophobia  and  neuralgic  pains  in  the  head  are  often  present 
and  add  greatly  to  the  patient's  misery.  Frontal  headache  is  constant  and 
severe,  and  tinnitus  and  fulness  of  the  head  are  also  annoying  symptoms. 
Some  deafness  may  be  present.  Associated  with  these  symptoms  the  patient 
often  has  marked  systemic  depression  and  wretchedness  with  great  mental 
depression. 

On  examining  the  mucous  membrane  of  the  nose  there  is  found  undue 
pallor  in  long-standing  cases  which  is  not  to  be  expected  when  inflammation 
is  present.  If  a  probe  is  touched  to  the  mucous  membrane  patches  of 
hypersesthesia  are  discovered,  as  evidenced  by  sudden  severe  sneezing  and 
other  signs  of  acute  irritation. 

The  attack  is  prone  to  persist  as  long  as  the  patient  remains  exposed  to  the 
cause,  and  upon  his  removal  from  exposure  may  cease  almost  as  speedily  as 
it  came  on.  In  cases  in  which  a  reflex  asthma  due  to  the  nasal  irritation 
ensues  the  patient  may  become  a  chronic  asthmatic  even  if  the  hay  cold 
disappears. 

Prognosis. — ^The  outlook  for  cure  in  the  affection  is  not  good  unless  the 
patient  can  go  away  to  a  resort  where  the  cause  does  not  exist  for  a  certain 
length  of  time  each  year.  So  far  as  life  is  concerned  it  never  endangers 
it,  but  if  the  disease  produces  vital  depression  it  undoubtedly  increases 
the  susceptibility  to  other  diseases.  The  patient  can  be  comforted  by  the 
statement  that  the  attacks  stop  or  diminish  in  many  cases  after  forty  years 
of  age. 

Treatment. — A  competent  rhinologist  should  always  be  asked  to  correct 
all  nasal  irregularities  during  the  period  of  quiescence,  and  the  physician 
should  correct  any  gouty  or  lithsemic  state  by  the  use  of  ordinary  exercise, 
a  good  diet,  and  the  use  of  the  salicylates,  or  bitter  tonics  with  arsenic  to 
improve  the  state  of  the  mucous  membranes  in  general.  Not  infrequently 
good  results  follow  the  use  of  30  grains  of  phosphate  of  sodium  in  a  cup 
of  hot  water  before  breakfast,  given  to  stimulate  the  gastroduodeno- 
hepatic  glands.  In  other  cases  salicylate  of  sodium  in  10  grain  doses  or 
salol  may  be  used  for  this  purpose.  These  measures  and  the  resort  to  a 
region  free  of  the  exciting  cause  in  the  autumn  months  are  the  prophylactic 
measures.  A  sea  voyage  usually  confers  complete  immunity  if  taken  at  the 
proper  time  of  year,  and  sometimes  residence  at  some  mountain  resort  does 
likewise,  particularly  if  the  altitude  is  very  great. 

In  the  way  of  local  treatment  for  the  attack  the  swollen  mucous  mem- 
branes may  be  constricted  by  the  appKcation  of  a  solution  of  adrenalin 
chloride  1 :  5000,  and  after  this  is  done  the  parts  may  be  washed  with  a 
mild  alkaline  spray  like  Dobell's  solution  or  normal  salt  solution  which  has 
been  warmed.  After  this  is  done  the  cocaine  solution  and  the  antipyrin 
solution  recommended  for  acute  coryza  may  be  employed  and  finally  the 
parts  coated  by  the  use  of  the  spray  of  menthol  and  camphor  named  in  that 
article. 

Within  the  last  few  years  several  attempts  to  produce  immunity  to 
hay  fever  by  the   use  of   preparations  of  golden   rod   and  ragweed   have 


ACUTE  CATARRHAL  LARYNGITIS  369 

been  attempted,  the  patients  taking  them  for  some  time  before  the  time  of 
an  attack  in  the  hope  that  they  would  not  suffer  from  the  disease.  This 
plan  has  not  so  far  proved  very  successful. 

Still  more  recently  Dunbar,  of  Hamburg,  claims  to  have  isolated  a  toxin 
from  the  pollen  of  certain  plants,  and  by  giving  it  to  horses  produced  an 
antitoxic  serum  which,  he  states,  will  protect  a  susceptible  person.  This 
is  not  used  hypodermically,  but  is  dried,  mixed  with  sugar  of  milk,  and  then 
finely  triturated.  A  small  part  of  this  powder  is  to  be  snuffed  up  the  nose. 
When  it  is  desired  to  use  the  remedy  in  the  eyes  the  fluid  serum  is  employed. 
The  value  of  this  method  is  still  undecided. 


EPISTAXIS. 

Etiology. — Nose-bleed  is  due  to  many  different  causes,  chiefly  traumatic. 
The  condition  only  concerns  us,  from  the  medical  standpoint,  when  it  develops 
as  a  result  of  lesions  in  the  nasal  cavities  or  in  the  course  of  the  infectious 
diseases,  or  in  cases  of  heart  disease  in  which  there  is  cephalic  congestion. 
Occasionally  it  occurs  in  very  plethoric  persons  after  severe  exercise,  and  in 
them  it  may  be  a  beneficial  condition. 

Severe  nasal  hemorrhage  usually  arises  from  an  ulcer  on  the  nasal  septum, 
from  cardiac  disease,  the  commonest  lesion  being  mitral  disease,  and  in 
typhoid  fever  as  one  of  the  prodromes.  Occasionally  it  is  a  desperately 
persistent  state  in  haemophilia,  and  even  more  rarely  it  seems  to  be  of  the 
nature  of  vicarious  menstruation.  Sometimes  it  is  a  manifestation  of  blood 
dyscrasia,  as  in  leukaemia. 

Treatment. — The  treatment  consists  in  plugging  the  nostrils  with  cotton, 
if  necessary  saturating  the  cotton  with  adrenalin  chloride  1:2000,  and  in 
compressing  the  artery  on  the  upper  lip  near  the  nose  by  pushing  it  against 
the  jaw-bone.    Internal  measures  are  usually  unnecessary  and  useless. 


DISEASES  OF  THE  LARYNX. 

ACUTE  CATARRHAL  LARYNGITIS. 

Definition. — ^Acute  laryngitis,  or  acute  catarrh  of  the  larynx,  is  an  inflam- 
mation of  the  mucous  membrane  lining  the  larynx,  as  a  result  of  which 
there  is  more  or  less  loss  of  voice,  or  aphonia,  and  perhaps  a  sense  of  con- 
striction or  respiratory  oppression. 

Etiology. — This  condition  arises  as  a  result  of  any  factor  which  directly 
causes  irritation  of  the  laryngeal  mucous  membrane,  such  as  the  inhalation 
of  irritant  vapors  or  dust.  In  some  cases  the  inhalation  of  cool  and  damp 
24 


370  DISEASES  OF  THE  LARYNX 

air  produces  like  effects,  particularly  if  the  voice  has  been  used  much 
before  the  exposure.  Indirectly  it  arises  as  the  result  of  getting  the  body 
chilled  in  a  cold  wind  after  exercise,  and  in  still  other  cases  it  seems  to  be, 
at  least  in  part,  due  to  some  disorder  of  metabolism,  whereby  gouty  con- 
ditions ensue,  and  these  in  turn  cause  laryngeal  inflammation  by  some 
indirect  effect  when  the  voice  is  much  used.  Another  cause,  particularly  in 
the  case  of  children,  is  "  mouth-breathing,"  which  permits  the  air  unmoistened 
by  the  nasal  chambers  to  pass  over  the  laryngeal  surface.  In  still  other 
instances  it  arises  as  a  complication  of  one  of  the  acute  infectious  dis- 
eases, as  influenza  and  of  hay  fever.  The  possible  diphtheritic  origin  of 
acute  laryngitis,  especially  in  children,  should  never  be  overlooked. 

Pathology. — ^The  inflammation  of  the  laryngeal  mucous  membrane  is 
precisely  like  that  of  mucous  membranes  elsewhere,  except  for  the  fact  that 
glandular  tissue  is  quite  scarce  in  these  parts,  and  so  there  is  but  little 
mucus  secreted  even  if  a  considerable  amount  of  inflammatory  exudate 
takes  place  in  the  tissues  beneath  the  mucous  membrane.  The  desquamation 
of  epithelial  cells  and  the  presence  of  dead  leukocytes  cause  the  secretion 
to  be  white  and  tenacious,  and  the  congestion  of  the  bloodvessels  gives 
rise  to  a  sense  of  tightness  in  the  laryngeal  box  which  is  distressing.  As 
the  congestion  decreases  the  process  of  regeneration  in  the  epithelial  cells  and 
submucous  tissues  takes  place,  secretion  becomes  more  profuse,  and  per- 
fect recovery  ensues. 

Symptoms. — The  patient  finds  it  difficult  to  develop  the  full  resonance 
of  his  voice  and  often  single  words  in  a  sentence,  or  all  the  words,  are 
spoken  somewhat  huskily  owing  to  failure  to  move  the  vocal  bands  as 
readily  as  in  health.  There  is  a  sense  of  tightness  in  the  larynx  and  even 
aching  pain  may  be  present.  In  some  cases  hoarseness  is  the  only  symptom, 
but  in  others  the  loss  of  voice  is  complete.  Speech  at  this  time  is  often  so 
painful  that  the  patient  endeavors  to  avoid  conversation. 

An  examination  of  the  laryngeal  mucous  membrane  at  this  time  will 
reveal  marked  redness  and  hypersemia  and  even  small  punctiform  hemor- 
rhages may  be  seen,  particularly  if  the  patient  has  repeatedly  and  violently 
endeavored  to  clear  his  throat  by  hawking  or  coughing.  The  ventricular 
bands  are  swollen,  and  this  may  be  the  chief  cause  of  the  loss  of  voice,  for 
it  often  happens  that  the  vocal  cords  escape  the  inflammatory  process.  In 
other  cases  the  edges  of  the  glottic  opening,  the  epiglottis,  and  the  mucous 
membrane  over  the  arytenoids  are  inflamed. 

As  the  process  proceeds  secretion  is  begun  and  small  particles  of  mucus 
are  occasionally  coughed  up.  This  is  particularly  apt  to  occur  after  severe 
coughing  in  the  morning  in  order  to  dislodge  inspissated  mucus.  The 
masses  expectorated  are  often  distinctly  purulent,  and  discolored  with  soot 
if  the  patient  lives  in  a  city.  Secretion  gradually  becomes  more  profuse. 
Pain  disappears  and  the  voice,  which  has  been  whispering,  becomes  hoarse 
and  coarse  in  character,  certain  words  which  require  effort  being  sounded 
with  difficulty.  Finally  the  voice  recovers  its  normal  tone  and  the  attack 
is  over. 

Diagnosis. — Care  should  be  taken  that  sudden  attacks  of  hoarseness  are 
not  considered  as  due  to  simple  catarrhal  laryngitis  until  the  possibility  of 


CHRONIC  CATARRHAL  LARYNGITIS  371 

diphtheria  is  excluded  by  a  thorough  examination  of  the  throat  and  larynx. 
This  is  particularly  important  in  children.  In  adults  the  possibility  of 
aneurysm,  tuberculosis,  papilloma,  and  syphilis  should  not  be  forgotten. 

Prognosis. — The  prognosis  is  always  good  as  to  recovery  if  the  exciting 
cause  is  removed. 

Treatment. — ^The  treatment  of  acute  laryngitis  consists  primarily  in  remov- 
ing the  cause.  If  irritant  dusts  are  present  the  patient  must  not  be  exposed 
to  them,  and  if  the  outside  atmosphere  is  raw  and  cold  he  must  be  kept 
in-doors  until  recovery  takes  place.  When  a  gouty  diathesis  underlies  the 
condition  the  salicylates  should  be  freely  used  in  the  form  of  salicin,  5  grains 
three  or  four  times  a  day,  and  the  vegetable  salts  of  potassium,  such  as  the 
citrate,  be  given  freely.  About  the  neck  may  be  fastened  a  capsicum  draft, 
or,  if  this  is  not  to  be  had,  a  folded  handkerchief  should  be  wrung  in  cold 
water  and  laid  upon  the  larynx,  being  immediately  covered  by  a  cloth  or 
piece  of  flannel,  which  is  bound  around  the  neck.  The  cold  compress  is 
promptly  changed  to  a  warm  compress  by  the  heat  of  the  body,  and  this  acts 
favorably  upon  the  local  inflammation  beneath.  The  air  of  the  room  in 
which  the  patient  is  to  sleep  or  rest  during  the  day  should  be  kept  well 
moistened  by  steam  disengaged  by  a  bronchitis  kettle  or  by  adding  pieces 
of  unslaked  lime  to  a  tub  of  water.  Into  the  water  in  the  bronchitis  kettle 
may  be  placed  a  few  grains  of  menthol  if  it  is  desirable  to  exercise  a  very 
sedative  effect,  and  the  patient  should  be  forbidden  to  go  into  any  cold 
rooms  or  hallways.  A  hot  mustard  foot-bath  and  a  hot  lemonade  with  a 
drachm  of  sweet  spirit  of  nitre  at  bedtime  to  produce  sweating  is  also  useful, 
or  a  dose  of  Dover's  powder  may  be  ordered  if  the  patient  is  an  adult. 
Kyle  recommends  the  use  of  tablets  of  y^-q  grain  of  pilocarpine  every  hour 
for  four  doses,  or  if  it  is  important  to  attempt  to  abort  the  disease  he  suggests 
the  use  of  5  to  10  drops  of  dilute  nitric  acid  in  water  every  hour  for  three 
doses,  and  then  every  two  hours  for  two  doses.  This  often  gives  temporary 
relief  if  it  does  no  permanent  good. 

If  by  any  chance  the  inflammation  involves  the  glottis  and  seems  to 
endanger  life,  intubation  or  tracheotomy  is  necessary. 

For  the  hoarseness  and  thick  secretion  of  the  stage  of  convalescence 
benzoate  of  soda  or  of  ammonia,  in  10  grain  doses  three  times  a  day,  are 
useful,  or  10  grains  of  ammonium  chloride  may  be  given  thrice  a  day  in 
licorice  and  water.  In  still  other  cases  terpin  hydrate  in  the  dose  of  a 
teaspoonful  of   the  elixir  every  three  hours  may  be  used. 


CHRONIC  CATARRHAL  LARYNGITIS. 

Symptoms. — Chronic  catarrh  of  the  larynx  is  characterized  by  chronic 
hoarseness,  by  constant  clearing  of  the  throat  in  an  endeavor  to  speak 
clearly,  and  finally,  in  severe  cases,  by  ulceration  of  the  laryngeal  mucous 
membrane.  Not  rarely  after  a  period  of  rest  the  patient  finds  that  after 
the  first  few  words  his  voice  forsakes  him,  or,  instead,  he  may  find  that 
if  speaking  is  difficult  at  the  beginning  it  becomes  more  easy  as  exercise 
limbers  up  the  infiltrated  muscles  and  engorged  mucous  membrane. 


372  DISEASES  OF   THE  LARYNX 

Pathology. — Pathologically  the  condition  is  characterized  by  chronic 
engorgement  of  the  minute  bloodvessels,  thickening  of  the  mucous  mem- 
brane, and  even  infiltration  of  the  submucous  tissues  and  the  laryngeal 
muscles.  If  this  process  persists  for  any  length  of  time  sufficient  infiltration 
may  be  present  to  become  unabsorbable  and  thus  cause  permanent  alteration 
in  the  character  of  the  voice.  Not  rarely  there  is  thickening  and  swelling 
of  the  pharyngeal  tissues  as  well,  and  the  tonsils  are  the  seat  of  chronic 
lymphoid  changes.  Spots  of  ulceration  may  develop  between  the  arytenoid 
cartilages. 

Diagnosis. — As  stated  in  the  article  on  Tuberculosis,  hoarseness  which  is 
persistent  should  always  be  carefully  investigated,  as  it  often  is  due  to  tuber- 
culosis or  syphilis,  or  even  papilloma.  When  it  is  due  to  aneurysm  the  laryn- 
goscope will  usually  reveal  one  cord  paralyzed,  and  when  due  to  syphilis 
the  history  of  the  patient  and  the  benefit  produced  by  specific  treatment 
must  be  noted.  In  persons  of  advanced  years  the  possibility  of  malignant 
growth  must  be  considered. 

Treatment. — ^The  treatment  consists  in  the  maintenance  of  cleanliness  and 
free  secretion  in  the  upper  respiratory  tract  by  the  use  of  alkaline  sprays 
and  nasal  douches.  To  the  larynx  itself  a  spray  of  alumnol  (3  per  cent, 
solution)  may  be  apphed  every  second  day.  The  use  of  tobacco  and  alcohol 
should  be  forbidden  and  the  liver  and  kidneys  kept  active  by  mild  alkaline 
purges  and  diuretics.  Tonics  to  the  general  system,  such  as  phosphorus, 
arsenic,  and  sometimes  iron,  particularly  the  syrup  of  the  iodide  are  useful. 

(EDEMATOUS  LARYNGITIS. 

Definition. — (Edema  of  the  larynx  occurs  as  an  acute  affection,  occasion- 
ally of  such  a  severe  degree  that  it  endangers  life.  It  is  essentially  an  acute 
celluhtis  of  the  laryngeal  tissues,  and  when  it  involves  the  upper  part  of 
the  larynx  in  particular  it  is  called  oedema  of  the  glottis. 

Etiology. — (Edema  of  the  larynx  is  far  more  frequently  due  to  injury 
than  to  any  other  cause,  and  in  many  instances  is  produced  by  the  inhalation 
of  irritant  vapors  or  fumes.  The  only  cases  I  have  seen  have  been  due  to 
the  patient  attempting  to  swallow  ammonia  water  undiluted,  which  both  by 
actual  contact  of  the  fluid  with  the  pharynx  and  of  the  fumes  with  the  larynx 
has  caused  serious  respiratory  distress.  Another  traumatic  cause  is  fracture 
of  the  larynx,  as  by  throttling  or  other  injury.  Of  the  non-traumatic 
causes  we  find  that  acute  inflammations  in  other  parts  may  be  provocative  of 
this  state,  as,  for  example,  tonsillar  abscess  with  inflammation  of  the  adjacent 
tissue  gradually  extending  to  the  larynx.  Sometimes  it  ensues  as  a  result 
of  grave  lesions  in  the  cartilages  of  the  larynx,  as  in  the  chondritis  arising 
in  typhoid  fever,  or  even  in  scarlet  fever  in  association  with  the  develop- 
ment of  the  "collar  of  brawn."  Infection  by  the  staphylococcus  or  strepto- 
coccus of  the  perilaryngeal  tissues,  the  floor  of  the  mouth  or  pharynx  (as  in 
Ludwig's  angina)  may  extend  to  the  epiglottis  and  larynx.  While  often  an 
infection,  it  may  arise  in  the  course  of  some  affection  characterized  by  wide- 
spread oedema,  as  Bright's  disease  or  chronic  heart  disease,  and  so  appear  to 
have  a  dropsical  origin. 


(EDEMATOUS  LARYNGITIS  373 

Pathology. — The  condition  of  oedema  of  the  larynx,  as  its  name  impHes, 
depends  upon  the  extravasation  of  fluid  into  the  submucous  tissues,  producing 
an  oedema  or  hydrops  of  the  part,  which  is  practically  always  of  an  inflam- 
matory origin.  This  swelling  may  involve  ah  the  laryngeal  structures 
equally  and  even  extend  well  along  the  trachea.  In  mild  cases  the  parts 
affected  are  not,  however,  seriously  disorganized,  and  the  swelling  may 
disappear  as  rapidly  as  it  came  on,  leaving  behind  it  little  trace  of  its  exist- 
ence. In  fatal  cases  the  swelling  is  usually  found  at  autopsy  to  have  largely 
disappeared,  although  the  parts  may  be  red  and  inflamed  and  somewhat 
relaxed.  In  such  cases  the  microscope  commonly  shows  a  serous,  or  sero- 
fibrinous, suffusion  of  the  affected  tissues,  the  exudate  containing  a  varying 
number  of  leukocytes.  In  other  cases  the  submucous  and  even  the  peri- 
laryngeal tissues  may  be  infiltrated  by  pus,  diffuse  suppurative  interstitial 
laryngitis,  a  most  fatal  disease. 

Symptoms. — With  the  onset  of  this  condition  several  characteristic  symp- 
toms at  once  develop,  namely,  impairment  of  the  voice,  stridulous  or  labored 
breathing,  manifestly  due  to  laryngeal  obstruction,  and  increasing  cyanosis. 
The  patient  is  uncomfortable  if  lying  down,  and  is  more  easy  when  sitting 
up  and  leaning  forward.  The  tissues  adjacent  to  the  larynx  may  be  swollen 
and  the  patient,  if  unable  to  speak,  points  appealingly  to  his  larynx. 

In  some  instances  a  state  of  chronic  oedema,  due  to  heart  or  renal  disease, 
may  ensue,  which  is  rarely  so  severe  or  as  pressing  for  rehef  as  is  the  acute 
malady. 

Diagnosis. — Difficult  laryngeal  breathing  may  be  due  to  a  laryngeal  crisis 
in  locomotor  ataxia  or  to  the  lodgement  of  a  foreign  body  in  the  larynx. 
These  conditions  should  be  excluded  before  the  physician  decides  that 
oedema  is  the  cause  of  the  illness.  Aneurysm  of  the  aorta  may  produce 
severe  laryngeal  symptoms  by  pressure  on  the  laryngeal  nerves,  and  in 
children  retropharyngeal  abscess  may,  by  rupture  or  pressure,  produce  some- 
what similar  symptoms. 

Prognosis. — In  the  absence  of  virulent  symptoms  the  prognosis  is  usually 
favorable  even  if  the  symptoms  are  severe,  provided  that  when  they  appear 
the  physician  is  ready  to  give  relief  by  intubation  or  tracheotomy.  If  the 
oedema  is  due  to  the  inhalation  of  irritating  vapors  and  the  lower  respiratory 
tract  is  involved  in  the  inflammatory  process,  the  prognosis  is,  of  course, 
very  grave. 

Treatment. — ^The  treatment  consists  in  the  administration  of  an  active 
saline  purge  to  deplete  the  vascular  system,  and  the  setting  free  of  steam 
from  a  bronchitis  kettle  in  the  air  of  the  room  in  which  the  patient  lives. 
To  the  water  in  the  kettle  may  be  added  a  few  grains  of  menthol  for  its 
soothing  influence  on  the  laryngeal  mucous  membrane.  A  10  per  cent, 
solution  of  alumnol  may  be  sprayed  into  the  larynx  for  its  astringent  effect. 
When  the  oedema  arises  as  a  complication  of  renal  or  cardiac  disease  and 
is  part  of  a  general  tendency  to  anasarca,  so  active  a  purge  as  elaterium  or 
colocynth  is  indicated  to  remove  fluid  from  the  body,  and  a  hot  pack  may 
be  used  to  cause  sweating  if  the  heart  is  strong  enough  to  stand  it.  The 
use  of  pilocarpine  for  this  purpose  is  unwise,  because  it  is  so  prone  to  cause 
pulmonary  oedema.     When  the  laryngeal  obstruction  becomes  marked  it 


374  DISEASES  OF   THE  LARYNX 

may  be  necessary  for  the  physician  to  quickly  perform  intubation  or  trach- 
eotomy, but  while  he  should  be  prepared  to  do  so  at  any  moment  it  is  scarcely 
necessary  to  add  that  tracheotomy  should  only  be  done  as  a  last  resort. 


SPASMODIC  LARYNGITIS. 

Definition, — Spasmodic  laryngitis,  sometimes  called  "  spasmodic  croup,"  or 
"  false  croup  "  in  distinction  from  diphtheria  or  true  croup,  is  a  condition  of 
acute  laryngeal  catarrh  involving  the  mucous  membrane  in  the  region  of 
the  glottis,  and  resulting  in  swelling  of  those  parts,  so  that  the  ingress  and 
egress  of  air  is  difficult.  The  spasm  of  the  laryngeal  muscles,  while  it  aids 
in  producing  the  symptoms,  is  really  of  secondary  importance  as  compared 
to  this  swelling. 

Etiology. — In  the  past  it  was  customary  to  consider  spasmodic  croup  a 
disease  in  itself.  We  now  know  that  it  is  a  symptom  depending  upon  several 
causes,  some  of  which  are  external,  some  internal.  Appearing  as  it  does 
almost  always  in  children  between  one  and  six  years,  but  sometimes  persist- 
ing in  its  occurrence  up  to  puberty,  it  depends  chiefly  upon  rickets  or  mal- 
nutrition, the  presence  of  postnasal  adenoids,  which  make  the  child  a  mouth 
breather,  or  to  some  defect  in  the  nose,  which  causes  the  same  condition. 
In  some  instances  errors  in  diet  before  retiring  to  bed  seem  to  precipitate 
an  attack.  Of  the  external  causes  which,  however,  are  only  active  in  those 
who  have  a  tendency  to  attacks  of  this  affection,  may  be  mentioned  furnace- 
heated  air,  which  is  so  dry  and  dusty  that  if  the  child  is  a  mouth  breather 
the  larynx  becomes  rapidly  dry  and  irritated.  An  acute  coryza  may  also 
bring  on  an  attack  in  that  it  causes  mouth  breathing. 

Treatment. — The  treatment  is  evident  from  what  has  just  been  said.  It 
may  be  divided  into  two  parts,  that  for  the  relief  of  the  attack  and  that 
for  the  cure  of  the  underlying  causes. 

When  any  sign  of  croup  is  manifested  the  nurse  should  place  1  or  2  grains 
of  menthol  in  the  bowl  of  a  dry  spoon  and  heat  it  over  a  gas  jet  or  lamp. 
This  sets  free  in  the  air  of  the  room  the  menthol  vapor  and  soothes  the 
laryngeal  mucous  membrane.  If  the  attack  is  well  developed  the  nurse 
should,  in  addition,  disengage  from  a  bronchitis  kettle  steam  laden  with 
menthol,  or  with  oil  of  pine  and  oil  of  eucalyptus,  in  the  proportion  of  15 
drops  of  each  in  the  water  in  the  kettle  or  on  the  sponge  usually  placed  in 
its  neck  or  spout.  Internally  a  dose  of  5  to  10  grains  of  bromide  of  sodium 
may  be  given  in  syrup,  and  over  the  larynx  should  be  placed  a  compress 
wrung  in  hot  or  cold  water. 

For  the  prevention  of  future  attacks  the  child  should  be  relieved  of  ade- 
noids or  enlarged  tonsils,  should  receive  proper  diet  and  tonics  if  rachitic, 
and  should  sleep  in  a  bronchitis  tent  if  the  larynx  is  irritable.  A  sponge 
loaded  with  cold  water  may  be  sopped  upon  the  skin  over  the  larynx 
every  morning  to  improve  its  vascular  tone. 


TUBERCULOUS  LARYNGITIS  375 


TUBERCULOUS  LARYNGITIS. 

Definition. — As  its  name  implies,  tuberculous  laryngitis  is  due  to  the 
presence  of  the  Bacillus  tuberculosis  in  the  laryngeal  tissues  and  the  conse- 
quent development  therein  of  miliary  or  larger  tubercles.    (See  Tuberculosis.) 

Etiology. — In  the  vast  majority  of  cases  of  laryngeal  tuberculosis  the 
infection  is  secondary  to  pulmonary  disease,  and  is  due  to  infection  of  the 
larynx  by  the  sputum  which  the  patient  coughs  up,  or  by  direct  extension 
from  below  upward.  In  rare  instances  it  is  undoubtedly  a  primary  affection. 
I  have  had  such  a  case  under  my  care  while  writing  this  article.  As  in 
tuberculous  infection  in  other  parts  there  must  be,  in  addition  to  the  presence 
of  the  bacillus,  a  susceptibility  to  infection,  or  one  acquired  by  general  or 
local  lowering  of  vitality.  This  disease  occurs  most  commonly  in  males 
between  twenty  and  thirty  years  of  age. 

Pathology. — Here,  as  elsewhere  in  the  body,  the  development  of  tubercles 
takes  place  by  leukocytic  migration  and  the  proliferation  of  cells,  and  is 
accompanied  by  the  closing  of  bloodvessels  and  the  necrosis  of  the  masses 
formed,  followed  by  breaking  down  and  escape  of  the  cheesy  material,  and 
the  production  of  ulcers  in  the  laryngeal  mucous  membrane.  As  the  process 
of  infiltration  proceeds  the  perichondrium  is  attacked  and  necrosis  takes 
place  in  the  laryngeal  cartilages. 

In  many  other  parts  of  the  body  the  system  makes  efforts  at  repair,  so  that, 
even  if  the  disease  ultimately  wins  the  battle,  evidences  of  an  active  defence 
can  be  recognized  ;  but  in  the  larynx  it  very  commonly  happens  that  no 
such  reparative  or  protective  process  occurs,  and  this  is  one  of  the  reasons 
why  the  malady  is  so  rarely  cured.  In  some  cases  the  infectious  process  takes 
on  some  of  the  aspects  of  a  tumor,  a  tuberculoma,  manifesting  a  tendency 
to  infiltration  and  induration,  with  but  httle  inclination  to  ulceration. 

Symptoms. — There  are  few  maladies  which  present  such  a  distressing 
picture  of  suffering  as  does  laryngeal  tuberculosis.  The  loss  of  voice,  which 
permits  speech  only  with  great  effort,  cuts  off  the  patient  from  pleasant 
intercourse  with  friends  and  from  expressing  any  but  his  most  urgent 
needs,  and  then  only  with  great  pain  and  effort.  The  thickening  of  adjacent 
tissues  nearly  always  makes  swallowing  most  difficult  and  painful,  and  for 
this  reason  urgent  thirst  must  be  satisfied  with  but  one  swallow  of  water. 
The  same  dysphagia  makes  the  use  of  solid  food  impossible  and  the  taking 
of  liquid  nourishment  almost  so,  yet  the  patient  cannot  combat  the  malady 
unless  well  nourished.  Because  of  these  factors  and  the  constant  pain  and 
loss  of  sleep,  the  loss  of  weight  in  laryngeal  tuberculosis  is  often  extra- 
ordinary, almost  equalling  that  seen  in  some  cases  of  malignant  growth 
elsewhere. 

In  the  earlier  stages  the  loss  of  voice  and  constant  discomfort  in  the  larynx 
may  be  the  only  symptoms.  Cough  is  present  in  all  cases  to  some  extent, 
and  is  often  exceedingly  painful.  After  all  the  muscles  about  these  parts 
have  had  their  action  inco-ordinated  by  direct  infiltration  or  disordered 
nerve  supply,  particles  of  food  get  into  the  larynx  and  cause  spasm  and  pain 
which  is  insufferable. 


376  DISEASES  OF   THE  LARYNX 

A  careful  examination  of  the  chest  wall  will  reveal  in  most  cases  some 
tuberculous  focus. 

If  the  laryngoscope  is  used  in  the  early  stages,  an  acute  hypersemia  may 
be  found,  but  in  the  chronic  type  the  appearance  will  be  that  of  marked 
local  anaemia.  A  tuberculous  lesion  may  be  found  in  the  epiglottis,  from 
whence  it  gradually  passes  downward,  or  the  disease  may  begin  below  the 
cords  and  work  its  way  upward.  These  tuberculous  areas  are  composed 
of  small  nodules  or  swellings  which  are  hypergemic  in  the  acute  cases  and 
anaemic  in  the  chronic  cases.  As  these  nodules  grow  they  may,  by  their 
mere  mechanical  presence,  cause  obstruction  to  free  respiration.  The 
infiltration  of  the  epiglottis  becomes  marked,  and  the  mucous  membrane 
may  become  dotted  by  a  multitude  of  small,  yellow  tubercles  which  are  easily 
recognized.  These  break  down  and,  having  done  so,  form  small  ulcers  which 
coalesce  and  form  larger  areas  of  ulceration.  Comparatively  rarely  the  vocal 
cords  develop  tiny  vegetations. 

Diagnosis. — ^The  discovery  of  a  pulmonary  tuberculous  process  in  the 
presence  of  the  hoarseness,  which  is  persistent  and  does  not  clear  up  under 
the  ordinary  treatment  for  acute  or  chronic  laryngitis,  raises  a  suspicion 
of  the  tuberculous  character  of  this  malady  at  once.  In  syphilitic  laryngitis 
the  history  of  the  patient,  the  reddened  areola  about  the  ulcers,  and  the 
presence  of  signs  of  syphilis  elsewhere  will  aid  the  diagnosis.  From  carci- 
noma of  the  larynx  we  can  separate  tuberculous  laryngitis  by  the  fact  that 
the  former  disease  occurs  as  a  single  new-growth  in  a  person  who  is  usually 
past  the  period  of  life  in  which  tuberculosis  is  prevalent. 

Prognosis. — The  prognosis  is  most  unfavorable  even  in  cases  seen  in 
the  early  stages,  because  the  ability  to  carry  on  repair  in  these  tissues  is  so 
poor  and  because  experience  has  taught  us  that  these  cases  rarely  recover. 

Treatment. — ^The  treatment  of  laryngeal  tuberculosis  can  be  carried  out 
only  by  a  skilled  and  dexterous  laryngologist.  Even  in  his  hands  it  may 
cause  much  distress  and  pain.  In  the  hands  of  the  t}To  clumsy  handling 
is  probably  worse  than  useless.  For  the  palliation  of  the  condition  and  of 
the  suffering  the  parts  may  be  sprayed  with  peroxide  of  hydrogen  followed 
by  a  mild  alkahne  solution,  and  these  in  turn  by  a  spray  containing  menthol 
5  grains,  oil  of  sandal-wood  5  minims,  and  liquid  albolene  1  ounce.  General 
tonic  treatment  such  as  is  used  in  all  cases  of  tuberculosis,  vnth  careful 
feeding,  is  essential.  As  a  rule,  the  patient  should  avoid  high  altitudes, 
particularly  if  they  are  windy,  as  the  drying  of  the  mucous  membrane 
increases  discomfort  in  the  larynx. 


SYPHILITIC  LARYNGITIS. 

Etiology. — S}^hilis  of  the  larynx  appears  during  the  secondary  and  ter- 
tiary stages  of  the  disease.  In  the  secondary  stage  it  may  amount  to  nothing 
more  severe  than  hypersemia  or  er}i;hema,  such  as  is  usually  met  with  in 
ordinary  acute  catarrhal  laryngitis,  but  in  other  instances  mucous  patches 
develop,  which  are  most  numerous  about  the  aryepiglottic  folds,  the  region 
of  the  vocal  cords,  the  arytenoid  cartilages,  and  on  the  edges  of  the  epiglottis. 


ACUTE  CATARRHAL  BRONCHITIS  377 

If  active  treatment  is  instituted  they  usually  readily  yield,  but  they  may 
become  distinct  ulcers.  When  these  heal  there  may  be  sufficient  thickening 
of  the  parts  to  cause  permanent  hoarseness. 

Tertiary  syphilis  appears  in  the  larynx  as  a  diffuse  or  circumscribed 
gummatous  growth,  which  usually  attaclcs  the  epiglottis,  the  cords,  and 
the  posterior  wall  of  the  larynx,  causing  thickening  and  infiltration  of  the 
tissues,  and  finally  ulceration  of  the  surface  in  some  instances.  The  cicatri- 
zation of  the  ulcers,  or  sclerosis  of  areas  by  infiltration,  may  cause  stenosis 
and  distortion  of  the  laryngeal  wall. 

Symptoms. — The  symptoms  are  hoarseness  and  loss  of  voice,  but  pain  is 
rarely  present. 

Diagnosis. — The  diagnosis  is  based  on  a  history  of  syphilitic  infection  or 
by  the  finding  of  evidences  of  syphilis  and  by  the  relief  which  follows  specific 
treatment.  Tuberculous  ulceration  is  not  so  rapid  in  its  development  and 
the  patient  reacts  to  tuberculin.  Further  than  this,  in  syphihs  the  upper 
surface  and  in  tuberculosis  the  lower  surface  of  the  epiglottis  is  usually 
affected.  From  malignant  growth  of  the  larynx  syphilis  is  separated  by 
the  fact  that  the  ulcer  is  solitary  in  epithelioma. 

Prognosis. — The  prognosis  is  good  if  treatment  is  used  early,  before  the 
stage  of  ulceration  is  well  developed.  After  ulcers  have  become  deep  and 
severe  they  may  be  healed  by  treatment,  but  cicatricial  contractions  neces- 
sarily appear  as  healing  goes  on. 

Treatment. — The  treatment  consists  of  iodide  of  potassium  and  the  mer- 
curials, as  in  other  cases  of  syphilis.     (See  Syphilis.) 


DISEASES  OF  THE  BRONCHI. 

ACUTE  CATARRHAL  BRONCHITIS. 

Definition. — Acute  bronchitis  is  an  inflammation  of  the  bronchial  tubes 
which  is  usually  confined  almost  entirely  to  the  mucous  membrane  lining 
them. 

History. — Bronchitis  has  been  recognized  as  a  distinct  condition  for  many 
centuries.  It  was  not,  however,  until  the  early  part  of  the  nineteenth  cen- 
tury that  this  term  was  used  to  describe  the  condition  now  under  discussion, 
when  Badham,  in  England,  and  Franck,  in  Germany,  first  employed  this 
term.  As  with  many  other  diseases  involving  the  thoracic  organs,  a  clear 
description  of  the  pathological  condition  was  first  given  to  us  by  the  French 
physician  Laennec. 

Distribution. — Acute  bronchitis  is  a  disease  which  occurs  in  all  parts  of 
the  world,  but  it  affects  chiefly  the  inhabitants  of  those  regions  in  which 
the  climate  is  moderately  cold  and  raw,  and  where  the  degree  of  humidity 
in  the  atmosphere  is  high.    On  the  other  hand,  hot  and  dry  portions  of  the 


378  DISEASES  OF   THE  BRONCHI 

earth's  surface  are  usually  free  from  this  disease.  Another  important  factor 
in  its  prevalence  is  sudden  changes  of  temperature  and  the  prevalence  of 
cold  winds  laden  with  moisture.  For  these  reasons  the  disease  is  most  fre- 
quent at  those  times  of  the  year  when  sudden  changes  of  temperature  are 
apt  to  occur,  and  therefore  is  commonly  met  with  in  the  late  winter  and 
early  spring  months. 

Etiology. — The  etiology  of  acute  bronchitis,  so  far  as  external  influences 
are  concerned,  has  just  been  described.  In  a  goodly  number  of  cases, 
practically  in  all,  it  is  probable  that  micro-organisms  have  much  to  do  with 
the  development  of  the  disease,  and  that  the  primary  hypersemia  and  con- 
gestion of  the  bronchial  mucous  membrane  is  due  to  the  exposure  of  the 
surface  of  the  body  to  external  influences  and,  to  a  slight  degree,  to  the 
passage  over  the  bronchial  mucous  membrane  of  an  atmosphere  which, 
because  of  its  physical  condition,  is  irritating  to  these  parts.  It  is  a  well- 
known  clinical  fact  that  exposure  of  the  surface  of  the  body  to  cold  seems 
to  be  followed  by  congestion  of  the  bronchial  mucous  membrane,  and  that 
this  actually  takes  place  has  been  proved,  first,  by  experiments  upon  animals, 
and,  second,  by  observations  upon  man.  Thus,  it  is  possible  by  the  external 
application,  alternately,  of  heat  and  cold  to  the  upper  portions  of  the  thorax 
to  produce  great  changes  in  the  capillary  circulation  of  the  larynx  and 
trachea  and  probably  the  bronchial  mucous  membrane  as  w^elL 

Much  depends,  too,  upon  the  general  health  of  the  patient  who  is  exposed 
to  the  provoking  causes  which  have  just  been  named.  Strong,  hearty,  or 
robust  individuals  who  have  a  well-balanced  circulation  and  elastic  blood- 
vessels frequently  suffer  from  no  pulmonary  inconvenience  from  exposure, 
but  persons  who  have  been  enfeebled  by  disease,  or  by  advancing  years,  or 
those  who  are  very  young  frequently  suffer  from  such  a  severe  congestion, 
and  it  may  produce  fatal  consequences.  Bronchitis  is  also  not  rarely  the 
result  of  an  inflammatory  process  which  begins  higher  up  in  the  respiratory 
tract  and  extends  to  the  tubes.  Practically  all  acute  infections  of  the  lung 
also  produce  some  bronchial  inflammation. 

So,  too,  any  condition  of  cardiac  or  renal  disease  which  impairs  circula- 
tory activity  is  exceedingly  prone  to  render  the  patient  susceptible  to  this 
form  of  inflammation.  We  find,  therefore,  that  acute  bronchitis  is  a  disease 
which  is  most  prevalent  in  infancy  and  old  age,  and  it  is  entirely  competent, 
at  these  two  periods  of  life,  to  produce  death  if  it  is  present  in  a  severe  form. 
Those  w^ho  have  been  attached  to  the  departments  for  children  in  large 
hospitals  cannot  fail  to  have  been  impressed  mth  the  very  great  frequency 
of  this  disease  in  the  winter  months,  and  also  with  its  rarity  among  the 
adults  who  come  to  the  same  institution  for  various  ailments. 

Both  sexes  are  equally  prone  to  suffer  from  acute  bronchitis,  but  it  is 
more  frequently  met  with  in  males  because  males  are  more  exposed  to  the 
provoking  causes  than  females. 

Certain  of  the  acute  infectious  diseases  very  strongly  predispose  to  this 
malady.  Thus,  it  is  nearly  always  present  in  a  well-developed  form  in  a 
case  of  measles,  even  when  that  disease  is  present  in  a  mild  form.  Again, 
there  are  but  few  cases  of  tvphoid  fever  which  do  not  have  a  certain  amount 
of  bronchitis. 


ACUTE  CATARRHAL  BRONCHITIS  379 

The  reason  that  bronchitis  so  frequently  compHcates  cardiac  disease 
depends  upon  the  intimate  relationship  between  the  circulation  in  the 
lungs  and  the  right  side  of  the  heart,  for  the  bronchial  veins  open  into  the 
venae  azygos  and  the  superior  intercostals,  and  so  are  intimately  connected 
with  the  right  side  of  the  heart.  These  bronchial  veins  also  anastomose 
closely  with  the  pulmonary  veins,  and  so  valvular  disease  which  results 
in  congestion  of  the  right  side  of  the  heart  naturally  tends  to  produce  a 
disturbance  of  the  circulation  in  the  bronchial  mucous  membrane. 

When  emphysema  of  the  lungs  is  present  the  coincident  bronchitis  is 
really  due  to  two  causes :  first,  the  congestion  of  the  right  side  of  the  heart 
which  is  so  apt  to  ensue  in  emphysema,  and,  second,  the  pathological 
changes  in  the  heart  result  in  impairment  of  the  bronchial  circulation. 
On  the  other  hand,  bronchitis  sometimes  leads  to  emphysema.  These 
affections  are  therefore  interactive. 

There  are  three  other  important  etiological  factors  in  the  production  of 
bronchitis  which  must  also  be  considered.  The  first  of  these  is  the  inhala- 
tion of  irritant  gases  or  vapors,  producing  what  is  known  as  acute  traumatic 
bronchitis.  The  second  is  the  inhalation  of  dust.  These  dusts  may  be 
vegetable,  animal,  or  mineral  in  their  origin.  Sometimes  all  three  forms 
are  combined.  Finally  there  can  be  no  doubt  that  the  inhalation  of  various 
micro-organisms  may  result  in  bronchial  infection. 

Of  the  forms  of  dust  which  produce  bronchitis  we  find  that  vegetable 
dust  seems  to  be  the  most  frequent  cause. 

That  form  of  bronchitis  which  most  frequently  follows  the  inhalation 
of  irritant  vapors  or  gases  is  seen  in  persons  who  have  been  exposed  to 
ammonia  fumes,  irritating  smoke,  or  to  chlorine  gas.  Another  form  of 
local  irritation  producing  bronchitis  is  that  which  is  seen  in  large  cities 
which  are  heavily  veiled  with  smoke  and  fog.  Thus,  in  the  city  of  London 
the  particles  of  moisture  in  the  air  become  coated  with  the  sooty  materials, 
and  so  evaporation,  even  in  houses  which  are  fairly  well  heated,  is  greatly 
impaired,  and  the  fog  penetrates  in-doors.  As  a  result  the  frequency  of 
acute  bronchitis  is  greatly  increased  in  London  in  those  seasons  of  the  year 
in  which  these  fogs  are  prevalent,  and  the  mortality  of  chronic  bronchitis 
is  wonderfully  increased  at  these  times.  So  powerful  an  influence  do  these 
deleterious  factors  exercise  that  it  is  a  well-known  fact  that  the  mortality  in 
the  city  of  London  may  be  doubled  in  those  weeks  in  which  the  fog  is  present. 
Thus,  on  some  occasions  the  mortality  is  as  high  as  46  per  cent,  as  against 
an  ordinary  death  rate  of  about  18  per  cent.  The  deaths  from  diseases  of  the 
respiratory  organs  rose  on  one  occasion  from  415  per  week  to  994  per  week 
during  the  prevalence  of  a  dense  fog.  Of  these,  694  were  due  to  bronchitis 
and  185  to  pneumonia.  That  this  increase  was  due  to  the  fog  and  not  to 
the  other  conditions  of  the  climate  is  proved  by  the  fact  that  a  similar 
increase  in  mortahty  did  not  take  place  in  surrounding  provincial  cities 
and  towns.  These  facts  are  well  emphasized  by  West  in  his  well-known 
book  upon  Diseases  of  the  Organs  of  Respiration. 

The  micro-organisms  infecting  the  bronchial  mucosa  are  the  pneumo- 
coccus,  which  is  most  common;  Friedlander's  bacillus,  the  Streptococcus 
pyogenes,  and  the  pyogenic  staphylococci.     The  Klebs-Loeffler  bacillus  is 


380  DISEASES  OF  THE  BRONCHI 

usually  present  in  the  bronchitis  which  complicates  diphtheria.  In  some 
cases  of  bronchitis  additional  micro-organisms  have  been  found,  such  as 
the  Bacillus  typhosus,  Bacillus  coli  communis,  and  various  forms  of  fungi. 
In  most  instances,  however,  bronchitis  is  polymicrobic  in  origin,  and  it  is 
often  impossible  to  decide  what  organism  is  the  primary  infecting  agent. 

Prevention. — Acute  bronchitis  can  only  be  prevented  by  proper  care  of 
the  general  health,  by  proper  clothing,  and  by  the  avoidance  of  climatic 
influences  which  are  known  to  be  deleterious.  Persons  who  have  learned 
by  experience  that  they  are  peculiarly  susceptible  to  the  various  provoking 
causes  named,  should,  by  change  in  climate  or  occupation,  avoid  these 
various  causes  of  irritation. 

Pathology  and  Morbid  Anatomy. — Acute  bronchitis  is  characterized  by 
hypersemia  and  swelling  of  the  mucous  membrane  lining  the  bronchial 
tubes,  accompanied  by  some  infiltration  of  the  submucous  tissues.  At  first 
there  may  be  an  almost  total  absence  of  secretion  or  undue  dryness  of  the 
surface  involved,  but  very  soon  the  engorged  mucous  glands  begin  to  pour 
out  into  the  lumen  of  the  tubes  considerable  quantities  of  mucus,  which  also 
soon  contains  epithelial  cells  coming  from  the  lining  of  the  glands  them- 
selves and  from  the  surface  of  the  mucous  membrane  as  well.  Leukocytes, 
which  have  undergone  diapedesis,  as  they  do  in  all  acute  inflammatory 
processes,  are  also  present,  and  even  red  blood  cells  may  be  seen.  A 
similar  extravasation  of  red  cefls  may  also  take  place  into  the  submucosa, 
and,  escaping  on  the  surface  tinge  the  sputum.  In  the  smaller  bronchi 
the  lining  epithehum  may  be  cast  ofl^  in  shreds,  and  if  the  inflamma- 
tion is  intense,  we  may  find  the  tubes  almost  or  completely  closed,  with 
resulting  capillary  bronchitis  or  suffocative  catarrh.  By  the  extension  of 
the  inflammation  to  the  peribronchial  tissues  and  the  pulmonary  alveoli 
there  is  developed  a  bronchopneumonia.  (See  Bronchopneumonia.)  As 
recovery  takes  place  the  dead  epitheliufn  and  extravasated  cells  are  expelled 
from  the  tubes  by  coughing,  and  new  epithehum  is  developed  from  deeper 
layers  of  cefls.  Sometimes,  particularly  when  a  large  number  of  infecting 
micro-organisms  are  present,  the  sputum  is  distinctly  purulent.  When 
bronchial  inflammation  persists  for  any  length  of  time,  or  the  attacks  are 
frequently  recurrent,  permanent  thickening  of  the  submucosa  results.  This 
fibrosis  may  extend  to  adjacent  structures  (peribronchitis)  or  be  continuous 
with  the  increased  fibrous  tissue  of  chronic  interstitial  pneumonia. 

Symptoms. — The  symptoms  of  acute  bronchitis  can  be  divided  into  three 
stages,  namely,  that  of  onset,  the  stage  of  profuse  secretion,  and  the  stage 
of  convalescence. 

In  the  stage  of  onset  there  may  be  a  chill,  which  usually  is  not 
severe;  a  short,  dry  cough  which  may,  by  its  persistance,  be  annoying, 
and,  owing  to  the  dry  and  inflamed  state  of  the  mucous  membrane  of  the 
bronchial  tubes,  be  distressing  because  of  the  soreness  or  pain  it  produces 
under  the  sternum.  If  the  degree  of  swelling  of  the  mucous  membrane 
is  marked,  there  may  be  a  sense  of  oppression,  and  the  breathing  may  be  a 
little  quickened.  The  temperature  of  the  body  is  usually  not  much  above 
normal  in  the  adult,  but  in  children  it  is  often  as  high  as  102°  or  even  103°, 
and  the  pulse  is  apt  to  be  rapid  in  direct  proportion  to  the  degree  of  fever. 


ACUTE  CATARRHAL  BRONCHITIS  381 

Auscultation  at  this  time  reveals  an  increased  roughness  of  the  inspiratory 
or  expiratory  bronchial  sounds,  and  perhaps  a  few  dry  rales  between  the 
shoulder-blades. 

In  the  second  stage  there  is  a  disappearance  of  the  soreness  in  the 
chest,  but  the  cough  may  be  persistent,  and  is  more  or  less  productive 
of  expectoration  of  mucopurulent  material.  Febrile  movement  continues 
if  that  symptom  has  been  present  earlier.  The  pulse  is  but  slightly 
quickened  and  auscultation  reveals,  particularly  over  the  bronchial  tubes 
posteriorly,  large,  moist  rales  and  rhonchi. 

The  duration  of  an  attack  of  acute  bronchitis  rarely  exceeds  ten  days 
to  two  weeks,  and  is  often  shorter  than  this. 

Treatment. — The  treatment  of  acute  bronchitis  divides  itself  into  two 
parts:  that  part  which  is  devoted  to  allaying  the  inflammation  in  its  early 
stages,  and  that  which  is  directed  toward  the  dissipation  of  the  results  of 
the  inflammation  after  it  has  peen  present  for  some  days.  In  the  early  stage 
no  better  remedy  can  be  administered  internally  than  a  prescription  which 
contains  in  each  dose  -|  a  drachm  of  syrup  of  ipecac  and  1  teaspoonful  to 
2  teaspoonfuls  of  the  official  liquor  potassii  citratis  of  the  United  States 
Pharmacopoeia.     This  should  be  administered  every  three  or  four  hours. 

If  cough  is  an  annoying  symptom,  and  there  is  much  pain  in  the  chest, 
Dover's  powder  may  be  given  to  an  adult  in  the  dose  of  2  or  3  grains  every 
three  or  four  hours  until  10  grains  have  been  taken.  A  mustard  plaster  may 
be  applied  to  the  chest,  back  and  front,  or  the  thorax  may  be  rubbed  with 
ammonia  liniment  or  with  chloroform  liniment.  In  children  a  very  useful 
counterirritant  application  to  the  chest  is  1  drachm  of  the  oil  of  amber  in 
2  tablespoonfuls  of  sweet  oil.  If  the  patient  be  a  child,  and  if  the  air  of 
the  bed-room  is  particularly  dry  and  irritating,  because  it  is  furnace-heated, 
much  relief  can  be  obtained  by  disengaging  a  small  quantity  of  steam. 
This  may  be  given  off  from  a  tea-kettle  which  is  kept  boiling  constantly, 
or  may  be  obtained  by  dropping  large  pieces  of  unslaked  lime  into  a  tub  of 
water.  It  is  probable  that  when  the  latter  procedure  is  resorted  to  the  air 
of  the  room  not  only  contains  an  extra  amount  of  moisture,  but  fine  particles 
of  lime,  which  act  advantageously  upon  the  bronchial  mucous  membrane. 

If  the  evidences  of  bronchial  irritation  are  very  marked,  the  patient, 
whether  he  be  an  adult  or  a  child,  should  sleep  in  a  bronchitis  tent.  A 
bronchitis  tent,  it  will  be  remembered,  consists  in  a  tent-like  arrangement 
of  sheets  spread  over  the  bed,  and  resting  upon  four  corner  sticks,  one  of 
which  is  tied  to  each  corner  of  the  bed.  Under  this  canopy  the  patient  will 
have  plenty  of  air,  and  the  steam  from  a  kettle  can  be  disengaged  within  its 
confines.  If  necessary,  1  or  2  grains  of  menthol  may  be  added  to  the  hot 
water  every  two  or  three  hours.  In  other  instances  the  bronchial  irritation 
will  be  greatly  soothed  by  pouring  into  the  boiling  water  a  tablespoonful  of 
a  mixture  composed  of  equal  parts  of  compound  tincture  of  benzoin,  oil 
of  eucalyptus,  and  oil  of  pine. 

After  secretion  has  begun  to  form  in  the  secondary  stage  of  acute  bron- 
chitis it  then  becomes  necessary  to  administer  not  sedatives,  but  stimulant 
expectorants,  and  of  these  chloride  of  ammonium,  without  any  doubt,  is 
usually  followed  by  the  best  results.    From  5  to  10  grains  of  this  drug  may 


382  DISEASES  OF  THE  BRONCHI 

be  given  with  equal  parts  of  the  fluid  extract  of  Ucorice  and  water  every 
four  or  five  hours  to  an  adult,  and,  if  cough  is  excessive,  ^  of  a  grain  of 
sulphate  of  codeine  or  20  drops  of  paregoric  may  be  added  to  each  dose. 
Under  the  influence  of  this  remedy  the  expectoration  of  yellow  or  muco- 
purulent sputum  is  at  first  increased,  but  at  the  end  of  twenty-four  or  forty- 
eight  hours  the  quantity  diminishes. 

When  there  seems  to  be  lack  of  secretion,  the  compound  licorice  mixture 
of  the  United  States  Pharmacopoeia,  which  contains  a  small  quantity  of 
tartar-emetic,  may  be  used  in  place  of  the  plain  extract  of  licorice  just 
named.  If  for  any  reason  the  cough  and  expectoration  persist  and  do  not 
diminish  under  the  use  of  the  chloride  of  ammonium,  we  may  give  with 
advantage  5  to  10  minims  of  the  oil  of  sandal-wood  in  capsules,  three  or  four 
times  a  day.  Other  patients  do  well  at  this  time  if  they  receive  5  minims 
of  the  oil  of  eucalyptus  in  capsules  three  times  a  day.  The  latter  remedy, 
however,  is  quite  apt  to  disorder  the  stomach.  Another  very  valuable 
remedy  in  the  secondary  stage  of  bronchitis,  to  promote  expectoration,  is 
terpin  hydrate,  which  is  best  given  in  the  form  of  an  elixir,  dose,  a  tea- 
spoonful,  and  which  may  be  much  increased  in  its  efficiency  if  to  each 
dose  is  added  ^  of  a  grain  of  heroin,  or  ^  of  a  grain  of  codeine  sulphate. 
The  dose  of  terpin  hydrate  is  from  2  to  5  grains  four  times  a  day,  but 
in  obstinate  cases  larger  doses  may  be  administered.  Terebene  may  also 
be  given  in  capsules  in  the  dose  of  5  minims  three  or  four  times  a  day. 

If  the  general  nutrition  of  the  patient  is  not  good  and  he  seems  somewhat 
debilitated,  the  employment  of  cod-liver  oil,  or  syrup  of  iodide  of  iron,  in 
moderate  doses,  will  often  produce  the  most  advantageous  results  at  this  stage 
of  the  illness. 

CHRONIC  CATARRHAL  BRONCHITIS. 

Definition  and  Symptoms. — By  chronic  bronchitis  is  meant  a  condition  in 
which  there  exists  a  chronic  inflammatory  process  in  the  bronchial  mucous 
membrane,  as  a  result  of  which  the  patient  suffers  from  cough  and  the 
expectoration  of  thick,  mucopurulent  sputum.  When  uncomplicated  there 
is  no  febrile  movement  in  association  with  this  condition,  nor  is  there,  as 
a  rule,  any  loss  of  flesh  or  impairment  of  the  general  health.  It  may  be 
regarded  as  a  subacute  continuation  of  an  acute  cold.  The  chief  objection 
to  the  term  "  chronic  bronchitis  "  is  that  it  so  often  is  applied  by  the  careless 
or  ignorant,  or  by  those  who  wish  to  use  an  euphemism,  to  designate  a  far 
more  serious  condition,  such  as  pulmonary  tuberculosis  or  bronchiectasis. 

Treatment. — The  treatment  of  chronic  bronchitis  is  practically  identical 
with  that  of  the  later  stages  of  the  acute  form,  which  has  just  been  described, 
but  the  most  important  thing  for  the  physician  to  do,  to  whom  is  presented 
a  so-called  case  of  chronic  bronchitis,  is  to  carefully  exclude  tuberculosis  or 
renal  disease  as  causative  factors  in  the  case.  Many  cases  of  so-called  chronic 
bronchitis  are  treated  for  weeks  with  ordinary  expectorants  when  tuberculosis 
is  present  or  Bright's  disease  is  the  real  cause  of  the  disorder. 


BRONCHIECTASIS  383 


BRONCHIECTASIS. 


Definition. — Bronchiectasis,  as  its  name  implies,  is  a  condition  in  which 
the  bronchial  tubes  are  dilated.  This  dilatation  may  occur  in  three  forms, 
namely,  the  cylindrical  or  fusiform,  the  saccular,  and  the  trabecular  or 
moniliform.  The  first  of  these  is  the  only  true  type  of  bronchiectasis,  but 
the  other  forms  are  those  most  commonly  met  with. 

The  disease  is  not  common  in  its  well-developed  form.  If  we  combine 
the  statistics  of  the  Brompton  Hospital,  of  London,  with  those  of  Biermer 
and  Willigk,  we  find  that  in  8144  autopsies  bronchiectasis  was  found  in  about 
4  per  cent.  These  are,  however,  postmortem  figures,  and  do  not  represent 
a  certain  proportion  of  cases  which  do  not  come  to  autopsy  because  of  a 
respiratory  ailment. 

Etiology,  Pathology,  and  Morbid  Anatomy. — The  saccular  form  is  common 
in  adults,  and  when  it  is  present,  the  lung,  at  autopsy,  contains  one  or 
more  saccules,  or  globular  cavities,  which  usually  are  not  very  large,  but  may 
be  the  size  of  a  small  lemon.  These  cavities  or  open  spaces,  when  large, 
are  due  not  only  to  simple  dilatation  of  the  bronchi,  but  to  involvement  of 
the  surrounding  tissues  as  well,  and  their  walls  are  composed  of  parts  of 
the  bronchial  tubes  and  thick  connective  tissue  which  has  been  formed  in 
part  as  the  result  of  chronic  inflammatory  changes,  the  lung  tissue  having 
undergone  fibroid  change.  Sometimes  these  spaces  are  filled  with  thickened, 
inspissated  secretion,  and  seem  like  closed  cavities.  It  is  readily  seen, 
therefore,  that  the  differentiation  between  this  state  and  fibroid  phthisis 
(see  Tuberculosis  of  the  Lung),  so  called,  may  be  by  no  means  easy,  par- 
ticularly as  these  pouches  may  become  infected,  ulcerate,  and  really  form 
small  abscesses. 

The  trabecular  form  is  still  less  a  true  bronchiectasis,  and  yet  it  is  the 
condition  most  commonly  met  with,  and  to  which  the  term  bronchiectasis 
is  most  frequently  applied.  It  consists  in  irregular  cavities  with  smooth 
Hnings,  which  cavities  are  surrounded  by  dense  walls  of  overgrown  con- 
nective tissue  which  do  not  contain  any  signs  of  remnants  of  the  tissues  of 
the  bronchial  tubes.  On  the  contrary,  the  only  relation  borne  by  the  bron- 
chial tube  to  such  a  cavity  is  that  it  forms  the  trabeculse  with  the  atrophied 
bloodvessels.  These  cavities  are  often  joined  one  to  another  by  openings, 
so  that  the  lung  may  be  thoroughly  riddled  with  spaces  more  or  less  well 
filled  with  secretion. 

Cylindrical  bronchiectasis  (Figs.  51  and  52)  is  usually  developed  in  children 
as  the  result  of  strain  upon  the  bronchial  tubes  produced  by  the  violent 
efforts  in  whooping-cough  or  measles.  It  probably  depends  primarily  upon 
inherent  weakness  of  the  muscular  and  elastic  coats  of  the  tubes.  The 
affected  bronchus  is  uniformly  dilated  in  its  entire  circumference  for  a  con- 
siderable distance,  and  this  dilatation  may  be  so  great  that  its  calibre  is 
increased  to  twice  or  thrice  the  normal.  In  other  instances  it  is  dilated  in 
sections,  with  a  normal  or  nearly  normal  calibre  between. 

When  bronchiectasis  occurs  in  the  saccular  and  trabecular  type  it  is  a 
subacute  or  chronic  disorder,  and  results  from  chronic  inflammation  of  the 


384 


DISEASES  OF  THE  BRONCHI 


bronchial  tubes,  with  resulting  atrophy  of  the  elastic  and  muscular  coats. 
Of  the  provoking  causes  influenza  is  an  important  factor,  i^nother  cause  is 
the  progress  of  cicatricial  or  cirrhotic  change  in  the  pulmonary  parenchyma, 
which,  as  it  proceeds,  distorts  the  bronchial  tubes,  narrowing  them  in  some 
places  and  widening  them  in  others.  In  other  instances  it  can  be  readily 
understood  how  chronic  thickening  of  the  visceral  layer  of  the  pleura  may 
so  result.  In  still  others  a  localized  bronchiectasis  may  be  caused  by  the 
entrance  of  a  foreign  body. 


Fig.  51 


Bronchiectasis,  originating  in  acute  lobar  pneumonia.  Marked  saccular  and  cylindrical  dilatations 
with  a  large  gangrenous  cavity  in  the  middle  lobe.  Duration  eleven  months.  From  a  case  under  the 
care  of  Dr.  Maguire.  Dr.  Barty  Bang.  (Brompton  Hospital  Museum.  Scottish  Medical  and  Surgical 
Journal.) 


The  influence  of  age  in  the  development  of  the  various  types  of  bronchi- 
ectasis is  quite  noteworthy.  Cylindrical  dilatation  is  largely  a  condition 
limited  to  childhood,  and  the  saccular  and  trabecular  types  are  chiefly  met 
with  in  adults.  It  has  been  thought  by  some  physicians  that  the  latter  forms 
occur  with  increasing  frequency  as  old  age  is  approached,  but  the  statistics  of 
Barty  King  indicate  that  the  age  incidence  of  the  pure  type  is  from  thirty 
to  forty  years.    Thus,  53.1  per  cent,  of  his  cases  occurred  between  twenty 


BRONCHIECTASIS 


385 


and  forty  years.     The  same  observer  places  the  proportions  of  the  two  sexes 
as  77  per  cent,  in  males  and  23  per  cent,  in  females. 

Symptoms. — The  symptoms  of  bronchiectasis  naturally  vary  greatly  with 
the  form  of  the  disease  which  is  present.  Cough  of  severe  degree  may  be 
considered  the  most  constant  of  them  all.  This  cough  is  peculiar  in  that 
in  many  cases  it  is  particularly  severe  in  the  morning,  persisting  until  the 
patient  has  rid  his  dilated  and  feeble  bronchi  of  the  secretions  which  have 
accumulated  in  them  during  the  night.  Not  only  is  this  cough  peculiar  in 
this  respect,  but  it  not  infrequently  happens  that  the  patient,  after  a  pro- 


FiG.  52 


Cylindrical  bronchiectasis.     A  typical  case.       Dr.  Barty  King.      (St.  Thomas'  Hospital  Museum. 
Scottish  Medical  and  Surgical  Journal.) 


longed  attack  of  coughing  which  is  unproductive,  is  enabled  to  get  rid  of 
a  large  quantity  of  sputum,  which  may  come  away  in  a  gush  or  which 
may  not  be  dislodged  until  by  some  change  in  posture  drainage  from  the 
bronchiectatic  area  can  take  place. 

The  sputum  is  also  somewhat  characteristic,  for  it  is  often  grayish- 
brown  in  appearance,  somewhat  fetid  in  odor,  and  separates  when  placed 
in  a  glass  into  three  layers,  the  upper  one  brownish  and  thin,  the  second 
one  mucoid,  and  the  third  granular  and  filled  with  dead  epithelial  cells  and 
pus  corpuscles.  This  lower  layer  also  contains  large  crystals  of  the  fatty 
25 


386  DISEASES  OF  THE  BRONCHI 

acids  and  crystals  of  hsematoidin.  The  sputum  is  so  distinctly  purulent 
that  it  may  closely  resemble  that  expectorated  in  cases  of  pulmonary 
abscess,  a  resemblance  still  further  increased  by  the  fact  that  it  may  be 
extremely  fetid.  It  is  not  nummular,  as  in  many  cases  of  phthisis,  and  it 
rarely  contains  elastic-tissue  fibres,  which  is  of  some  importance  in  dif- 
ferential diagnosis.  Fever  is  usually  not  present  unless  the  purulent  process 
in  the  bronchi  is  marked  and  septic  absorption  results.  An  additional  symp- 
tom, sometimes  met  with,  is  hcemopiysis  from  ulceration  of  a  bloodvessel. 
The  physical  signs  of  bronchiectasis  have  little  about  them  that  is  distinctly 
characteristic,  and  for  this  reason  an  absolute  diagnosis  may  be  difficult  or 
impossible  unless  the  lesions  are  so  far  advanced  as  to  have  affected  the 
whole  lung  and  caused  akeration  in  the  configuration  of  the  chest.  When 
the  bronchiectatic  spaces  or  cavities  are  large  the  physical  signs  are  prac- 
tically identical  with  those  of  pulmonary  tuberculosis  with  cavity  forma- 
tion;'but  there  is  this  important  difference,  namely,  that  the  cavities  in 
tuberculosis  are  commonly  apical  while  the  cavernous  breathing  of  bron- 
chiectasis is  usually  most  marked  near  the  base.  The  physical  signs  of 
cavity  formation  also  vary  with  the  condition  of  the  cavity — that  is,  whether 
it  is  full  of  secretion  or  empty,  and  therefore  change  in  the  patient's  posi- 
tion, and  cough  with  expectoration,  may  cause  very  great  differences  both 
in  examination  by  auscultation  and  percussion.  Loud,  moist  rales  and 
amphoric  breathing  may  be  present. 

Diagnosis. — -It  is  manifest  from  what  has  just  been  said  that  the  differ- 
ential diagnosis  of  bronchiectasis  from  pulmonary  tuberculosis  may  be  quite 
difficult  and,  indeed,  impossible  in  certain  cases,  for  it  not  uncommonly 
happens  that  a  superficial  dilated  and  sacculated  area  in  the  lung  gives,  on 
auscultation  and  percussion,  physical  signs  which  are  identical  with  those 
which  are  produced  in  pulmonary  tuberculosis  with  cavity.  The  presence  of 
tubercle  bacilli  and  of  yellow  elastic  tissue  in  the  sputum,  of  hectic  fever,  of 
rapid  loss  of  flesh,  and  of  night-sweats  point  to  tuberculous  infection.  Another 
useful  differential  point  is  the  fact  that  in  tuberculosis  the  cavity  is  usually 
at  the  apex,  whereas  in  bronchiectasis  it  is  lower  down  in  the  lung.  Still 
another  point  is  that  the  patient  is  rarely  as  ill  as  in  tuberculosis,  and  can 
get  about  year  after  year  unless  some  acute  intercurrent  pulmonary  malady 
intervenes. 

Further  than  this,  bronchiectasis  and  pulmonary  tuberculosis  may  exist 
simultaneously.  Thus,  in  68  cases  of  bronchiectasis  observed  by  Trajan- 
owski,  21  occurred  in  individuals  who  were  affected  with  phthisis,  and  in 
75  autopsies  on  individuals  who  died  from  phthisis  Wilson  Fox  found 
bronchiectasis  in  27  cases.  Twenty-one  (21)  were  of  the  fusiform  variety 
and  six  (6)  were  saccular. 

Complications. — Haemoptysis,  as  a  complication  of  bronchiectasis,  is  rarely 
severe  and  occurred  in  Barthez's  cases  16  times  out  of  39  cases.  Grainger 
Stewart  met  with  it  3  times  in  8  cases,  and  Fowler  met  with  it  14  times 
in  35  cases.    Three  of  these  cases  were  tuberculous.^ 

Another  complication  is  rheumatoid  arthritis.    I  have  recently  had  a  case 

^  For  some  of  the  cases  in  French  literature  see  De%'ic  and  Bertier,  Lyon  medical,  January,  1904. 


BRONCHIECTASIS  387 

under  my  care  in  which,  after  many  years  of  chronic  bronchiectasis,  a  maiden 
lady  developed  multiple  arthritis,  and  in  the  course  of  a  few  weeks  became 
completely  disabled.  Sometimes  no  more  serious  joint  difficulties  arise  than 
swelling  of  the  finger-joints  and  clubbing  of  the  finger-tips,  with  incurvation 
of  the  nails,  or  the  case  develops  true  pulmonary  osteoarthropathy.  The 
joint  complications  are  probably  septic  in  origin.  Pulmonary  gangrene  may 
also  develop,  and  Duret  has  operated  on  such  cases  with  success. 

Brain  abscess  may  arise  from  a  septic  focus  in  bronchiectasis. 

Cyanosis  and  dyspnoea  on  exertion  are  such  constant  symptoms  that  they 
can  scarcely  be  considered  as  complications. 

When  we  consider  the  state  of  the  tissues  involved  we  can  readily  under- 
stand how  readily  a  septic  bronchopneumonia  may  be  developed  in  these 
cases,  either  as  a  result  of  direct  extension  of  the  inflammatory  process  from 
the  area  primarily  involved,  or  by  the  inspiration  into  other  parts  of  the 
lung  of  septic  material  during  paroxysms  of  coughing. 

Prognosis. — This  depends  upon  the  state  of  the  patient's  health,  the 
presence  or  absence  of  sepsis,  and  the  presence  or  absence  of  tuberculous 
infection.  In  severe  forms  the  health  is  greatly  impaired.  Recovery  from 
the  condition  itself,  if  it  be  well  developed,  is  manifestly  impossible.  Never- 
theless, life  may  continue  for  many  years. 

Treatment. — The  treatment  of  well-developed  bronchiectasis  can  be  only 
palliative.  Once  the  condition  of  dilatation  of  the  bronchial  tubes  has 
been  established,  it  is  evident  that  they  cannot  be  brought  back  to  their 
normal  calibre.  On  the  other  hand,  in  the  early  stages  of  bronchiectasis, 
much  can  be  done  in  the  way  of  palliative  treatment.  It  is  a  mistake,  how- 
ever, to  give  sedatives  to  control  the  cough  unless  the  cough  is  so  excessive 
that  it  materially  interferes  with  sleeping  and  eating,  for  cough  is  a  measure 
designed  by  nature  to  rid  the  dilated  tubes  of  the  secretions  which  certainly 
do  harm  if  they  are  retained.  Ordinarily,  expectorant  remedies  cannot  be 
expected  to  do  as  much  good  as  they  do  in  ordinary  cases  of  bronchitis. 
The  best  to  be  employed  are  creosote  in  doses  of  3  to  5  minims  three  or 
four  times  a  day;  guaiacol  in  the  dose  of  3  minims  three  times  a  day,  or 
guaiacol  carbonate  in  the  dose  of  3  grains  three  times  a  day.  In  some 
instances  much  good  follows  the  administration  of  a  mixture  containing 
iodide  of  ammonium.  Still  other  cases  are  benefited  by  the  chloride  of 
ammonium. 

It  must  not  be  forgotten  that  many  cases  of  bronchiectasis  which 
have  lasted  for  some  years  suffer  as  well  from  feebleness  and  dilatation 
of  the  right  side  of  the  heart,  and  the  degree  of  cyanosis  and  dyspnoea  on 
exertion  can  be  much  decreased  by  the  administration  of  small  and  con- 
tinuous doses  of  digitalis  or  strophanthus,  and,  in  some  instances,  by  the 
proper  use  of  strychnine.  A  certain  amount  of  rest  in  bed  or  on  a  couch 
every  day  is  very  advisable;  and  if  the  patient  seems  to  have  great  difficulty 
in  expectorating  the  contents  of  certain  cavities,  experiments  should  be 
made  with  different  postures  to  determine  that  in  which  the  cavity  is  most 
easily  drained,  and  he  should  be  instructed  to  take  this  posture  in  order 
to  avoid  prolonged  and  exhausting  spells  of  coughing. 

Within  the  last  few  years  a  number  of  clinicians  have  warmly  advocated 


388  DISEASES  OF   THE  BRONCHI 

the  employment  of  intratracheal  injections  of  medicaments  in  cases  of 
bronchiectasis.  Various  mixtures  have  been  employed,  of  which  perhaps 
the  most  popular  have  contained  menthol,  guaiacol,  ohve  oil,  or  albolene. 
They  do  little  good.  In  other  instances,  asserted  good  results,  so  far  as 
elimination  of  the  symptoms  are  concerned,  have  followed  the  inhalation 
of  various  drugs,  such  as  the  vapor  of  chloride  of  ammonium,  creosote, 
and  tar. 

So  far  as  climatic  treatment  is  concerned,  these  patients  should  carefully 
avoid  high,  dry  altitudes,  and  should  resort  to  hill  altitudes  or  the  seaside 
resorts,  unless  the  latter  are  too  damp,  in  which  case  the  drier  places  must 
be  sought,  as,  for  example,  Thomasville,  Georgia;  Lakewood,  New  Jersey, 
or  some  similar  spot  not  too  near  the  sea,  where  there  is  a  sandy  soil  and 
a  heavy  pine  growth.  Such  patients,  too,  should  be  warned  of  the  danger 
of  complications  which  may  follow  exposure  to  sudden  changes  of  temper- 
ature and  to  wet,  and  should  wear  flannels  next  to  the  skin  all  the  year 
round,  if  possible,  to  avoid  chilling  the  surface.  If  these  precautions  are 
taken,  the  greater  amount  of  time  spent  in  the  fresh  air  the  better,  as  in-door 
life  for  these  patients  is  disadvantageous  if  the  climate  is  at  all  suitable  to 
their  condition. 


FIBRINOUS  BRONCHITIS. 

Definition. — Fibrinous  bronchitis  is  an  exceedingly  rare  affection,  char- 
acterized by  the  formation  of  a  fibrinous  exudate  which  makes  a  cast  of  the 
bronchial  tubes.  As  ordinarily  observed  it  is  in  no  way  related  to  diphtheria, 
in  which  disease,  however,  casts  of  the  larynx  and  trachea  and  even  of  the 
bronchial  tubes  sometimes  form. 

Etiology. — The  cause  of  this  strange  affection  is  practically  unknown. 
When  it  occurs  as  a  complication  or  sequel  of  other  diseases,  it  seems  to 
bear  no  relation  to  them  save  that  of  coincidence.  The  condition  is  much 
more  frequent  in  males  than  in  females,  and  is  not  particularly  prone  to 
occur  at  any  particular  age.  West  states  the  youngest  case  recorded  is 
four  years  of  age,  and  the  oldest  seventy-two  years.  It  has  occurred  more 
frequently  after  acute  croupous  pneumonia  and  during  the  progress  of 
pulmonary  tuberculosis  and  ordinary  chronic  bronchitis  than  in  other 
maladies,  but  its  occurrence  in  these  affections  is  not  sufficiently  constant 
to  justify  us  in  considering  that  these  relationships  are  direct.  In  some 
instances  it  is  associated  with  the  presence  of  mitral  disease  of  the 
heart. 

Pathology. — The  casts  when  expelled  are  found  to  be  composed  of  masses 
of  gelatinous  or  pulpy-looking  material  which,  when  floated  in  water  or 
carefully  spread  upon  a  glass  surface,  are  found  to  be  in  the  form  of  the 
bronchial  tubes;  sometimes  even  of  the  smaller  tubes.  The  casts  are  tough 
and  yellowish-white  in  appearance,  and  many  are  composed  of  fibrin  in 
which  may  be  found  white  blood  cells  and  epithelium  from  the  bronchial 
mucous  membrane.  Other  casts  contain  no  demonstrable  fibrin,  but  are 
rich  in  mucin.    Whether  they  are  distinct  forms  or  altered  fibrinous  casts 


FIBRINOUS  BRONCHITIS 


389 


is  not  known.  The  cast  may  be  hollow  or  filled  with  gelatinous  mucus. 
It  is  a  curious  fact  that  these  casts  may  form  without  resulting  in  serious 
lesions  of  the  lining  membrane  of  the  tubes,  for  even  the  epithelial  lining 
of  the  bronchial  tubes  may  not  be  found  seriously  impaired  after  a  cast  is 
thrown  off  (Fig.  53). 

As  the  affection  is  very  rare,  and  still  more  rarely  causes  death,  we  know 
comparatively  little  of  its  true  morbid  anatomy.  Sometimes  casts  have  been 
found  at  autopsy  when  the  condition  was  not  suspected  to  be  present,  and 
in  other  cases  in  which  casts  had  been  thrown  off  in  life  none  have  been 
found  at  the  postmortem. 


Fig.  53 


2  cm. 
Cast  from  a  case  of  fibrinous  bronchitis. 


m 


Symptoms. — The  symptoms  of  fibrinous  bronchitis  chiefly  consist 
severe  attacks  of  cough  and  dyspnoea,  the  cough  being  an  effort  to  dislodge 
the  membrane  and  the  dyspnoea  the  result  of  the  obstruction  to  the  respi- 
ration. Sometimes  the  dyspnoea  has  been  quite  urgent,  but  it  has  usually 
been  almost  completely  reUeved  after  the  cast  is  expelled.  This  expulsion 
of  a  cast  may  occur  once  in  a  lifetime,  once  in  several  weeks,  once  in  several 
days,  or  several  casts  may  be  expelled  in  one  day.  Rarely  the  formation  of 
a  cast  suggests  periodicity.  While  the  cough  is  usually  severe  in  the  effort 
to  dislodge  the  exudate,  the  expulsion  may  be  readily  accomplished.  Occa- 
sionally hcemoptysis  complicates  the  case,  usually  amounting  to  nothing  more 


390  DISEASES  OF   THE  BRONCHI 

than  slight  streaking  of  the  expelled  membrane,  but  in  other  instances 
the  bleeding  is  quite  profuse.  The  blood  comes  from  the  bronchial,  not  from 
the  pulmonary,  vessels.  Fever  may  be  present  in  the  acute  cases,  but  is 
usually  absent  in  the  more  chronic  ones. 

Diagnosis. — This  condition  must  be  separated  from  diphtheria,  which  can 
be  done  by  the  absence  of  false  membrane  in  the  fauces  and  larynx;  from 
croupous  pneumonia,  which  is  possible  by  reason  of  the  absence  of  the 
fever  and  other  signs  of  that  disease;  and  from  foreign  bodies  in  the  air- 
passages,  which  cause  dyspnoea  and  violent  attacks  of  cough,  by  the  history 
of  the  patient. 

Prognosis. — The  prognosis  as  to  return  of  the  disorder  is  bad,  as  most 
cases  suffer  from  recurrence,  although  acute  cases  in  which  complete  recovery 
has  occurred  have  been  reported.  In  regard  to  the  effect  of  the  disease  on  life 
it  may  be  said  that  this  varies  greatly  with  the  general  state  of  the  patient's 
health  and  upon  the  gravity  of  the  diseases  which  are  associated  with  it. 

In  cases  with  no  grave  complications  recovery  may  be  expected  in  a 
majority,  both  as  to  complete  temporary  recovery  and  recurrence. 

Treatment. — ^The  only  plan  of  treatment  which  has  proved  itself  of  value 
in  a  sufficient  number  of  cases  to  be  regarded  with  any  confidence  is 
the  use  of  iodide  of  potassium  in  full  doses.  Some  patients  seem  to  be 
made  more  comfortable  by  the  inhalation  of  steam.  Climatic  change  is 
often  essential,  and  Southern  California,  or  Florida,  or  Madeira,  may  be 
resorted  to. 

BRONCHIAL  ASTHMA. 

Definition. — Strictly  speaking,  the  word  "  asthma  "  may  be  applied  to  any 
condition  in  which  the  respiration  is  labored  and  difficult,  but  in  medicine 
it  is  most  commonly  used  to  describe  a  condition  of  difficult  breathing  due  to 
constriction  of  the  bronchial  tubes  and  further  narrowing  of  their  calibre  by 
swelling  of  the  mucous  membrane  lining  them.  This  state  of  spasm  of  the 
bronchial  muscle  fibres  and  hypersemia  of  the  mucous  membrane  depends 
upon  a  neurosis.  This  neurosis  may  arise  in  turn  from  a  large  number  of 
causes,  all  of  which  probably  exercise  their  influence  through  the  pneumo- 
gastric  nerves. 

It  is  unfortunate  that  the  term  "asthma"  has  also  been  applied  to  labored 
breathing  due  to  various  toxsemias,  such  as  ureemia  and  the  coma  of  diabetes. 
Renal  disease  may,  it  is  true,  indirectly  produce  true  asthma,  but  this  word 
ought  not  to  be  applied  to  that  form  of  labored  breathing  in  which  there  is 
no  swelling  or  spasm  of  the  sort  described  in  the  preceding  paragraph.  The 
term  asthma  is,  therefore,  used  in  this  article  to  mean  bronchial  asthma. 

Etiology. — The  cause  of  asthma  in  many  cases  cannot  be  determined,  and 
in  some  persons  it  is  evidently  due  to  some  lack  of  stability  in  the  nervous 
control  of  the  bronchial  tubes.  In  others  the  asthmatic  attack  arises 
because  of  the  inhalation  of  bad  air,  which  acts  as  an  irritant  to  the  respiratory 
tract,  either  because  of  the  state  of  the  atmosphere  itself  or  because  the  air  is 
laden  with  dust.  The  influence  exercised  by  the  atmosphere  in  producing 
asthmatic  attacks  is  very  great  and  varies  in  different  cases  to  an  extraor- 


BRONCHIAL  ASTHMA  '  391 

dinary  degree.  ]\Iere  impurity  of  the  air  has  little  to  do  with  this  influence  in 
some  cases.  Thus,  I  had  under  my  care  an  old  man,  from  a  healthy  country 
district  in  Pennsylvania,  who  came  to  Philadelphia  to  get  relief  from  nightly 
attacks  of  asthma.  Without  any  treatment  the  severity  of  the  attacks  dimin- 
ished when  he  breathed  city  air  on  the  level  of  the  street,  dust  laden  though 
it  was,  and  his  attacks  ceased  entirely  so  long  as  he  remained  in  a  private 
room  of  the  fifth  floor  of  the  Jeft'erson  Hospital,  where  there  was  less  dust, 
but,  perhaps,  more  smoke  and  gas  from  the  neighboring  chimneys.  In  other 
instances  gases  or  fumes,  as  from  coal  or  arsenic,  produce  an  attack,  and  in 
still  others  the  patient  only  suffers  at  that  season  of  the  year  when  the  pollen 
of  certain  plants  or  flowers  is  set  free.  For  this  reason,  sufferers  from  "hay 
fever"  often  suffer  from  asthma,  since  the  exciting  causes  of  both  states  are 
present,  namely,  a  respiratory  neurosis  and  the  irritants  in  the  air. 

In  still  other  cases  the  cause  lies  in  the  system  of  the  patient  and  does  not 
come  from  outside.  Thus  certain  persons  who  are  sufferers  from  gout  will  occa- 
sionally have  attacks  of  asthma,  just  as  they  have  pain  in  the  toe  or  soreness 
in  the  voluntary  muscles  ;  and,  again,  it  not  uncommonly  happens  that  persons 
who  have  an  unstable  nerve  supply  to  the  bronchial  tubes  have  an  attack  of 
asthma  if  exposed  to  great  cold  or  if  they  have  a  slight  bronchial  congestion 
due  to  this  cause.  So,  too,  such  persons  may  be  seized  with  an  attack  as  the 
result  of  great  physical  weariness  or  of  nervous  excitement,  and  it  by  no 
means  rarely  happens  that  feebleness  of  the  heart,  which  results  in  poor  cir- 
culation in  the  lungs,  produces  a  seizure  in  susceptible  persons.  Such  a  case 
is  called  one  of  "  cardiac  asthma."  In  other  instances  deficient  activity  of  the 
kidneys  produces  indirectly  a  similar  seizure  or  so-called  "renal  asthma." 
In  some  cases  great  acidity  of  the  stomach,  and  the  various  forms  of  indigestion, 
reflexly  provoke  an  attack  through  the  gastric  fibres  of  the  vagus  nerves. 

The  nervous  mechanism  whereby  an  asthmatic  seizure  is  produced  is  sup- 
posed to  be  as  follows:  The  control  of  the  circulation  in  the  bronchial 
mucous  membrane,  and  of  the  muscular  fibres  controlling  the  bronchial  tubes, 
resides  in  the  vagus  nerves,  which  possess  efferent  and  afferent  fibres,  not  only 
connected  with  the  lungs,  but  with  the  stomach  and  heart  as  well.  There  are 
also,  in  all  probability,  fibres  which  indirectly  connect  the  nasal  mucous  mem- 
brane -^nth  the  vagus.  Certain  causes  of  irritation  acting  upon  the  respiratory 
and  gastric  and  cardiac  fibres  of  the  vagus  give  rise  to  an  afferent  impulse  sent 
to  the  vagus  centre,  and  this  in  turn  results  in  the  irradiation  of  an  efferent 
impulse  to  the  bloodvessels  in  the  bronchial  mucosa  and  to  the  bronchial 
muscular  fibres,  whereby  the  tubes  are  constricted,  the  mucous  membrane 
becomes  swollen,  and,  in  addition,  secretion  takes  place,  which  aids  in  ob- 
structing still  further  the  smaller  tubes. 

Pathology  and  Morbid  Anatomy. — The  pathology  of  this  condition  has 
been  described  in  part  in  the  preceding  paragraph.  The  morbid  change 
which  is  manifest  is  the  engorgement  of  the  mucous  membrane,  the  thick, 
viscid,  bronchial  secretion,  and  the  spasm  of  bronchial  tubes.  About  this 
subject  many  earnest  discussions  have  taken  place  and  the  profession  are 
not  in  accord.  Brodie  and  Dixon  speak  of  four  theories  as  to  the  cause  of 
the  attack,  but  believe  that  the  spasm  of  the  bronchial  muscle  is  the  essential 
factor.     The  other  possible  factors,  in  their  opinion,  are  swelling  of  the 


392  DISEASES  OF   THE  BRONCHI 

bronchial  mucosa,  the  so-called  reactionary  hypersemia  of  Traube  or  vaso- 
motor turgescence  of  Weber,  bronchiolitis  exudativa  of  Curschmann,  and, 
lastly,  a  reflex  spasm  of  the  respiratory  muscles. 

The  morbid  anatomy,  unless  secondary  conditions  arise,  is  nil,  for  with 
the  disappearance  of  the  attack  the  lungs  attain  their  normal  state  within 
a  short  time.  It  is  only  when  repeated  attacks  of  asthma  occur  that  the 
patient  as  a  consequence  suffers  from  chronic  bronchitis,  emphysema,  or 
bronchiectasis,  although,  if  a  single  attack  is  very  severe,  he  may  develop 
bronchopneumonia,  particularly  if  exposed  to  cold  and  dampness. 

The  chest  of  the  asthmatic  patient,  who  has  suffered  from  this  disease  for 
many  years,  is  usually  like  that  of  pulmonary  emphysema  in  its  configura- 
tion, and  if  the  disease  be  present  in  early  life,  when  the  chest  is  very  pliable, 
a  "pigeon-breast"  may  be  developed,  or  a  well-marked  Harrison's  groove 
may  be  seen.^ 

In  most  instances  in  which  asthma  has  been  present  for  years  the  heart 
undergoes  dilatation  and  hypertrophy,  particularly  on  the  right  side,  and 
its  beat  may  be  quite  feeble  if  hypertrophy  has  not  fully  compensated  for 
the  dilatation.  Secondarily,  these  cardiac  changes  may  result  in  hepatic  and 
renal  congestion. 

The  scanty  sputum  which  is  expelled  by  asthmatic  patients  possesses  in 
many  instances  peculiarities  which  are  pathognomonic.  This  sputum,  if 
examined,  is  found  to  contain  little  lumps  or  balls,  which,  if  they  are  teased 
out  on  a  plate  of  glass  placed  on  a  black  background,  are  found  to  consist 
of  minute  curls  or  twisted  fibres,  in  form  not  unlike  the  curls  of  hair  on  a 
child's  head.  These  curls  are  called  "  Curschmann's  spirals,"  and  in  their 
folds  are  found  crystals  of  the  fatty  acids,  the  so-called  "  Charcot-Leyden 
crystals."  That  fatty  acids  are  present,  however,  is  denied  by  many.  Thus, 
Goodhart  and  Taslett  think  these  curls  are  related  to  the  casts  of  fibrinous 
bronchitis,  and  they  point  out  that  such  casts  frequently  show  twists  or 
spiral  terminations.  Hoffmann  thinks  the  terminal  bronchioles  are  spiral 
in  form. 

Before  and  during  an  attack  of  pure  bronchial  asthma  there  is  an 
extraordinary  increase  in  the  number  of  eosinophiles  in  the  blood.  This 
eosinophilia  is  said  not  to  occur  in  cases  of  renal  and  cardiac  asthma. 

Symptoms. — The  symptoms  of  spasmodic  or  bronchial  asthma,  in  well- 
developed  cases,  are  very  typical.  The  patient  usually  retires  to  bed  per- 
fectly well  and  wakes  at  midnight  or  in  the  early  morning  with  a  sense  of 
intense  dyspnoea  and  oppression,  which  may  be  so  severe  as  to  seem  to  threaten 
death  from  asphyxia,  but  death  never  occurs  in  an  attack  from  this  cause. 
The  attitude  of  the  patient  suffering  from  asthma  is  most  characteristic.  If 
he  is  in  bed  he  sits  up  and  places  his  hands  back  of  him  on  the  mattress,  so  as 
to  support  himself  in  that  posture  which  will  enable  him  to  use  his  auxiliary 
muscles  of  respiration  to  the  greatest  possible  extent.  His  respirations  are 
labored,  his  brow  is  covered  with  sweat,  and  his  face  is  at  first  anxious  and 
pale,  and  then  cyanosed  and  livid.  The  efforts  at  inspiration  and  expiration 
are  forcible,  but  the  chest  has  the  appearance  of  distention,  since  the  inter- 

1  "Harrison's  groove"  is  that  depression  which  begins  at  the  sternum  at  the  attachment  of  the  seventh 
or  eighth  rib,  and  extends  backward  in  the  line  of  the  ribs  toward  the  axilla. 


BRONCHIAL  ASTHMA  393 

costal  spaces  are  often  unduly  full,  and  the  anterior  portion  of  the  thorax 
is  elevated.  The  difficulty  under  which  the  patient  labors  is  that  he  retains 
in  his  chest  an  excess  of  air  which  has  become  vitiated,  but  which  he  cannot 
expel,  and  therefore  he  has  no  room  for  fresh  air.  The  condition  is  rather 
one  of  difficult  expiration  than  of  difficult  inspiration.  Owing  to  the  great 
shortness  of  breath  the  patient  is  often  unable  to  speak  except  in  a  whisper, 
and  speaks  but  a  word  or  two  with  each  breath.  The  superficial  veins  are 
engorged.  The  urine  during  an  attack  is  often  scanty  and  heavily  loaded 
with  urates,  but  after  the  attack  it  is  often  passed  in  large  quantities,  and 
is  clear  and  limpid. 

The  attack  may  last  from  half  an  hour  to  several  hours,  and  leaves  the 
patient  quite  exhausted.  In  some  instances,  with  the  passing  of  the  seizure, 
almost  total  respiratory  relief  follows,  but  in  most  cases  some  dyspnoea  per- 
sists for  several  hours,  and  cyanosis  may  be  present  till  all  respiratory  diffi- 
culty is  relieved.  If  the  degree  of  relief  is  sufficient  to  permit  sleep,  the  patient 
may  be  sufficiently  rested  to  attend  to  business  the  following  day,  but  in  the 
majority  of  cases  this  is  impossible,  or  at  least  inadvisable,  because  of  the 
fatigue,  the  weak  condition  of  the  heart  and  lungs  from  the  effects  of  the 
attack,  and  the  presence  of  the  bronchitis  and  bronchial  secretion,  which  may 
result  in  fatal  bronchopneumonia  if  the  patient  is  not  very  prudent  as  to 
exposure. 

Diagnosis. — The  history  of  the  attack,  in  its  mode  of  onset  and  subsequent 
development,  renders  a  diagnosis  easy.  The  duty  of  the  physician  is  to  dis- 
cover, if  possible,  the  cause  of  the  attack  and  remove  it,  resting  confident 
that  asthma  is  always  a  symptom  and  not  a  disease.  The  physical  signs  present 
in  an  attack  are  very  characteristic.  In  the  early  stages  auscultation  reveals 
harsh  bronchial  breathing,  with  musical  rales,which  may  be  scattered  here  and 
there  through  the  chest,  and  owing  to  the  disturbed  respiratory  cycle  it  may 
seem  as  if  one  part  of  the  lung  does  not  expand  simultaneously  with  the  other 
parts.  When  the  attack  is  well  developed  the  difficult  passage  of  air 
through  the  narrow  tubes  results  in  the  still  greater  development  of  musical 
sounds,  which  may  be  described  as  resembling  those  made  by  a  litter  of  mew- 
ing kittens  or  crying  puppies.  These  to-and-fro,  loud,  musical  rales,  widely 
diffused  through  both  lungs,  are  so  characteristic  of  the  asthmatic  patient  as 
to  make  the  diagnosis  certain  in  many  cases. 

There  is  one  condition  from  which  asthma  in  the  later  stages  must  be  care- 
fully separated,  namely,  that  of  pulmonary  oedema.  Aside  from  the  fact  that 
the  underlying  cause  of  pulmonary  oedema  is  often  serious  renal  disease,  and 
therefore  a  dangerous  state  deserving  recognition,  the  history  is  often  given 
of  previous  attacks  of  shortness  of  breath,  or  even  of  wheezing  respirations; 
and  the  physical  signs  in  the  later  stage  of  bronchial  asthma,  when  widely 
diffused  and  musical  moist  rales  are  heard,  may  not  differ  materially  from 
those  of  pulmonary  oedema,  since  musical  moist  rales  and  some  impairment  of 
resonance  on  percussion  may  be  present  in  this  condition  as  well.  In  spas- 
modic croup  the  obstruction  to  respiration  is  so  clearly  laryngeal  and  the 
chest  is  so  free  from  widely  diffused  rales  that  the  diagnosis  is  not  difficult, 
and  in  laryngeal  spasm  due  to  locomotor  ataxia  the  same  freedom  from 
musical  rales  in  the  chest   again  enables  us  to   make  a  differentiation. 


394  DISEASES  OF  THE  BRONCHI 

Sometimes  labored  respiration  resembling  that  of  spasmodic  asthma  occurs 
in  acute  pneumothorax,  but  the  physical  signs  are  so  different  that  no 
difficulty  is  experienced  in  separating  these  two  conditions. 

Prognosis.— The  prognosis  as  to  recovery  from  an  individual  attack  of 
asthma  is  very  favorable,  even  if  it  be  exceedingly  severe,  provided  that  no 
acute  complication  arises.  The  prognosis  as  to  recovery  from  the  tendency 
to  asthma  is  very  bad,  for  the  history  of  the  vast  majority  of  cases  is  that 
they  have  recurrences.  It  is  only  in  those  cases  in  which  there  is  a  manifest 
exciting  cause,  external  or  internal,  which  can  be  removed,  that  a  favorable 
prognosis  as  to  the  future  can  be  advanced.  The  tendency  of  spasmodic 
asthma  to  produce  bronchopneumonia,  emphysema,  dilatation  of  the  right 
side  of  the  heart,  and  secondary  circulatory  feebleness  must  never  be  for- 
gotten ;  but,  on  the  other  hand,  it  is  remarkable  that  very  many  asthmatics 
live  to  moderate  old  age  without  being  invalided. 

Treatment. — The  treatment  of  spasmodic  asthma  may  be  divided  into  three 
parts :  that  devoted  to  the  prevention  of  the  attack,  the  relief  of  a  parox}^sm 
whicli  is  present,  the  removal  of  the  underlying  causes  and  of  the  sequelae 
which  are  produced  by  the  attack.  It  has  already  been  pointed  out  that  cer- 
tain conditions  of  the  atmosphere  and  the  presence  of  certain  kinds  of  dust 
in  the  air  strongly  predispose  certain  individuals  to  attacks  of  asthma.  On 
the  principle  that  an  ounce  of  prevention  is  worth  a  pound  of  cure,  it  is 
evident  that  asthmatic  patients  should  be  exposed  as  little  as  possible  to  such 
provoking  causes,  and  if  they  must  of  necessity  sleep  in  a  room  the  air  of 
which  has  been  heated  by  a  furnace,  steam  should  be  disengaged  in  the  air 
of  this  room,  so  that  it  will  not  be  unduly  dry.  Such  patients  should  be  sub- 
jected to  a  careful  examination  of  the  nasal,  pharyngeal,  and  tracheal  mucous 
membranes,  with  the  object  of  discovering  whether  they  suffer  from  any 
localized  spot  of  hyperaesthesia  in  these  mucous  membranes,  for  it  not  infre- 
quently happens  that  foreign  bodies  or  dry  air  may  irritate  these  spots  and 
so  reflexly  produce  an  attack.  Indeed,  in  some  cases  of  so-called  "nasal 
asthma  "  it  is  possible  by  touching  a  hypereesthetic  spot  on  the  nasal  mucous 
membrane  to  precipitate  an  attack  of  spasmodic  asthma.  Such  hyper- 
eesthetic  spots  should  be  removed  by  the  application  of  the  cautery  where  it 
can  be  employed. 

For  the  relief  of  the  attack  of  asthma  itself  when  it  is  threatened,  the  inhala- 
tion of  nitrite  of  amyl  and  the  drinking  of  strong,  black  coffee  may  be  resorted 
to,  or  a  hypodermic  injection  of  morphine  and  atropine  may  be  given. 

When  the  attack  is  developed,  an  innumerable  number  of  drugs  have 
been  recommended  by  various  practitioners  and  by  a  still  greater  number 
of  sufferers.  Among  the  older  remedies,  without  doubt,  belladonna  and 
its  sister  drugs  possess  the  confidence  of  a  large  number  of  the  profession; 
but  none  really  exercise  a  powerful  curative  influence,  unless  they  are  given 
in  doses  which  are  so  large  as  to  be  almost  capable  of  producing  moderate 
poisoning.  These  drugs  probably  act  by  their  depressant  influence  upon 
the  vagus  nerve,  and  by  altering  the  circulation  in  the  capillaries  supplying 
the  bronchial  mucous  membrane.  They  are  particularly  useful  in  those 
cases  of  asthma  in  which,  during  the  attack,  there  is  formed  a  considerable 
quantity  of  bronchial  secretion,  and  they  are  the  chief  ingredients,  with 


BRONCHIAL  ASTHMA  395 

nitrate  of  potassium,  of  most  of  the  proprietary  cigarettes  and  powders  which 
are  burned  in  the  patient's  room. 

Of  the  so-called  depressant  remedies  for  asthma,  we  have  lobeha,  which 
is  very  highly  thought  of  by  many  practitioners,  particularly  in  England. 
On  the  other  hand,  some  physicians  are  afraid  of  this  drug,  because  of 
the  depressant  influence  upon  the  heart.  It  is  not  to  be  emploved  when 
the  heart  is  feeble.  When  the  heart  is  strong,  it  should  be  given  in  full 
doses,  if  given  at  all.  As  much  as  ^  to  1  drachm  of  the  tincture  should 
be  given  in  one  dose,  and  repeated  in  the  dose  of  10  minims  every 
half-hour  or  hour  until  the  patient's  circulation  is  markedly  depressed 
and  the  skin  is  relaxed  and  perspiring.  These  doses  may  produce  nausea 
and  even  vomiting,  but  the  associated  relaxation  often  will  abort  an 
attack,  whereas  smaller  doses  which  do  not  produce  vomiting  may  pro- 
duce more  profound  circulatory  symptoms,  since  all  of  the  drug  is 
absorbed  and  none  lost  by  emesis.  Pilocarpine  may  also  be  employed  in 
those  cases  of  spasmodic  asthma  in  which  there  seerns  to  be  an  excessive 
dryness  of  the  bronchial  mucous  membranes.  But  the  fact  that  this  drug 
in  some  cases  seems  to  depress  the  heart  seriously,  and  in  others  cause  an 
excessively  profuse  outpouring  of  bronchial  secretion,  has  properly  prevented 
its  general  employment.  Many  patients  experience  great  relief  in  the 
early  stages  of  an  attack  if  they  receive  a  hypodermic  injection  of  \  grain 
of  morphine  with  yz^  grain  of  atropine.  In  a  disease  which  recurs  fre- 
quently, as  does  asthma,  this  use  of  morphine  is  always  dangerous,  in  view 
of  the  possibility  of  establishing  the  morphine  habit.  Furthermore,  the  after- 
depressant  effects  of  the  drug  upon  the  following  day  often  renders  the 
remedy  almost  as  bad  as  the  disease. 

For  internal  administration  in  the  treatment  of  asthma,  there  is  no 
drug  which  meets  as  many  indications  in  as  many  cases  as  nitroglycerin.  If 
the  attack  is  threatened  y^  or  even  -g^  of  a  grain  should  be  given  hypo- 
dermically,  and  the  same  dose  may  be  repeated  every  hour  or  two,  particu- 
larly if  the  patient  is  one  of  advanced  years  and  has  a  somewhat  high  arterial 
tension.  In  some  cases  the  inhalation  of  a  few  minims  of  nitrite  of  amyl, 
poured  upon  a  handkerchief,  will  serve  to  abort  a  threatened  attack  or  to 
modify  the  severity  of  one  which  is  already  well  developed. 

In  those  cases  where  there  is  great  irritability  of  the  nervous  system 
underlying  the  asthmatic  attack,  the  occasional  use  of  the  bromides  may  be 
advantageous,  but  they  are  of  little  value  for  the  prevention  of  an  individual 
attack,  and  their  continued  use  between  attacks  is  obviously  unwise.  The 
same  opinion  may  be  expressed  in  regard  to  the  employment  of  chloral,  which 
has  the  additional  disadvantage  that  the  chloral  habit  may  be  instituted,  or 
that  the  heart  may  be  depressed  to  an  undue  degree. 

For  many  years  the  author  has  employed  a  compound  in  tablet  or  elixir 
in  the  treatment  of  asthma,  both  as  a  preventive  remedy  and  as  a  cure  for 
individual  attacks,  and  has  gotten  results  from  it  which  cause  him  to  regard 
this  formula  with  considerable  favor.  It  is  now  placed  on  the  market  by 
all  large  manufacturing  druggists. 


gr-  ij- 
gr.  -^U- 


396  DISEASES  OF  THE  BROXCIII 

JJ . — Sodii  iodidl 

Potas.  bromidi  . 

Ext.  eupliorbise  piluli ferae    . 

Nitrogh'cerini    . 

Tinct.  lobelise    . 
Ft.  in  tabel.  vel  capsiil.  No.  i. 
S. — One  every  four  to  six  hours. 

It  must  never  be  forgotten,  however,  that  asthma  is  a  symptom  rather  than 
a  disease,  and  that  the  remedies  which  prove  useful  in  one  case  may  in 
another  prove  entirely  useless,  because  in  each  instance  the  underlying  cause 
of  the  malady  is  quite  different.  It  is  this  fact  which  has  probably  caused 
some  physicians  to  speak  in  high  praise  of  certain  remedies  in  the  treat- 
ment of  spasmodic  asthma,  while  others  with  equal  experience  assert  that 
they  have  gotten  no  good  results  from  the  employment  of  such  drugs. 

Reference  has  already  been  made  to  the  value  of  supplying  asthmatic 
patients  with  moist  air,  particularly  when  they  hve  in  furnace-heated  houses. 
It  is  the  author's  constant  habit,  when  cases  of  asthma  come  under  his 
care  to  place  them  in  a  bronchitis  tent.  To  the  air  of  this  tent  is  sup- 
plied a  small  quantity  of  steam,  with  the  result  that  the  patient  has  a  great 
diminution  in  the  degree  of  dyspnoea,  and  frequently  gets  some  hours  of 
refreshing  sleep.  An  additional  advantage  in  putting  these  patients  in  a 
bronchitis  tent  is  that  it  requires  them  to  remain  in  bed,  and  so  gives  rest 
to  the  heart,  which  organ  is  often  sadly  in  need  of  relief,  since  the  difficulty 
of  breathing  and  the  lack  of  sleep  throws  upon  it,  day  after  day,  in  some 
patients,  a  very  severe  strain.  In  some  instances  the  addition  of  a  few 
grains  of  menthol  to  the  boihng  water  seems  to  increase  the  efficiency  of 
the  bronchitis  tent.  In  still  others  equal  parts  of  oil  of  pine,  oil  of  euca- 
lyptus, and  compound  tincture  of  benzoin  may  be  added,  in  the  quantity 
of  a  tablespoonful  or  two  to  the  boihng  water,  with  benefit  to  the  patient. 

In  all  cases  of  asthma  the  physician  should  carefully  examine  the  heart, 
and  if  there  are  any  evidences  of  feebleness  and  dilatation  of  the  right  side 
of  the  heart,  as  manifested  by  venous  engorgement,  and  the  extension  of 
cardiac  dulness  downward  and  to  the  right,  small  doses  of  strophanthus 
or  digitahs  should  be  given.  In  some  cases  in  which  the  cardiac  difficuhy  is 
marked  during  the  attack,  fuU  doses  of  Hoffmann's  anodyne  are  advisable. 
These  drugs  may  be  assisted  in  their  stimulating  influence  by  one  or  two 
hypodermic  injections  of  strychnine. 

It  is  also  the  duty  of  the  physician  in  all  these  cases  to  carefully  and 
repeatedly  examine  the  urine,  since  renal  disease  sometimes  produces  true 
asthmatic  seizures,  and  still  more  commonly  produces  attacks  of  dyspnoea, 
which  the  patient  may  call  asthma,  but  which  are  reaUy  those  of  true 
urajmic  poisoning.  Then,  too,  if  asthma  is  present  with  a  moderate  degree 
of  albuminuria  without  casts,  this  albuminuria  may  aid  the  physician  in  de- 
termining that  the  heart  is  yielding  under  the  strain,  since  this  albuminuria 
is  frequently  due  to  renal  congestion,  resulting  from  a  feeble  circulation. 
The  albuminuria  disappears,  the  urinary  flow  becomes  more  profuse,  and 
the  heart's  action  gets  better  under  the  administration  of  digitalis  or  stro- 
phanthus, combined  with  rest,  as  already  indicated. 


BRONCHOPNEUMONIA  397 

DISEASES  OF  THE  LUJS'GS. 

BRONCHOPNEUMONIA. 

Definition. — Catarrhal  pneumonia,  lobular  pneumonia,  or  bronchopneu- 
monia is  an  acute  inflammation  of  the  small  bronchioles  and  of  the  tissues 
immediately  surrounding  them  and  their  attached  lobules,  and  primarily 
involves  the  lobules,  rather  than  the  lobes  as  does  the  croupous  type  of 
pulmonary  consolidation.  It  is  called  bronchopneumonia  because  of  this 
primary  inflammation  of  the  smaller  bronchi,  and  it  is  called  lobular 
pneumonia  because  it  affects  the  lung  by  lobules  rather  than  by  lobes. 
More  commonly  still  it  is  designated  catarrhal  pneumonia,  since  it  usually 
follows  inflammatory  changes  in  the  mucous  membrane  of  the  bronchial 
tubes.  No  single  or  specific  micro-organism  is  the  cause  of  bronchopneu- 
monia, but  it  is  due  to  infection  of  the  bronchi  and  adjacent  tissues  by 
many  pathogenic  germs. 

As  with  typhoid  fever,  so  with  bronchopneumonia:  Gerhard,  a  Phil- 
adelphia student  of  Louis,  in  Paris,  was  the  first  person  to  clearly  differ- 
entiate bronchopneumonia  from  croupous  pneumonia  (1834),  although  as 
early  as  1823  Seger  had  separated  the  pneumonia  of  adults  from  this  form 
which  is  that  which  commonly  affects  children. 

Distribution. — Bronchopneumonia,  because  of  its  various  causes,  is  found 
everywhere  throughout  the  world. 

Etiology. — Frequently  bronchopneumonia  is  due  to  the  micrococcus  of 
croupous  pneumonia,  which  for  some  unknown  reason  fails  to  produce  a 
croupous  exudate  in  a  single  lobe  or  in  several  lobes,  as  is  usual  when  that 
organism  enters  the  lung  in  an  adult.  In  other  instances  pyogenic  organisms 
such  as  the  streptococcus  or  staphylococcus  are  responsible  for  the  disease. 
Thus,  in  103  cases  of  bronchopneumonia  examined  by  Netter,  Weichsel- 
baum,  and  Pearce,  the  streptococcus  was  found  in  about  30  and  the  pneu- 
mococcus  in  29.  AVhen  associated  with  other  organisms  the  number  of 
instances  in  which  these  cocci  were  found  was  much  greater.  Primary 
bronchopneumonia  is  usually  due  to  the  pneumococcus,  and  secondary 
bronchopneumonia  to  the  streptococcus. 

When  such  a  specific  malady  as  diphtheria  is  the  primary  cause  of  the 
illness  the  Klebs-Loeffler  bacillus  is  the  most  frequent  cause  of  the  pneu- 
monic lesions.  Thus,  in  62  cases  of  bronchopneumonia  following  diphtheria 
examined  by  Pearce,  this  organism  was  found  52  times  and  the  strepto- 
coccus 27  times.  In  still  others  the  bacillus  of  Pfeiffer  (that  of  epidemic 
influenza)  brings  on  an  attack.  The  tubercle  bacillus  not  rarely  is  respon- 
sible for  the  inflammatory  process,  and  almost  any  pathogenic  organism 
entering  the  lower  bronchial  tubes  may  act  as  an  exciting  cause.  Doubtless 
these  organisms  often  gain  access  to  the  bronchioles  in  periods  of  good 
health  without  producing  evil  effects,  but  if  by  chance  there  is  present  a 
general  or  local  impairment  of  vital  resistance  pathological  changes  ensue. 

Bronchopneumonia  is  usually  said  to  be  capable  of  division  into  two 


398  DISEASES  OF  THE  LUNGS 

types,  namely,  the  primary  and  secondary.  The  primary  form  is  met  with 
in  children  and  adults  who  are  usually  in  poor  health  with  diminished 
vitality,  and  seems  to  have  its  onset  with  the  development  of  an  acute  "cold." 
It  is  most  commonly  met  with  in  infants,  and  in  them,  as  has  just  been  stated, 
is  usually  a  pneumococcus  infection,  although  true  croupous  pneumonia  at 
this  age  is  not  common.  The  secondary  type  is  much  the  more  frequent  of 
the  two;  indeed,  it  may  be  considered  the  rule  that  bronchopneumonia 
occurs  as  a  secondary  affection  in  the  vast  majority  of  cases,  for  nearly 
always  there  is  a  history  of  a  previous  acute  or  subacute  bronchitis,  or  of 
some  disease  which  predisposes  to  such  a  condition,  as  whooping-cough, 
measles,  or  influenza. 

In  adults  there  is  usually  the  history  of  a  severe  cold  affecting  the  upper 
respiratory  tract,  or  of  the  use  of  an  anaesthetic  drug  by  inhalation, 
which  has  at  one  and  the  same  time  irritated  the  air-passages  and  per- 
mitted the  entrance  of  saliva  or  particles  of  mucus  or  food  containing 
many  micro-organisms  which  produce  infection.  A  similar  result  may 
accrue  in  instances  in  which  no  such  drug  is  employed.  Thus,  in  some 
asthmatics  during  the  progress  of  an  attack  there  may  be  drawn  into  the 
air-passages  micro-organisms  from  the  mouth  or  tiny  particles  of  food. 
In  individuals  suffering  from  the  coma  of  alcoholism,  cerebral  congestion, 
uraemia,  or  apoplexy,  with  stertorous  breathing,  the  same  accident  may 
ensue.  Such  a  form  of  infection  may  occur  in  the  coma  following  an  epileptic 
seizure.  In  some  instances  the  presence  of  an  ulcerative  laryngitis,  due  to 
syphilis,  tuberculosis,  or  malignant  disease  produces  an  infection  in  this 
manner.  Bulbar  paralysis,  or  that  due  to  diphtheria,  may  also  provoke 
this  type  of  pneumonia.  In  many  cases  of  severe  illness,  as  in  typhoid 
fever,  with  foul  secretions  in  the  nose  and  mouth,  this  method  of  infection 
ensues  because  the  ordinary  sensitiveness  of  the  glottic  mucous  membrane, 
and  that  of  the  trachea,  is  obtunded  by  the  dryness  of  these  parts  or  by 
the  benumbing  effects  of  the  disease.  This  form  of  the  disease  is  called 
aspiration  pneumonia,  or  the  "  Schluck-pneumonie  "  of  the  Germans.  Old 
age  and  debility  are  also  predisposing  causes. 

Prevention.— From  what  has  been  said  it  is  evident  that  the  secondary 
forms  of  bronchopneumonia  are  capable  of  prevention,  at  least  to  some 
extent.  Perfect  cleanliness  of  the  mouth  is  one  of  the  methods  of  prophy- 
laxis, in  that  it  prevents  the  inhalation  from  the. oral  cavity  of  infecting 
micro-organisms.  So,  too,  during  the  course  of  measles  and  whooping- 
cough  careful  avoidance  of  exposure  and  the  use  of  a  bronchitis  tent  to 
allay  bronchial  irritation  is  preventive  in  its  influence.  If  local  lesions 
in  the  upper  respiratory  tract  exist,  they  should  be  modified  or  removed  by 
proper  treatment. 

Frequency. — Bronchopneumonia  is  an  exceedingly  common  disease 
probably  outranking  in  frequency  its  sister  malady,  croupous  pneumonia. 
As  a  terminal  infection  it  causes  death  in  many  maladies  otherwise  almost 
never  fatal  in  themselves,  such,  for  example,  as  whooping-cough  and  measles, 
both  of  which  have  a  high  mortality  in  very  young  children  from  this  very 
cause.  Thus,  out  of  446  cases  of  bronchopneumonia  in  children  cited  by 
Holt,  it  followed  or  complicated  whooping-cough  66  times  and  measles 


BRONCHOPNEUMONIA  399 

89  times.  It  is  a  noteworthy  fact  that  bronchopneumonia  is  the  type 
which  is  particularly  common  in  infancy,  while  croupous  pneumonia 
is  generally  a  disease  of  later  life.  In  the  child  under  five  years  it  is  very 
common,  and  fatal  in  direct  proportion  to  the  youth  of  the  patient,  whereas 
croupous  pneumonia  is  rare  in  this  period  of  life,  and  very  rarely  is  fatal 
at  this  time.  Out  of  Holt's  426  cases,  53  per  cent,  occurred  in  the  first  year 
of  life  and  33  per  cent,  in  the  second  year. 

Pathology  and  Morbid  Anatomy. — This  form  of  pneumonia,  at  least  in  its 
earlier  stages,  occurs  in  patches  which  cause  the  lung  to  present  during  life 
physical  signs,  and,  after  death,  macroscopic  appearances,  ordinarily  quite 
distinct  from  those  of  the  solidified  or  hepatized  lung  of  croupous  pneumonia. 
Macroscopically  the  lung  presents  a  mottled  appearance  because  its  surface 
represents  three  conditions  of  the  pulmonary  parenchyma,  namely,  (a)  areas 
of  consolidation,  (b)  areas  of  atelectasis  or  collapse,  and  (c)  areas  of  emphv- 
sema,  or  enlargement,  of  groups  of  vesicles  due  to  overdistention,  resulting 
from  collapse  of  adjacent  lobules.  The  consolidated  areas  are  pinkish, 
reddish,  or  grayish-yellow  in  hue,  the  emphysematous  patches  are  paler 
and  crepitate  when  touched,  while  the  collapsed  portions  are  bluish  or 
mahogany  in  color  and  depressed  below  the  rest  of  the  cut  surface  of  the 
lung. 

The  inflammatory  process  usually  begins  in  the  smaller  bronchi  and 
extends  from  them  to  the  tissues  immediately  adjoining,  forming  patches  of 
consolidation,  which  are  deep  red  in  hue,  and  which  extend  farther  and 
farther  from  their  original  site,  until  perchance  they  coalesce  and  form 
fairly  large  airless  consolidations.  As  the  margin  of  the  inflammatory  zone 
extends,  the  primary  area  of  inflammation  undergoes  necrotic  degenerative 
changes,  loses  its  red  appearance,  and  may  become  grayish,  through  granular 
and  fatty  degeneration  of  the  exudate.  This  inflammatory  exudate  not  only 
invades  the  peribronchial  tissues,  but  the  vesicles  as  well,  so  that  they  are 
rendered  airless.  If  the  lung  be  cut  across  these  patches  of  consolidation 
will  project  slightly,  and  in  the  centre  of  each  can  be  seen  the  cross-section 
of  the  primarily  involved  bronchus,  which  looks  whitish,  and  from  which 
mucopus  may  exude.  In  some  instances  in  which  the  infection  is  severe 
and  the  inflammatory  process  rapid,  the  mucopurulent  character  of  the 
exudate  into  the  bronchial  tubes  is  very  well  developed,  and  this  purulent 
process  may  extend  into  the  peribronchial  spaces  and,  in  septic  cases,  cause 
small  pyogenic  foci.  The  exudate  itself  is  composed,  as  would  be  expected 
from  the  character  of  the  lesions,  of  serum,  red  cells,  epithelial  cells  which 
have  separated  from  the  bronchial  and  vesicular  walls,  and  a  large  number 
of  leukocytes,  and  in  varying  numbers  the  associated  bacteria. 

The  exudate  contains  much  less  fibrin  than  it  does  in  croupous  pneu- 
monia, and  a  copious  fibrinous  deposit  on  the  pleura  is  exceptional. 

If  the  inflammation  of  the  walls  of  the  bronchial  tubes  is  severe  they 
become  thickened  and  swollen,  and  therefore  their  lumen  is  greatly  decreased 
or  even  occluded.  This  result  is  greatly  aided  by  their  becoming  plugged 
with  the  mucus  and  dead  cells,  and  so  it  not  infrequently  happens  that  a  cer- 
tain area,  or  several  areas,  of  the  vesicular  portion  of  the  lung  is  deprived 
of  air  and  undergoes  collapse  or  atelectasis. 


400  DISEASES  OF  THE  LUNGS 

It  is  worthy  of  note  that  catarrhal  pneumonia  is  in  the  great  majority 
of  instances  present  in  both  lungs,  and  that  it  is  not  usually  conspicuous  in 
the  bases  posteriorly.  The  anterior  portions  of  the  lungs  and  particularly 
the  apices,  except  in  tuberculous  cases,  show  little  involvement  unless  the 
lesions  are  well  developed  elsewhere. 

The  exudate  in  bronchopneumonia  undergoes  resolution,  as  do  most 
inflammatory  exudates,  by  the  degeneration  of  the  extravasated  and  des- 
quamated elements  and  their  speedy  absorption  or  expectoration.  With 
this  process  the  material  plugging  the  bronchial  tubes  disappears  and  the 
collapsed  vesicles,  upon  receiving  their  normal  supply  of  air,  expand  so 
that  complete  recovery  ensues. 

When  this  does  not  take  place  we  find  the  development  of  dense  con- 
nective tissue  about  the  air  tubes  and  between  the  air  spaces,  which,  as 
it  increases  in  degree,  causes  thickening  and  induration.  As  this  process 
increases  the  connective  tissue  distorts  the  lung  so  that  the  bronchi  are 
twisted  or  bent,  patches  of  vesicular  tissue  collapse,  secretion  is  retained  in 
the  bronchial  tubes,  and  as  a  result  chronic  bronchial  inflammation,  dila- 
tation, or  sacculation  of  these  tubes  occurs,  and  the  patient  becomes  a 
sufferer  from  chronic  bronchitis,  with  bronchiectasis  or  a  chronic  broncho- 
pneumonia. 

In  other  instances  old  tuberculous  lesions  are  rendered  active  by  the 
acute  bronchopneumonia,  or  a  new  tuberculous  infection  is  superadded, 
so  that  the  case  speedily  passes  into  a  well-developed  pulmonary  tuber- 
culosis. In  still  other  instances  the  whole  process  from  the  very  beginning 
is  really  due  to  the  Bacillus  tuberculosis,  and  the  patient  rapidly  develops 
unmistakable  evidences  of  tuberculous  infection,  the  microscope  showing, 
sooner  or  later,  the  presence  of  these  organisms  in  the  sputum.  In  such 
cases  the  exudate  in  the  air  cells  goes  on  to  caseation,  and  may  become 
encapsulated  or  disseminated,  depending  upon  the  virulence  of  the  organ- 
ism and  the  resistance  of  the  patient. 

Symptoms. — ^The  symptomatology  of  bronchopneumonia  varies  with  the 
primary  cause.  If  it  be  primary  it  naturally  presents  symptoms  which 
differ  somewhat  from  those  which  it  presents  when  it  is  secondary,  and 
follows  some  more  or  less  prolonged  and  exhausting  malady.  Then,  too, 
the  symptoms  naturally  vary  with  the  age  of  the  patient  attacked,  with  the 
areas  of  the  lungs  which  are  involved,  and  with  the  severity  of  the  illness 
which  has  preceded  it. 

For  the  ready  study  of  the  symptoms  of  bronchopneumonia  we  may 
therefore  form  at  least  three  classes  of  cases:  those  which  are  distinctly 
primary,  those  that  are  clearly  secondary,  and  those  which  involve  the 
small  bronchioles  very  early  in  the  attack,  producing  what  is  known  as 
acute,  suffocative  catarrh. 

When  the  child  is  attacked  with  the  primary  form  of  bronchopneumonia 
there  is  usually  a  chill  at  onset,  which  varies  greatly  in  its  severity,  in  some 
cases  being  so  slight  that  it  is  scarcely  noted,  and  in  others  amounting  to  a 
true  rigor.  Commonly  there  is  a  history  that  the  child  has  been  exposed 
to  cold  and  wet.  As  in  all  inflammatory  conditions  in  childhood,  there  is 
a  sharp  rise  in  temperature,  almost  from  the  very  first  an  increase  in  the 


BRONCHOPNEUMONIA 


401 


respiratory  rate,  and,  it  may  be,  very  considerable  evidence  of  respiratory 
difficulty. 

It  is  curious  to  note  how  the  severity  of  the  symptoms  of  catarrhal  pneu- 
monia vary  in  different  children.  Some  become  dyspnceic  very  early,  and 
others  suffer  very  little  respiratory  embarrassment  through  the  whole  course 
of  the  malady. 

So  sudden  may  be  the  onset  in  this  primary  form  of  bronchopneumonia 
that  it  may  be  practically  impossible  for  the  physician  to  separate  it  from 
croupous  pneumonia,  particularly  as  children  suffering  from  the  latter  dis- 
ease rarely  bring  up  rusty  sputum,  and  also  because  they  frequently  have  a 
pulse  rate  which  is  higher  in  proportion  to  the  respirations  than  that  ratio 
which  is  common  in  croupous  pneumonia  in  adults.  Cerebral  symptoms 
may  also  be  present,  just  as  they  are  in  croupous  pneumonia;  and  this  is  not 


Fig. 54 


tB 


Lung  of  a  child.  Catarrhal  pneumonia  following:  measles.  In  the  upper  left  quadrant  is  part  of  the 
wall  of  a  small  bronchus,  the  epithelium  of  which  is  desquamating  (.4) ;  several  air  vesicles  contain- 
ing catarrhal  exudate  are  shown  (B).  The  connective  tissue  of  the  bronchus  and  the  intervesicular 
structure  are  slightly  oedematous  and  the  seat  of  considerable  leukocytic  infiltration  (C). 

surprising  in  view  of  the  fact  already  pointed  out,  that  the  pneumococcus 
is  the  micro-organism  most  frequently  responsible  for  both  forms  of  pneu- 
monia in  children.  For  this  reason,  probably,  primary  catarrhal  pneu- 
monia in  children  not  infrequently  ends  by  crisis,  and  recovery  may  speedily 
take  place  after  a  very  few  days  of  illness.  Indeed,  the  outlook  in  a  case  of 
this  kind  in  an  otherwise  healthy  child,  which  is  not  very  young,  is  usually 
favorable.  , 

The  symptoms  of  the  onset  of  secondary  bronchopneumonia  vary  greatly 
from  those  just  described.  Instead  of  having  a  sharp  onset  the  onset  is 
insidious.  A  child  having  been  ailing  from  some  other  malady  for  a  number 
of  days  or  weeks,  is  found  to  have  an  accession  of  fever,  to  be  languid,  to 
have  a  rapid  pulse,  to  have  a  very  marked  increase  in  respiratory  rate,  and 
26 


402 


DISEASES  OF  THE  LUNGS 


the  skin  is  found  to  be  hot  and  dry.  The  speed  of  the  pulse  is  often  exces- 
sive, reaching  150  to  200  a  minute;  but  in  this  disease,  as  in  all  others,  its 
quality  is  of  as  great  importance  as  its  speed.  An  irregular  pulse  is  of  evil 
import.  The  cough  is  fairly  constant  and  sometimes  produces  pain,  and  if 
the  area  involved  is  at  all  large  respiratory  embarrassment  is  early  mani- 
fested. This  is  shown  by  the  increased  number  of  respirations,  by  the  fact 
that  they  are  somewhat  labored,  and  also  by  the  fact  that  the  intercostal 
spaces  are  frequently  drawn  in  by  the  suddenness  of  the  inspiratory  move- 
ment. Auscultation  will  probably  reveal  in  the  smaller  bronchial  tubes 
some  fine  rales,  with  exaggerated  inspiratory  and  somewhat  prolonged 
expiratory  sounds.  The  breathing  is  of  the  exaggerated,  puerile  type;  the 
couo-h  is  unproductive.  Percussion  for  the  first  twenty-four  hours  of  the 
attack  may  reveal  practically  nothing.  This  is  in  part  due  in  children  to 
the  resiliency  of  the  entire  chest,  so  that,  unless  very  gentle  percussion  is 
exercised,  the  resonance  of  neighboring  parts  may  cover  the  impaired 
resonance  of  the  consolidated  area.  Again,  those  areas  which  have  under- 
gone compensatory  dilatation  possess  a  hyperresonance  which  may  cover 
the  impairment.  If,  however,  the  pathological  lesion  is  well  developed,  at 
the  end  of  twenty-four  or  forty-eight  hours  careful  percussion  will  usually 
reveal  distinct  impairment  of  resonance,  particularly  if  the  lesions  are,  as 
is  common,  chiefly  at  the  bases  posteriorly. 

If  the  disease  is  severe  the  symptoms  of  dyspnoea  may  become  distressingly 
well  marked,  and  cyanosis  may  become  constant,  the  child  being  so  short  of 
breath  that  it  ceases  to  cry,  and,  indeed,  may  have  difficulty  in  taking  liquids 
because  of  its  dyspnoea;  that  is  to  say,  it  is  so  short  of  breath  that  it  cannot 
take  time  to  swallow.  Usually  at  this  time  the  expression  is  somewhat 
anxious.  If  the  dyspnoea  has  been  prolonged  enough  to  exhaust  the  child, 
and  the  accumulation  of  carbon  dioxide  in  the  blood  has  been  sufficient  to 
benumb  its  sensibilities,  it  is  Trmrkedly  apathetic.  These  symptoms  last  a 
variable  number  of  days,  but  usually  a  change  for  the  better  in  a  mild  case 
begins  to  be  noted  by  the  end  of  the  fifth,  sixth,  or  seventh  day,  and  with 
the  beginning  of  improvement  in  the  general  symptoms  auscultation  will 
reveal  that  the  rales  in  the  chest  are  more  moist,  that  on  coughing  they 
alter  in  quality  more  than  before,  and,  further,  air  will  be  found  passing 
through  portions  of  the  lung  which  heretofore  have  seemed  devoid  of  it. 

In  other  instances  the  disease  runs  a  much  longer  course,  and  the  child, 
after  hovering  between  life  and  death  for  a  number  of  days,  slowly  emerges 
from  its  illness,  and  the  physical  signs  in  the  lungs  equally  slowly  disap- 
pear. 

In  young  children  it  is  by  no  means  an  uncommon  occurrence  for  the  dis- 
ease to  spread  in  a  violent  form  into  the  smaller  bronchioles,  and  by  the 
swelling  of  the  mucous  membrane,  the  copiousness  of  the  exudate,  and 
the  wide  area  involved,  produce  what  is  known  as  acute  suffocative  catarrh, 
a  condition  which  at  one  time  was  considered  as  a  separate  entity  from 
bronchopneumonia,  but  which  is  now  recognized  as  being  simply  a  malig- 
nant form  of  the  disease  involving  a  large  number  of  the  smaller  bronchi- 
oles, and  so  greatly  interfering  with  respiration.  Another  term  which  has 
also  been  used  to  describe  this  condition  is  "capillary  bronchitis;"  in  other 


BRONCHOPNEUMONIA  403 

words,  this  name  is  meant  to  bring  out  the  fact  that  the  finer  bronchioles  are 
involved.  A  very  excellent  term  to  describe  this  form  of  the  disease  is  "acute 
disseminated  bronchopneumonia. " 

Capillary  bronchitis,  or  acute  suffocative  catarrh,  is  one  of  the  most  dis- 
tressing acute  maladies  which  affect  young  children.  Its  onset  is  usually 
very  rapid,  and  within  twelve  or  twenty-four  hours  the  child  may  be 
suffering  intensely  from  dyspnoea.  At  first,  the  dyspnoea  and  inability  to  get  a 
sufficient  quantity  of  oxygen  render  it  fretful  and  restless ;  but  very  soon  it 
becomes  weary,  and  with  the  weariness  of  the  general  system  there  develops 
a  weariness  of  the  respiratory  centre,  which  fails  to  send  out  sufficiently 
powerful  influences  to  cause  the  remaining  healthy  portion  of  the  lung  to 
be  completely  filled  at  each  inspiration.  Very  speedily,  too,  carbonic  acid 
gas  accumulates  in  the  blood  and  benumbs  the  respiratory  centre,  so  that 
within  twenty-four  or  thirty-six  hours  after  the  beginning  of  the  malady 
the  child  may  lie  in  its  mother's  arms  limp  and  motionless  except  for  the 
rapid  respirations  which  are  required  to  maintain  life.  I  have  not  infre- 
quently seen  a  child  in  this  condition  as  limp  as  it  is  when  under  the  influ- 
ence of  ether  or  chloroform,  and  only  semi-conscious.  The  finger-nails  are 
livid,  the  lips  much  darker  than  normal.  The  mouth  is  apt  to  be  excessively 
dry,  owing  to  rapid  evaporation  of  moisture  from  the  high  fever  and  rapid 
breathing. 

During  a  portion  of  the  attack  the  respiratory  rate  may  become  as  high 
as  60  or  even  70  a  minute,  and  not  infrequently  death  comes  on 
as  a  combined  result  of  the  infection,  of  the  dilatation  of  the  right  side  of 
the  heart,  of  the  accumulation  of  carbon  dioxide  in  the  blood,  and  of  general 
nervous  exhaustion. 

Probably  the  most  characteristic  sjonptom  of  capillary  bronchitis  is  the 
intense  dyspnoea,  which  is  quite  as  acute  in  some  cases  as  it  is  in  diph- 
theria with  laryngeal  obstruction.  Indeed,  I  have  known  intubation  to  be 
done  in  a  case  of  capillary  bronchitis,  it  being  thought  that  the  child  had 
laryngeal  trouble  in  addition  to  its  pulmonary  difficulties,  although  no 
laryngeal  lesion  was  actually  present. 

The  temperature  in  cases  of  capillary  bronchitis  varies  very  greatly.  In 
some  patients  it  is  very  high,  rising,  it  may  be,  to  107°;  in  other  instances 
it  rarely  passes  above  101°  or  102°.  In  the  latter  type,  however,  there 
may  be  a  sharp  rise  a  few  hours  before  death.  At  the  time  of  death  the 
temperature  may,  superficially  at  least,  be  subnormal,  although  the  rectal 
temperature  may  be  high.  The  general  run  of  the  temperature  pursues 
no  definite  course  as  it  is  wont  to  do  in  croupous  pneumonia,  but  progresses 
very  irregularly. 

The  degree  of  fever  in  bronchopneumonia  of  the  secondary  type  is  of 
little  value  for  the  purpose  of  determining  the  severity  of  the  disease.  Some- 
times when  the  infection  is  quite  severe  the  temperature  may  not  rise  above 
101°  or  102°;  whereas  in  other  cases  which  are  really  less  ill,  it  may  reach 
105°  or  106°. 

Duration. — The  duration  of  bronchopneumonia  varies  very  greatly  with 
the  condition  of  the  child  at  the  onset  of  the  disease.  In  primary  broncho- 
pneumonia, occurring  in  an  otherwise  healthy  child,  the  malady  may  last  for 


J.04  DISEASES  OF  THE  LUNGS 

but  a  few  days,  and  it  is  a  noteworthy  fact  that  it  may  be  arrested  in  any 
stage  of  its  development,  so  that  recovery  may  speedily  take  place. 

In  secondary  bronchopneumonia  the  duration  is  apt  to  be  very  much 
longer  than  in  the  primary  form.  Under  these  circumstances  it  commonly 
runs  a  course  of  from  ten  days  to  two  weeks,  and  if  the  condition  of  the 
patient  is  seriously  impaired  at  the  time  of  its  onset,  it  may  last  for  three  or 
four  weeks.  Usually,  however,  during  the  last  ten  days  or  two  weeks  of  a 
prolonged  attack  of  this  character,  the  symptoms  are  much  modified  and 
the  temperature  is  but  a  Httle  above  normal.  ^Yhooping-cough,  wliich  is  a 
very  frequent  cause  of  bronchopneumonia,  runs  a  course  of  from  six  to 
twelve  weeks,  and  if  bronchopneumonia  develops  early  in  the  attack  of 
whooping-cough  the  persistency  of  the  spasmodic  seizures,  with  their  accom- 
panying bronchitis,  naturally  prolongs  the  duration  of  the  pulmonary  dis- 
order; whereas,  in  another  disease  like  measles,  which  runs  a  much  shorter 
course,  the  pulmonary  disorder  may  disappear  almost  as  soon  as  the  erup- 
tive disease,  although  very  often  it  persists  for  a  week  or  ten  days,  and  con- 
valescence from  measles  is  well  established.  Much  depends,  too,  as  to  the 
duration  of  the  malady,  upon  the  size  of  the  areas  of  consolidation  and  the 
presence  of  more  slowly  Hquidated  exudates.  Commonly,  the  greater 
the  area  infected,  the  greater  the  length  of  the  disease. 

Complications. — The  complications  of  bronchopneumonia  are  not  numer- 
ous. As  already  pointed  out,  it  occasionally  happens  that  tuberculosis 
develops  in  the  area  which  is  diseased.  More  rarely  still  the  infection 
of  the  peribronchial  tissues  is  so  severe  that  pulmonary  abscess  results. 
Pleuritis  is  rare  unless  there  happens  to  be  a  patch  of  consolidation  close  to 
the  pleura,  in  which  case  a  small  area  may  be  involved.  This  rarely  spreads 
and  still  more  rarely  is  accompanied  by  marked  effusion,  but  it  sometimes 
results  in  empyema. 

Diagnosis. — Bronchopneumonia  is  to  be  differentiated  from  ordinary  severe 
bronchitis  by  the  presence  of  patches  of  impaired  resonance  on  percussion, 
and  by  the  fact  that  during  the  course  of  an  acute  bronchitis  an  exacer- 
bation of  temperature  and  of  the  general  symptoms  of  severe  illness  ensue. 
Beyond  these  points  it  may  be  practically  impossible  to  separate  the  two 
maladies.  It  is  not  to  be  forgotten  that  bronchitis  is  not  associated  with 
hyperresonance  in  any  portion  of  the  chest  as  a  rule,  but  catarrhal  pneu- 
monia is  frequently  associated  with  this  physical  sign.  Percussion  in  capil- 
lary bronchitis  may  therefore  give  exaggerated  resonance  owing  to  the 
emphysematous  state  of  the  vesicular  parts  of  the  lung,  for,  as  in  asthma, 
the  difficulty,  which  often  exists,  is  an  inability  to  expire  some  of  the  air 
which  has  been  taken  in  by  forced  inspiration.  As  has  already  been  stated, 
hyperresonance  may  completely  take  the  place  of  impaired  resonance  due 
to  consolidation. 

From  croupous  pneumonia  bronchopneumonia  is  to  be  separated  by  the 
fact  that  its  onset  is  more  gradual  or  insidious,  by  the  intermittent  character 
of  the  fever,  and  by  the  irregular  distribution  of  the  physical  signs  in  the 
chest.  Another  important  differential  point  is  the  fact  that  catarrhal  pneu- 
monia is  usually  bilateral  and  joined  at  the  bases,  whereas  croupous 
pneumonia  is  not;  that  bronchopneumonia  is  usually  well  diffused,  and  in 


BRONCHOPNEUMONIA  405 

both  lungs,  whereas  the  croupous  type  is  usually  but  not  always  unilateral, 
and  commonly  limited  to  one  lobe.  Croupous  pneumonia  usually  ends  by 
crisis,  whereas  bronchopneumonia  may  end  by  lysis.  The  predominance  of 
severe  cerebral  or  meningeal  symptoms  is  rather  in  favor  of  the  croupous 
type  of  the  disease. 

In  many  cases  it  is  impossible  to  determine  whether  the  bronchopneu- 
monia is  due  to  the  pneumococcus  or  some  other  coccus,  or  is  the  result  of 
the  infection  by  the  tubercle  bacilli.  In  the  absence  of  enlargement  of  the 
mesenteric  glands  and  of  other  signs  of  tuberculous  infection,  the  differential 
diagnosis  between  bronchopneumonia  of  tuberculous  origin  and  that  due  to 
ordinary  causes  is  practically  impossible,  until  the  disease  has  advanced  so 
far  that  other  systemic  manifestations  of  tuberculous  infection  are  manifest. 

Sometimes  the  intermittent  and  irregular  temperature  curves  of  broncho- 
pneumonia suggest  the  possibility  of  malarial  infection.  The  differential 
diagnosis  in  a  case  of  malarial  infection,  with  bronchial  symptoms  like  those 
of  bronchopneumonia,  can  of  course  only  be  made  by  careful  examination 
of  the  blood,  and  by  a  more  careful  study  of  the  temperature  chart  than  is 
usual  in  the  ordinary  case.  Then,  too,  in  the  malarial  forms  of  the  disease 
the  symptoms  will  be  modified  or  arrested  by  the  use  of  quinine. 

As  already  pointed  out,  the  symptoms  of  bronchopneumonia,  in  children 
in  particular,  vary  to  an  extraordinary  degree  with  the  primary  illness  from 
which  the  patient  has  been  suffering.  Thus,  in  whooping-cough  the  onset 
of  the  disease  is  often  so  insidious  as  to  be  easily  overlooked  because  the 
rales  are  mistaken  for  those  of  the  usual  mild  bronchitis.  In  other  instances 
the  symptoms  may  be  those  of  tuberculous  or  acute  meningitis,  particularly 
in  rachitic  infants. 

Not  rarely  an  acute  diarrhoea  may  be  present,  the  stools  being  green  and 
containing  much  mucus,  some  of  which  is  due  to  a  coincident  gastrointestinal 
catarrh,  and  some  of  it  being  from  the  bronchial  tubes,  for  a  child  rarely 
expectorates,  and  usually  swallows  what  he  coughs  up  from  his  chest.  Be- 
cause of  the  associated  indigestion  there  may  be  vomiting  and  distention  of 
the  abdomen  by  gas,  which  factors  all  aid  in  increasing  the  adynamia,  and  in 
interfering  with  the  cardiac  and  pulmonary  activity.  These  facts  emphasize 
a  fact  too  frequently  overlooked,  namely,  that  the  condition  of  the  lungs 
should  always  be  carefully  investigated  in  all  cases  which  present  signs  of 
illness  elsewhere,  since  it  may  be  found,  to  the  physician's  surprise,  that 
the  pulmonary  condition  is  not  rarely  the  primary  underlying  cause. 

Prognosis. — The  prognosis  of  bronchopneumonia  varies  very  greatly 
with  the  underlying  cause  of  the  disease  and  with  the  age  of  the  patient. 
In  young  infants  it  is  an  exceedingly  fatal  malady,  whether  it  is  primary  or 
secondary,  and  during  the  first  year  of  life,  if  the  disease  is  well  marked, 
the  prognosis  is  always  unfavorable.  The  favorableness  of  the  prognosis 
increases  with  each  year  of  age.  Another  important  factor  in  the  prognosis 
of  these  cases  is  the  general  vitality  of  the  patient.  Children  who  are  natu- 
rally strong  and  healthy,  and  are  provided  with  good  air  and  sunshine,  have 
a  better  opportunity  than  those  who  live  in  poorly  constructed  dwellings 
with  bad  ventilation,  and  whose  primary  vitality  is  necessarily  limited. 
This  question  of  the  vitality  of  the  patient  is  a  most  important  factor  from 


406  DISEASES  OF  THE  LUNGS 

a  prognostic  standpoint,  and  therefore  if  the  child  has  been  much  weakened 
and  devitahzed  by  prolonged  illness,  or  has  had  its  heart  seriously  weakened 
by  the  prolonged  strain  of  severe  whooping-cough,  the  outlook  is  much  less 
favorable  than  if  the  disease  attacfe  the  child  who  is  suffering  from  a  mild 
attack  of  measles. 

The  mortality  of  bronchopneumonia  in  very  young  children  in  private 
practice  is  probably  about  30  per  cent.;  whereas  in  asylum  practice,  where 
it  is  impossible  to  provide  them  with  the  same  amount  of  fresh  air  and 
careful  nursing,  and  where  the  health  is  often  previously  impaired,  it  is  not 
infrequently  as  high  as  65  or  70  per  cent.  While  it  is  true  that  poorly 
nourished,  rachitic  children  are  very  apt  to  fall  victims  to  the  disease,  it  is 
also  a  fact  that  well-nourished,  stout,  fat  children  sometimes  have  marked 
difficulty  in  surviving  its  attack;  and  this  is  particularly  true  if  they  are 
"condensed-milk  babies,"  for  such  children  usually  have  low  vital  resist- 
ance. The  complicating  maladies,  as,  for  example,  active  diarrhoea  and 
indigestion  or  vomiting,  of  course  make  the  prognosis  very  uncertain, 
and  if  they  resist  treatment  are  still  more  cause  for  anxiety. 

Treatment. — In  the  treatment  of  bronchopneumonia  it  is  of  the  greatest 
importance  that  the  child  should  be  in  a  well- ventilated  room  which  received 
as  much  sunshine  as  possible,  for  bronchopneumonia  is  essentially  a  disease 
of  bad  ventilation.  The  temperature  of  the  room  should  be  kept  constant, 
and  every  care  should  be  exercised  that  it  is  not  damp.  If  possible,  it  should 
be  heated  by  a  stove,  or  by  an  open  fire,  rather  than  by  furnace-heated  air, 
and  if  it  is  necessary  to  heat  it  by  means  of  a  furnace,  care  should  be  taken 
that  the  air  of  the  room  should  not  be  allowed  to  become  unduly  dry.  This 
may  be  prevented  by  having  the  air  from  the  furnace  flue  pass  over  the 
surface  of  a  pan  of  water,  and  if  the  air  is  very  hot  and  thoroughly  dried  it 
is  better  to  set  free  in  the  air  of  the  room  a  certain  amount  of  steam  from 
a  tea-kettle,  a  pan  of  boiling  water,  or  by  occasionally  immersing  a  large 
piece  of  quicklime  in  a  bucket  of  water. 

There  can  be  no  doubt  that  the  influence  of  dusty,  impure,  or  dry  air  upon 
the  bronchial  mucous  membrane  in  cases  of  this  disease  is  most  deleterious, 
and  I  believe  that  in  many  instances  much  better  results  can  be  obtained  if 
it  is  possible  to  place  the  child  in  a  bronchitis  tent,  or  to  provide  the  air  of 
the  room  with  a  sufficient  degree  of  moisture  to  make  the  apartment  the 
equivalent  of  a  bronchitis  tent.  This  can  readily  be  accomplished  in  the 
way  just  suggested,  or  by  the  use  of  what  is  known  as  a  "croup  kettle," 
which  continually  sets  free  a  small  quantity  of  steam.  To  the  water  which 
is  placed  in  the  croup  kettle  1  or  2  grains  of  menthol  may  be  added  every 
two  or  three  hours,  and  in  some  instances,  for  their  soothing  influence,  a 
few  drops  of  oil  of  eucalyptus  and  compound  tincture  of  benzoin  may  be 
so  employed.  As  far  as  possible  the  patient  should  be  kept  quiet  in  bed, 
or,  in  the  case  of  little  children,  should  be  moved  as  little  as  is  consistent  with 
comfort;  but  if  the  child  is  very  ill,  it  should  not  be  allowed  to  lie  in  one 
posture  hour  after  hour,  but  occasionally  be  changed,  lest  hypostatic 
congestion  occur.  Easily  digested,  nutritious  food  should  be  given  in  small 
quantities  every  two  hours.  No  medicine  which  may  disturb  digestion 
should  be  given  to  a  child  in  its  food. 


BRONCHOPNEUMONIA  407 

In  the  way  of  external  applications  to  the  chest,  the  child's  back,  sides, 
and  front  may  be  rubbed  with  a  mixture  of  a  teaspoonful  of  turpentine 
and  three  tablespoonfuls  of  sweet  oil.  In  other  instances  a  weak  ammonia 
liniment  may  be  used,  or  in  still  other  cases  oil  of  amber,  in  the  strength  of  a 
teaspoonful  to  two  tablespoonfuls  of  sweet  oil.  These  methods  of  treatment 
provide  sufficient  counterirritation  and  do  not  maintain  the  febrile  tempera- 
ture as  do  the  poultice  or  cotton  jacket,  both  of  which  forms  of  application 
have  now  deservedly  gone  out  of  use,  as  it  is  inconceivable  that  they  can 
favorably  affect  the  lesion  in  the  lung,  and  they  certainly  increase  the  dis- 
comfort, the  fever,  and  the  irritation  of  the  child's  nervous  system. 

Stimulants  are  not  needed  in  all  cases  of  bronchopneumonia,  but  are 
used  wisely  in  a  larger  proportion  of  patients  than  in  those  who  suffer  from 
the  croupous  variety  of  the  disease,  because  bronchopneumonia,  as  has 
already  been  pointed  out,  usually  attacks  the  feeble  and  therefore  those 
who  commonly  need  stimulation.  The  quantity  of  stimulant  which  is 
given  varies  of  course  with  the  feebleness  of  the  heart  sounds,  the  condition 
of  arterial  tension,  and  the  degree  of  general  nervous  prostration.  One  of 
the  best  stimulants  which  can  be  used  is  the  carbonate  of  ammonium  in 
'the  dose  of  2  or  3  grains  every  three  or  four  hours  to  a  child  of  a  year  or 
two,  usually  giving  it  in  the  syrup  of  acacia  and  water.  Carbonate  of  ammo- 
nium, however,  acts  best  when  it  is  given  for  comparatively  short  periods  of 
time,  and  for  a  constant  stimulant  during  the  greater  portion  of  the  disease 
it  is  probable  that  brandy  occupies  the  first  place.  Care  should  be  exercised 
that  the  brandy  is  at  least  five  years  old,  and  that  it  is  as  bland  as  possible. 
It  should  be  given  very  well  diluted  by  water,  and  a  child  of  a  year  may 
take  as  much  as  half  an  ounce  to  an  ounce  in  twenty-four  hours  with 
advantage,  30  drops  being  given  every  two  or  three  hours. 

As  a  rapidly  acting  diffusible  stimulant  to  meet  critical  periods  of  depres- 
sion Hoffmann's  anodyne  in  the  dose  of  5, 10,  or  15  drops  maybe  employed 
in  young  children.  In  other  instances  y^Q-  grain  of  strychnine  may  be  used, 
or  a  larger  dose  than  this,  it  being  always  borne  in  mind  that  the  nervous 
system  of  a  child  is  exceedingly  susceptible  to  this  drug.  Like  the  carbon- 
ate of  ammonium,  strychnine  is  only  to  be  used  when  it  is  necessary  to 
bridge  an  exceedingly  critical  period.  If  the  dose  of  strychnine  is  to  be 
repeated,  -^\q  of  a  grain  is  a  sufficiently  large  amount.  This  quantity  may 
be  given  twice,  thrice,  or  four  times  in  twenty-four  hours,  but,  as  a  rule,  it  is 
unwise  to  continue  its  use  for  a  longer  period  than  this. 

Where  the  quantity  of  bronchial  secretion  is  considerable,  particularly 
in  many  cases  of  suffocative  bronchitis,  a  critical  period  may  be  weathered 
by  the  use  of  small  doses  of  atropine;  from  j-oVo"  ^^  -5^  of  a  grain  may  be 
given  every  two  or  three  hours  by  the  mouth,  or,  if  need  be,  -g-g-g-  to  -g^ 
may  be  given  hypodermically,  if  there  seems  to  be  danger  of  the  child 
drowning  in  its  own  secretions.  Oxygen  may  be  taken  by  inhalation  in 
some  cases  with  advantage. 

The  use  of  antipyretic  drugs  is  to  be  absolutely  condemned.  They  are 
even  more  dangerous  in  this  disease  than  in  croupous  pneumonia.  If  the 
temperature  is  so  high  as  to  be  dangerous  in  itself,  it  may  be  controlled  by 
cool  or  tepid  spongings,  with  gentle  friction;  by  the  use  of  cool  cloths  to 


408  DISEASES  OF  THE  LUXGS 

the  forehead,  or  an  ice-bag  apphed  to  the  head  if  cerebral  symptoms  are 
marked.  Sometimes,  too,  placing  the  child  in  a  tepid  bath  for  a  few 
moments  will  act  as  an  excellent  antipjTetic. 

When  the  symptoms  of  respiratory  oppression  are  marked  and  the  fever 
is  high,  it  is  often  advantageous  at  a  critical  period  to  dip  the  child  alter- 
nately in  cool  and  hot  water,  the  water  being  hot  enough  to  produce  distinct 
counterirritation  on  the  skin,  and,  reflexly,  to  arouse  the  dormant  nervous 
system.  Under  these  circumstances  the  child  often  rallies,  takes  deep 
inspirations,  dislodges  the  mucus  which  is  otherwise  obstructing  its  breath- 
ing, and  at  the  same  time  has  a  reduction  in  its  temperature.  Such  an 
alternate  hot  and  cold  plunge  bath  should  only  be  resorted  to  when  condi- 
tions are  desperate,  and  should  not  be  repeated  too  frecjuently.  A  tepid  bath, 
the  patient  being  immersed  or  simply  sponged,  will  also  very  frequently  allay 
restlessness  and  permit  quiet  sleep. 

In  the  protracted  cases  it  is  exceedingly  important  that  pure  air  and  good 
food  should  be  pro\aded.  Not  infrequently  the  child  which  fails  to  improve 
in  the  city  may,  when  carried  in  its  nurse's  arms  to  the  sea-shore  or  the 
mountains,  change  for  the  better  to  a  remarkable  degree  within  a  very  short 
period  of  time.  This  is  particularly  true  if  the  weather  is  oppressively  hot. 
Such  patients  also  may  be  benefited  in  some  instances,  particularly  during 
the  winter  months,  by  cod-liver  oil  inunctions,  and,  if  the  digestion  will 
stand  it,  by  the  administration  of  small  quantities  of  cod-liver  oil  or  the 
syrup  of  iodide  of  iron  by  the  mouth.  Sometimes  such  patients  are  also 
greatly  benefited  by  the  administration  of  the  hypophosphites. 

During  the  acute  stage  of  bronchopneumonia  there  is  little  use  in  employ- 
ing the  ordinary  expectorants.  During  the  stage  of  resolution,  if  the  secretion 
is  profuse,  small  doses,  such  as  1  or  2  grains  of  chloride  of  ammonium, 
with  fluid  extract  of  licorice  and  water,  may  be  given  tmce  or  thrice  a  day. 
Rarely  in  young  children  is  there  much  expectoration,  either  in  the  sense 
of  expelling  mucus  from  the  mouth  or  coughing  it  up  into  the  pharynx. 
The  younger  the  child  the  less  chance  there  is  of  freeing  its  bronchial  tubes 
of  secretion  by  coughing,  and  care  should  always  be  taken  that  the  admin- 
istration of  an  expectorant,  which  is  not  of  very  great  importance,  does  not 
disorder  the  digestion,  which  is  of  far  greater  importance  to  the  maintenance 
of  the  child's  health  and  strength  than  any  medicine  can  be. 

The  bronchopneumonia  of  adults  usually  follows  asthma  or  the  inspira- 
tion of  irritant  materials,  and  must  be  treated  in  much  the  same  manner  as 
that  just  described  for  bronchopneumonia  in  children,  except  that  the  doses 
should  be  larger  in  proportion  to  the  age  and  size  of  the  individual.  In 
nearly  all  cases  active  stimulation  is  required,  and  digitalis  and  strychnine 
are  particularly  useful.  Counterirritation,  freely  appHed  to  the  chest,  seems 
to  be  of  advantage  in  some  instances,  but  here  again  the  cotton  jacket  or 
the  poultice  ought  not  to  be  resorted  to,  as  they  simply  oppress  the  patient 
and  do  little  good. 

METASTATIC  PNEUMONIA. 

Definition. — By  the  term  metastatic  pneumonia  is  meant  a  condition  of 
consolidation  of  part  of  one  lung,  or  more  rarely  parts  of  both  lungs,  as 


METASTATIC  PNEUMONIA  409 

the  result  of  the  plugging  of  one  or  more  of  the  pulmonary  vessels  by  an 
embolus  which  is  of  septic  origin. 

Etiology  and  Pathology. — As  elsewhere,  emboli  reaching  the  lung  may  be 
(1)  simple  or  bland,  (2)  septic  or  infective;  either  of  these  may  be  massive 
or  small.  A  large  mass  thrown  into  the  pulmonary  artery  at  once  arrests 
the  flow  of  blood,  the  patient  gives  a  few  gasps,  possibly  has  a  convulsion, 
or  at  least  convulsive  movements,  and  dies.  Smaller  emboli,  if  numerous 
(an  embolic  shower),  may  induce  similar  phenomena.  The  simple  or  bland 
embolus  occludes  one  or  more  vessels,  and  leads  to  the  formation  of  a  hemor- 
rhagic infarct.  These  irregularly  shaped  or  conical  areas  vary  in  size, 
depending  upon  the  magnitude  of  the  occluded  vessel  and  the  efficiency  of 
the  collateral  circulation.  They  may  be  central  or  peripheral,  massive  or 
small,  single  or  multiple. 

The  question  of  autochthonous  embolism  is  of  pathological  rather  than 
clinical  interest. 

The  affected  area  is  airless,  denser  than  the  uninvolved  pulmonary  tissues, 
and  near  the  centre  it  is  dark  purple  or  almost  black  in  recent  infarcts,  black 
or  brownish-black  in  older  areas,  and  it  may  be  surrounded  by  a  zone  of 
reactionary  inflammation.  If  the  lesion  is  peripheral  the  indurated  area 
rises  above  the  level  of  the  pleura  and  is  frequently  covered  by  a  delicate 
stratum  of  fibrin.  Certain  pleurisies,  particularly  those  following  operations, 
have  been  attributed  to  pulmonary  infarction.  Histologically  such  areas 
when  recent  show  air  vesicles  occupied  by  blood  cells  and  fibrin  and  more 
or  less  interstitial  extravasation.  Later  the  erythrocytes  are  fragmented,  the 
leukocytes  increased,  phagocytes  abundant,  and  evident  reparative  processes 
in  progress. 

The  sputum  is  more  or  less  blood-stained,  and  when  the  infarcts  are 
large  or  numerous  it  may  be  intensely  so.  In  fat  embolism,  such  as  may 
accompany  fractures  of  the  long  bones,  oil  globules  may  be  demonstrable 
in  the  sputum. 

\Yhether  the  process  arises  to  the  dignity  of  a  pneumonia  depends,  of 
course,  upon  the  amount  of  accompanying  inflammation.  It  is  evident 
that  a  few"  small  infarcts  irregularly  distributed  may  give  rise  to  no  symp- 
toms because  of  the  insignificant  lesions  induced;  or,  on  the  other  hand, 
large,  or  multiple,  areas  may  be  accompanied  by  evident  lung  symptoms. 
Whether  inflammation  be  marked  or  slight  is  so  largely  dependent  upon  the 
presence  of  infection  that  in  the  absence  of  bacteria  the  name  metastatic 
pneumonia  is  scarcely  applicable. 

Embolism  due  to  fragments  of  neoplasms  entering  the  lungs  usually 
escapes  notice  until  the  proliferating  cells  give  rise  to  metastatic  tumors. 

The  most  important  and  gravest  type  of  metastatic  pneumonia  is  that 
seen  in  pyaemia. 

During  the  course  of  a  septic  process  in  any  part  of  the  body,  even  though 
it  may  be  so  minute  as  to  escape  notice  unless  carefully  sought,  it  is  possible 
for  a  small  clot  (embolus)  infected  by  micro-organisms  to  enter  the  circula- 
tion and,  being  carried  to  the  lung,  to  plug  one  of  the  vessels.  The  difference 
between  the  infarct  resulting  from  an  ordinary  embolus  and  the  lesion 
ensuing  from  one  of  septic  origin  is  very  marked,  for  in  the  latter  condition 


410  DISEASES  OF   THE  LUNGS 

there  speedily  develops  an  acute  local  process  due  to  the  rapid  extension 
of  the  infection  from  the  embolus.  In  this  way  the  immediate  neighborhood 
of  the  closed  vessel  becomes  engorged ;  polymorphonuclear  leukocytes  accum- 
ulate in  the  infected  area,  which  rapidly  undergoes  liquefaction,  necrosis,  and 
an  abscess  is  formed.  As  such  emboli  are  rarely  solitary,  multiple  foci  are 
prone  to  develop;  these  may,  by  extension,  become  confluent  or  successive 
embolic  showers  may  cause  closely  approximated  lesions  of  different 
ages. 

As  the  quantity  of  infective  material  and  its  distribution  constantly  varies, 
the  anatomical  result  of  such  conditions  can  rarely  be  the  same  in  any  two 
cases.  There  may  be  a  single  area  of  infection,  or  the  lung  may  be  riddled 
by  abscesses,  the  "pytemic  pneumonia"  of  old  writers. 

The  area  of  solidification  in  the  lung  may  resemble  the  patchy  state  seen 
in  bronchopneumonia  or  the  hepatized  appearance  of  croupous  pneumonia. 
There  is,  however,  this  important  difference  in  the  further  progress  of  the 
local  lesions  between  the  two  diseases  named  and  that  under  discussion,  for 
in  metastatic  pneumonia  the  inflammatory  process  usually  goes  on  to  suppu- 
ration, the  entire  infected  area  becoming  crowded  with  pus  cells  and  cocci, 
the  walls  of  the  vesicles  and  the  connective  tissue  of  the  lung  breaking  down 
instead  of  remaining  intact  as  in  most  cases  of  ordinary  pneumonia.  As 
a  result  we  find  one  or  more  abscesses  of  the  lung  which  may  rupture  into 
a  bronchus,  into  the  pleural  cavity,  or  even  through  the  diaphragm,  and  are 
practically  always  accompanied  by  marked  septic  fever. 

The  pleura  rarely  escapes,  and  empyema,  in  patients  surviving  sufficiently 
long,  is  not  uncommon.  As  the  abscesses  open  into  the  bronchi  and  eroded 
vessels  give  way,  pulmonary  hemorrhage  is  prone  to  occur.  Large  areas  of 
pulmonary  tissue  may  undergo  necrosis  and  further  complicate  the  case  by 
the  addition  of  pulmonary  gangrene. 

Symptoms. — The  symptoms  of  metastatic  or  septic  pneumonia  present  so 
little  that  is  characteristic  that  they  are  often  overlooked.  This  is  because 
the  lesion  in  the  lung  is  secondary  to  some  inflammatory  process  already 
present,  which  is  responsible  for  much  of  the  fever  and  other  signs  of  an 
infection.  In  the  midst  of  these  symptoms,  if  they  are  severe,  the  slight 
exacerbation  produced  by  the  embolism  is  not  recognized.  It  is  only  in 
those  cases  in  which  the  area  of  the  lung  involved  is  very  considerable  that 
pulmonary  signs  are  forced  upon  the  physician,  projecting  themselves,  as  it 
were,  above  those  already  present.  When  the  pulmonary  symptoms  are 
marked  they  so  closely  resemble  those  of  an  acute  pneumonia  that  not 
infrequently  the  diagnosis  of  an  intercurrent  pneumonia  is  made,  only  to  be 
modified  when  repeated  chills,  sweats,  and  a  temperature  chart  indicative  of 
sepsis  show  that  the  process  in  the  lung  is  septic.     (See  Pyaemia.) 

When  the  embolus  is  a  large  one  and  plugs  the  pulmonary  artery  at  its 
bifurcation,  death  suddenly  ensues. 

The  physical  signs  of  metastatic  pneumonia  are  practically  identical  in  the 
early  stage  of  the  affection  with  those  of  bronchopneumonia  or  croupous 
pneumonia,  for  the  consolidated  portion  of  the  lung  produces  dulness  on 
percussion,  bronchial  breathing,  and  increased  vocal  fremitus  and  resonance. 
Later,  when  the  consolidated  area  breaks  down  and  begins  to  undergo  sup- 


PNEUMONOCONIOSIS  411 

puration,  the  physical  signs  may  be  those  met  with  in  beginning  resolu- 
tion in  ordinary  croupous  pneumonia. 

Prognosis. — The  prognosis  in  metastatic  pneumonia  is  bad  because  it  is  a 
septic  process  and  also  because  it  is  a  serious  complication  added  to  a 
process  which  is  already  more  or  less  severe.  It  usually  ends  in  abscess  or 
gangrene,  and  these  affections,  particularly  the  latter,  are  fatal  in  the  great 
majority  of  cases.  In  the  rare  instances  in  which  recovery  takes  place  the 
health  of  the  patient  is,  as  a  rule,  permanently  impaired.  I  have,  however, 
seen  two  instances  followed  by  abscess  end  in  complete  restoration  to  health. 

Treatment. — There  is  no  specific  treatment  of  this  condition  unless  it  be 
known  that  the  streptococcus  is  the  cause  of  the  infection,  in  which  case 
antistreptococcic  serum  may  be  employed.  Even  in  these  instances,  how- 
ever, it  cannot  do  much  good  because,  after  the  pulmonary  vessel  is  mechan- 
ically closed  by  an  embolus,  no  treatment  can  bring  about  its  relief.  The 
most  that  the  serum  can  do  is  to  limit  the  degree  of  general  toxaemia. 

Ordinarily  the  treatment  must  consist  in  the  use  of  as  much  easily  assimi- 
lated food  as  the  patient  can  take  without  disordering  his  digestion,  the 
administration  of  proper  quantities  of  stimulants,  and  the  careful  control 
of  such  symptoms  as  may  become  excessive,  as,  for  example,  the  reduction 
of  high  temperature,  if  it  is  persistent. 


PNEUMONOCONIOSIS. 

Definition. — This  term  is  applied  to  a  state  of  the  lungs  in  which,  by 
reason  of  exposure  to,  and  inhalation  of,  various  kinds  of  dust  a  deposit  of 
the  foreign  body  takes  place  in  the  pulmonary  tissues  and  produces  secondary 
changes.  When  the  individual  is  exposed  to  coal-dust  in  sufficient  amount 
and  for  a  long-enough  period  to  cause  its  accumulation  in  the  lung,  the 
state  of  the  lung  is  called  "anthracosis;''  when  the  dust  is  derived  from  the 
grinding  of  iron  or  steel,  it  is  called  "siderosis ;"  when  the  dust  arises  from 
stones,  the  term  "  lithiasis"  or  "chalicosis"  is  employed.  Still  another  type 
of  foreign  body  capable  of  causing  pneumonoconiosis  affects  those  who  work 
in  large  textile  industries  and  shoddy  mills.  The  minute  particles  of  wool 
and  cotton,  and  of  the  clay  used  for  "sizing,"  often  cause  bronchitis  and 
favor  the  occurrence  of  phthisis.  The  dust  can  often  be  found  in  the  sputum 
of  such  patients.  Reference  to  this  type  of  the  disease  is  made  in  the  author's 
Fiske  Fund  Prize  Essay  for  1885.  Still  another  form  of  exposure  gives  rise 
to  "grain-shovellers'  disease,"  and  to  "potters'  rot." 

Etiology. — Under  ordinary  circumstances  the  respiratory  tract  is  able  to 
get  rid  of  minute  foreign  bodies  which  may  enter  it.  This  is  accomplished 
by  the  arrest  of  the  dust  in  the  nasal  and  pharyngeal  mucus,  and  by  the 
action  of  ciliated  epithelium  Hning  the  larynx,  trachea,  and  bronchial  tubes, 
which  continually  passes  along  toward  the  mouth  for  expectoration  any 
dust  particles  which  may  enter.  If  these  protective  measures  are  insufficient 
because  of  the  great  quantity  of  dust  inhaled,  or  where  after  a  time  this 
ciliated  epithelium  is  destroyed,  some  of  the  particles  are  carried  through 
the  mucous  membrane  and  are  arrested  in  the  nearby  connective  tissue; 


412  DISEASES  OF   THE  LUNGS 

but  if  the  amount  of  dust  is  so  large  that  even  this  third  barrier  is  passed, 
then  the  dust  particles  are  taken  up  by  the  lymphatics  and  carried  to  the 
bronchial  lymph  nodes,  or  to  the  interlobular  pulmonary  septa  under  the 
visceral  layer  of  the  pleura,  or  to  the  substernal  lymph  glands,  where  they 
are  deposited  and  remain  fixed.  Very  rarely  the  fine  particles  may  enter 
the  circulation  and  be  deposited  in  the  liver  and  spleen,  as  in  a  case 
reported  by  Welch,  or  they  may  be  even  excreted  in  the  urine. 

Pathology. — Up  to  this  stage  these  results  may  possess  no  pathological 
significance,  but  in  some  instances  the  presence  of  large  quantities  of  these 
foreign  bodies  produce  a  low-grade  inflammatory  process  in  the  lung  tissues 
which  results  in  overgrowth  of  connective  tissue;  that  is,  a  chronic  pro- 
ductive interstitial  pneumonia  or  pulmonary  sclerosis.  Occurring  inde- 
pendently of  the  interstitial  change,  or  associated  with  it,  there  is  quite 
constantly  a  subacute  or  chronic  bronchitis  and  emphysema,  and  finally 
areas  of  softening  take  place,  in  the  fibroid  portions  of  the  lungs,  which  are 
small  in  size  and  filled  with  dust-stained  fluid.  Sometimes  these  com- 
municate with  a  bronchial  tube  and  may  then  become  infected  and  ulcerate. 
These  ulcerated  patches  or  spots  of  softening  may  or  may  not  be  due  to 
infection  by  the  Bacillus  tuberculosis.  It  is  by  this  process  that  we  have 
established  "miners'  phthisis"  or  "grindstone  consumption"  and  "gold- 
dust  complaint"  of  the  lung.  So  common  is  this  condition  in  Sheffield, 
England,  that  it  has  been  called  "knife-grinders'  rot." 

Symptoms. — As  a  rule  symptoms  of  pulmonary  trouble  do  not  come  on 
in  serious  form  until  the  individual  has  been  exposed  for  some  months  or 
years,  when  chronic  cough,  dyspnoea,  and  loss  of  flesh  call  attention  to  the 
insidious  changes  in  the  lungs.  A  macroscopic  or,  when  this  fails,  a  micro- 
scopic examination  will  usually  reveal  the  dust  in  the  sputum,  and  the  his- 
tory of  the  case  renders  the  diagnosis  easy. 

Prognosis. — In  an  investigation  carried  on  at  Solingen,  Germany,  by 
Moritz,  it  was  found  that  there  were  no  fork-grinders  above  forty-five 
years  of  age  and  no  sword-grinders  above  fifty.  Of  the  total  number 
of  knife-grinders  employed,  only  5.5  per  cent,  were  over  forty  years  of  age. 
Of  the  scissors-grinders  there  were  8.4  per  cent,  above  forty.  The  fork-  and 
sword -grinders  work  with  dry  grinding  stones,  while  the  knife-  and  scissors- 
grinders  work  with  grinding  stones  which  are  constantly  kept  moist.  The 
relatively  greater  number  of  scissors-grinders  who  live  to  be  over  forty  is 
explained  by  the  fact  that  the  knife-grinders  sit  closer  to  their  machines 
than  the  scissors-grinders,  and  thus  inhale  more  dust. 

Peabody,  in  some  investigations  made  at  Sheffield,  England,  found  that 
the  average  period  of  knife-grinders  who  are  able  to  continue  their  work  is 
thirteen  years.  In  South  Africa,  Fox  states  that  the  duration  of  fife  in 
gold  mines  where  there  is  much  dust  from  blasting  is  only  four  years.  Out 
of  1377  rock-drill  miners,  225,  or  16.34  per  cent.,  died  in  two  and  a  half 
years. 

Treatment. — The  treatment  is  removal  from  exposure  and  the  use  of  the 
medicinal  measures  advised  in  the  articles  on  Chronic  Bronchitis  and 
Emphysema.  It  is  the  duty  of  all  employers  of  labor  in  dusty  places  to 
provide    free  ventilation,  both   to  dissipate  the  dust  and  to  diminish   the 


EMPHYSEMA   OF   THE  LUNGS  413 

chance  of  tuberculous  infection.  In  many  industries  the  employees  should 
use  moist  respirators  to  catch  the  dust  in  the  respired  air.  Moist  or  wet 
grinding  should  be  used  instead  of  dry  grinding  to  prevent  dust,  and 
workmen  known  to  be  tuberculous  should  be  excluded  from  the  workshop. 


EMPHYSEMA  OP  THE  LUNGS. 

Definition. — ^The  term  emphysema,  as  applied  to  disease  of  the  lung,  signifies 
a  condition  in  which  the  air  content  of  the  organ,  in  a  large  or  small  area, 
is  in  excess  of  the  normal.  Systematic  writers  ordinarily  make  it  include 
(1)  essential,  hypertrophic  or  large-lunged  emphysema;  (2)  atrophic  or 
senile  emphysema;  (3)  compensatory  emphysema,  a  form  of  vesicular  over- 
distention  due  to  inexpansion,  or  absence,  of  pulmonary  parenchyma  in 
some  juxtaposed  or,  less  commonly,  a  distant  area,  and  (4)  a  form  of  what 
occurring  elsewhere  is  ordinarily  termed  "surgical  emphysema,"  but  in  the 
lung  is  called  "interstitial,"  "interlobular,"  or  "  intervesicular  " — names  that 
indicate  the  location  of  the  air  and  differentiate  the  condition  from  the  first 
named  states  or  those  forms  in  which  the  abnormal  air  content  is  intravesicular 

Emphysema  has  also  been  divided  into  an  acute  and  chronic  form.  In 
point  of  time  the  interstitial  is  always  acute,  the  essential  and  atrophic 
always  chronic,  while  the  compensatory  may  be  either.  Some  writers 
apply  the  term  "acute"  to  that  condition  in  which  rapid  overdistention  of 
relatively  large  areas  occurs  as  a  result  of  violent  inspiratory  efforts,  or 
obstructed  expiration,  such  as  occurs  in  cardiac  asthma,  bronchial  obstruc- 
tion, and  allied  conditions. 

Briefly  described,  vesicular  emphysema  is  a  state  in  which  there  is  atrophy 
of  the  septa  between  the  air  cells  so  that  a  number  of  vesicles  coalesce. 
As  a  result  we  find  in  the  lung  many  small,  bladder-like  spaces  containing 
air.  Associated  with  this  minute  change  the  entire  lung  increases  in  bulk 
and  the  thoracic  cavity  is  usually  much  increased  in  all  its  diameters, 
especially  the  anteroposterior  and  the  vertical,  producing  the  so-called 
* '  barrel-shaped  chest. ' ' 

Etiology. — Much  difference  of  opinion  exists  as  to  the  primary  cause  of 
pulmonary  emphysema.  It  is  universally  acknowledged  that  the  condition 
develops  as  a  result  of  inadequacy,  either  congenital  or  acquired,  of  the 
supporting  elastic  tissue  between  the  vesicles;  but  one  school  of  pathologists 
maintains  that  the  giving  way  of  the  vesicular  walls  depends  upon  mechanical 
stress,  while  another  school  asserts  that  such  a  result  ensues  only  when  the 
normal  support  is  removed  through  failure  of  nutrition  in  these  parts  so 
that  atrophy  results.  The  author  is  convinced  of  the  correctness  of  the 
latter  view,  namely,  that  the  coalescence  of  the  vesicles  takes  place  only 
after  the  elastic  connective  tissue  has  become  wasted  as  the  result  of  im- 
paired circulatory  supply.  It  is  perfectly  true  that  great  pulmonary  stress 
tends  to  produce  emphysema  of  the  lung,  but  it  only  produces  this  state 
when  the  connective  tissue  is  unable  to  provide  proper  vesicular  support. 

Probably  in  a  large  proportion  of  cases  the  tendency  is  hereditary,  the 
defect  is  congenital,  and  the  tissues  succumb  as  soon  as  any  great  stress  is 


414  DISEASES  OF   THE  LUNGS 

put  upon  them.  If  this  primary  nutritional  feebleness  be  admitted  as  the 
fundamental  cause  of  the  condition,  it  is  easy  to  understand  how  it  is  that 
persons  so  affected  fall  victims  to  emphysema  when  attacked  by  spasmodic 
asthma,  or  when  following  occupations  which  produce  pulmonary  stress, 
and  it  also  makes  manifest  why  it  is  that  other  persons  exposed  to  equally 
severe  exciting  causes  escape. 

Frequency. — ^The  frequency  of  true  pulmonary  emphysema  is  difficult  to 
determine  because  many  of  the  mild  cases  are  overlooked,  and  patients  do 
not  present  themselves  for  treatment  until  the  disease  is  far  advanced. 
To  show  how  widely  statistics  may  vary  according  to  the  method  of  their 
collection,  it  is  interesting  to  note  that  Lebert  states  that  pulmonary  emphy- 
sema forms  about  5  per  cent,  of  all  diseases,  while  Virchow  found  in  nearly 
200,000  cases,  admitted  to  the  Charity  in  Berhn,  that  the  percentage  of 
emphysema  was  only  0.3,  a  result  confirmed  by  West  at  St.  Bartholomew's 
in  London.  The  disease  is  met  with  three  times  as  frequently  in  men  as 
in  women,  probably  because  they  are  exposed  to  its  secondary  causes  more 
constantly,  and  it  occurs  chiefly  between  the  ages  of  thirty  and  sixty  years. 
It  occurs  in  children,  but  rarely  before  they  are  ten  years  of  age,  although 
cases  as  young  as  two  years  of  age  have  been  recorded. 

Pathology  and  Morbid  Anatomy. — It  has  already  been  stated  that  the 
essential  characteristic  of  pulmonary  emphysema  is  the  wasting  of  the  inter- 
alveolar  tissues  so  that  coalescence  of  the  vesicles  takes  place.  As  a  result 
small,  bladder-like  spaces  are  formed,  the  lung  loses  its  elasticity,  and  so 
fails  to  expel  the  air  on  expiration,  with  the  result  that  the  quantity  of 
residual  air  is  greatly  increased.  This  results  in  dyspnoea  in  two  ways: 
first,  there  is  an  impaired  circulation  of  fresh  air  in  the  lung,  and,  second, 
there  is  a  decrease  in  the  area  of  the  vesicular  tissues,  so  that  a  much 
smaller  surface  is  afforded  for  the  absorption  of  oxygen. 

When  the  thorax  of  a  case  of  essential  emphysema  is  opened  the  lungs  do 
not  retract  as  do  healthy  lungs.  Indeed,  they  may  project  into  the  opening 
which  has  been  made.  The  left  lung  extends  so  far  forward  as  to  cover 
the  heart,  and  the  right  lung  may  overlap  the  edge  of  the  left.  Often  the 
epiclavicular  spaces  are  distended  by  lung  tissue,  and  if  the  disease  be 
marked  the  convexity  of  the  diaphragm  is  reduced,  with  consequent  dis- 
placement downward  of  the  adjacent  abdominal  viscera,  particularly  the 
liver. 

The  chest  is  changed  in  appearance  because  with  the  increase  in  the  size 
of  the  lungs  the  ribs  become  more  horizontal  and  the  intercostal  spaces  more 
bulging,  the  sternum  and  costal  cartilages  are  projected  forward,  and  the 
normal  dorsal  curvature  of  the  spine  is  exaggerated. 

When  the  lungs  are  removed  from  the  chest  it  is  found  that  they  possess 
four  peculiarities  aside  from  their  great  size:  they  are  pale  gray  in  color, 
unusually  free  from  blood,  dry,  and  when  pressed  between  the  fingers  they 
lack  the  crepitation  met  with  in  normal  lung-tissue.  A  noteworthy  change 
is  the  presence  of  dilated  pouches  or  bladder-like  protuberances  on  the 
surface  of  the  lung,  and  particularly  at  its  margins.  If  the  lung  be  cut, 
somewhat  smaller  spaces  will  be  found  scattered  through  it.  It  is  note- 
worthy that  in  emphysema  these  open  spaces  are  surrounded  by  thin  walls 


EMPHYSEMA   OF   THE  LUNGS 


415 


which  readily  collapse,  whereas  the  sacculations  of  saccular  bronchiectasis 
are  surrounded  by  areas  of  thickening  and  inflammatory  change. 

With  the  coalescence  of  the  air  spaces  the  capillaries  which  usually 
pass  between  the  vesicular  walls  disappear,  and  this  in  turn  diminishes  the 
number  of  pathways  by  which  the  blood  can  pass  from  the  right  to  the  left 
side  of  the  heart.  As  a  result  three  chief  circulatory  changes  ensue. 
Some  of  the  blood  finds  its  way  by  large  anastomotic  channels  from  one 
side  to  the  other,  and  so  is  imperfectly  oxidized.  The  increased  obstruc- 
tion to  the  flow  results  in  distention  and  arteriosclerotic  changes  in  the 
pulmonary  artery,  in  dilatation,  with  more  or  less  hypertrophy,  of  the 
right  ventricle  and  finally  in  dilatation  of  the  right  auricle.     Eventually, 

Fig.  55 


Section  of  anterior  margin  of  the  lung  from  a  case  of  essential  emphysema,  showing  the  wasting 
and  absorption  of  the  vesicular  walls. 


when  the  pathological  process  is  far  advanced  we  find  that  the  liver  is 
greatly  engorged  with  blood,  ascites  may  develop,  the  cardiac  failure 
rapidly  progresses,  and  death  results  from  the  various  sequences  of  the 
primary  lesions. 

Associated  with  emphysema  there  is  usually  more  or  less  well-developed 
chronic  bronchitis. 

Symptoms. — ^The  symptoms  of  emphysema  may  be  best  divided  into  the 
objective,  or  those  that  can  be  seen  by  the  physician,  and  the  subjective,  or 
those  described  by  the  patient. 

"Physical  Signs. — The  most  noteworthy  objective  signs  are  the  increase  in 
the  diameter  of  the  chest,  so  that  the  anteroposterior  diameter  equals  the 
lateral;  the  fulness  or  bulging  of  the  intercostal  spaces;  the  impaired  respir- 
atory movement  of  the  thorax,  which  may  seem  quite  fixed;  the  well-filled 


416 


DISEASES  OF   THE  LUNGS 


or  distended  cervical  vessels,  and  the  presence  in  the  epigastrium  of  the  apex 
beat  of  the  heart.  If  the  ease  is  severe  we  see  in  addition  to  these  signs 
^pulsations  of  the  jugular  veins,  labored  breathing,  cyanosis  of  the  lips, 
fulness  of  the  abdomen,  due  to  the  displaced  and  engorged  liver,  and  the 
accumulation  of  fluid  in  the  peritoneum.  Not  infrequently  inspection  of  the 
upper  part  of  the  epigastrium  reveals  a  network  of  enlarged  capillaries  in 
the  skin.    These  are  the  chief  signs  on  inspection. 

Fig.  56 


Lung,  anterior  aspect,  from  a  case  of  essential  emphysema.  The  large  bullae  on  the  anterior  margin 
of  the  middle  lobe  are  nearly  two  centimetres  in  diameter.  Smaller  vesicles  are  present  on  the 
anterior  margin  of  the  upper  lobe  and  along  the  diaphragmatic  border  of  the  lower  lobe.  The  apex  is 
but  slightly  involved,  but  in  some  cases  it  is  markedly  affected. 


On  further  careful  physical  examination  we  find  on  palpation  that  the 
apex  beat  cannot  be  felt  at  the  normal  area  near  the  nipple  because  it  is 
displaced  and  covered  by  the  enlarged  lung.  The  lower  margin  of  the  liver 
may  be  felt  as  low  as  the  navel.  Palpation  of  the  chest  while  the  patient 
speaks  reveals  a  marked  decrease  in  vocal  fremitus.  Percussion  gives  a 
high-pitched  resonant  note  all  over  the  chest,  particularly  over  the  upper 
lobes;  reveals  a  decrease  of  the  normal  area  of  cardiac  dulness;  shows  the 
liver  to  be  as  low  as  palpation  indicated  it  to  be,  and  gives  flatness  in  the 


EMPHYSEMA   OF   THE  LUNGS  417 

flanks  and  in  the  suprapubic  area  if  ascites  is  present.  Auscultation  reveals 
a  feeble  vesicular  murmur,  marked  prolongation  of  expiration  because  of  the 
inelastic  state  of  the  lung,  and  sometimes  there  can  be  heard  rales,  which 
are  due  to  the  associated  bronchitis.  A  curious  crackling  sound,  the 
cause  of  which  is  not  certain,  is  also  heard  sometimes.  It  is  not  due  to 
pleurisy  and  is  probably  produced  by  the  air  in  the  bladder-like  dilata- 
tions in  the  margins  of  the  lungs.  This  sound  is  usually  best  heard  at  the 
apices. 

Subjective  Signs. — The  symptoms  from  which  the  patient  complains 
are  chiefly  those  connected  with  respiration.  The  shortness  of  breath  varies 
greatly  in  different  cases.  In  some  it  is  constant.  In  others  it  is  only  devel- 
oped when  exercise  is  taken,  and  the  difference  in  its  degree  on  exertion 
varies  widely  in  different  individuals.  Often  dyspnoea  is  only  felt  on  warm, 
oppressive,  or  humid  days,  while  in  other  cases  any  exertion  whatever 
produces  such  severe  dyspnoea  that  the  patient  is  forced  to  rest.  This 
dyspnoea,  as  already  stated,  depends  upon  deficient  oxygenation  of  the 
blood,  upon  the  interference  with  the  action  of  the  right  side  of  the  heart, 
and  upon  the  inability  of  patient  to  take  fresh  air  into  his  lungs  in  large 
quantity  because  of  the  excess  of  residual  air  which  is  present. 

The  cough  in  some  cases  is  so  constant  as  to  greatly  annoy  the  patient.  In 
other  instances  it  is  almost  entirely  absent.  The  development  of  this  symptom 
largely  depends  upon  the  degree  of  bronchitis  which  is  associated  with  the 
emphysematous  change.  If  marked  bronchial  irritation  is  present,  the  cough 
is  not  only  annoying  because  of  its  persistency,  but  also  exhausts  the  patient, 
and  aids  in  the  dilatation  and  fatigue  of  the  right  side  of  the  heart.  The 
sputum  which  results  from  the  cough  varies  in  quantity  with  the  severity 
of  the  bronchitis  which  is  present,  and  is  not  peculiar  in  appearance  unless 
by  chance  the  patient  is  also  a  sufferer  from  asthma,  when  the  characteristics 
of  asthmatic  sputum  may  be  manifest.  The  digestive  disorders  sometimes 
complained  of  by  the  patient  depend  chiefly  upon  the  impairment  of  the 
circulation  in  the  liver,  stomach,  and  intestines,  produced  by  the  secondary 
cardiac  lesions.  Sometimes,  too,  the  urine  is  scanty,  owing  to  congestion 
of  the  kidneys  from  the  same  cause. 

Diagnosis — From  what  has  just  been  said  of  the  symptoms  and  typical 
signs  of  pulmonary  emphysema  it  is  evident  that  the  diagnosis  is  not  difficult. 
Indeed,  in  a  well-developed  case  there  is  probably  no  pulmonary  condition 
so  easily  recognized.  The  bilateral  increase  in  the  size  of  the  chest,  the 
narrowing  of  the  intercostal  spaces,  the  dyspnoea,  the  cyanosis,  the  prolonga- 
tion of  expiration,  the  hyper  resonance  on  percussion  are  all  to  be  noted  in 
forming  a  positive  conclusion  as  to  the  character  of  a  case.  It  is  not  necessary 
for  the  diagnosis  of  emphysema  that  deformity  of  the  chest  be  present 
Sometimes  a  marked  degree  of  pulmonary  change  exists  without  any  change 
in  the  shape  of  the  thorax. 

Emphysema  of  one  lung  is  practically  never  seen,  and  therefore  pneumo- 
thorax can  be  easily  separated  from  emphysema. 

Prognosis. — The  prognosis  of  emphysema  is  always  unfavorable;  at  least, 
so  far  as  complete  recovery  is  concerned.     In  many  cases,  however,  the 
progress  of  the  disease  is  so  slow  that  the  patient  may  live  for  years  with  a 
27 


418  DISEASES  OF   THE  LUNGS 

fair  degree  of  comfort.  Indeed,  in  some  instances  the  pathological  process 
becomes  stationary.  Patients  with  well-developed  emphysema  are,  however, 
rarely  fortunate  enough  to  develop  this  arrest  of  the  disease,  and  equally 
rarely  live  until  advanced  old  age,  usually  because  with  advancing  years 
the  muscle  fibre  of  the  right  side  of  the  heart  becomes  less  and  less  able  to 
stand  the  strain  which  is  thrown  upon  it. 

It  is  vitally  important,  so  far  as  prognosis  is  concerned,  for  patients  suf- 
fering from  pulmonary  emphysema,  to  avoid  exposure  to  sudden  changes 
of  temperature;  for  such  changes  may  produce  a  severe  bronchitis  or  pneu- 
monia, conditions  which  the  patient  is  ill  able  to  withstand.  The  presence 
of  a  persistent  chronic  bronchitis  renders  the  prognosis  more  grave^  than  if 
this  complication  does  not  exist.  Death  rarely  comes  on  suddenly  in  these 
patients,  but  slowly,  as  a  result  of  constantly  increasing  circulatory  failure. 
Lebert  asserts  that  one-third  of  these  cases  die  from  cardiac  dropsy,  and  the 
rest  from  pulmonary  congestion  and  gradual  feebleness,  with  slow  suffocation, 
increasing  cyanosis,  and  constantly  developing  bronchitis.  ^ 

Treatment. — The  treatment  of  pulmonary  emphysema  is,  unfortunately, 
very  limited.  There  is  no  curative  treatment.  The  most  that  the  physician 
can  do  is  to  improve  the  condition  of  the  circulation  and  the  nutrition  of  the 
patient,  and  to  prevent  him  from  throwing  severe  strain  upon  his  pulmonary 
tissues  and  his  circulatory  apparatus.  Where  the  patient  follows  an  occupa- 
tion which  is  manifestly  injurious,  he  must  be  advised  to  give  it  up,  and,  for 
that  matter,  to  avoid  all  violent  muscular  effort  which  will  throw  a  strain 
upon  his  heart  and  lungs.  Incipient  attacks  of  acute  bronchitis  should  be 
treated  at  the  earliest  possible  moment,  and,  if  chronic  bronchitis  is  present, 
the  remedies  which  are  commonly  given  for  that  disorder  should  be  em- 
ployed, care  being  taken,  however,  that  no  drug  is  given  which  tends,  on  the 
one  hand,  to  act  as  a  circulatory  depressant,  and,  on  the  other,  to  promote 
too  free  bronchial  secretion,  for  it  must  always  be  borne  in  mind  that  drugs 
of  this  character  may  precipitate  an  attack  of  profuse  bronchial  secretion, 
in  which  the  patient  may  drown  in  his  own  fluids. 

Many  of  these  patients  will  be  benefited  by  the  administration  of  5  grains 
of  carbonate  of  ammonium  and  5  grains  of  chloride  of  ammonium  given  in 
a  cachet,  or  capsule,  or  in  fluid  extract  of  licorice  and  water,  three  or  four 
times  a  day.  In  other  instances,  if  the  bronchitis  is  chronic  and  well 
marked,  creosote  or  guaiacol  may  be  used;  but  care  must  be  exercised  that 
they  do  not  disorder  the  stomach.  If  the  secretion  is  thick  and  tenacious, 
iodide  of  ammonium,  or  iodide  of  sodium,  in  the  dose  of  5  grains  three 
times  a  day,  is  useful,  care  being  taken,  however,  that  the  administration 
of  this  remedy  does  not  produce  too  free  bronchial  secretion.  It  must  also  be 
borne  in  mind  that  bronchitis  complicating  emphysema  is  not  infrequently 
the  result  of  impaired  cardiac  action,  and,  therefore,  that  the  best  treatment 
for  the  bronchitis  is  the  administration  of  cardiac  tonics,  such  as  small  doses 
of  digitalis,  3  to  5  minims  twice  or  thrice  a  day,  or  the  tincture  of  strophan- 
thus,  or,  in  other  cases,  the  administration,  for  a  few  days,  of  moderately 
large  doses  of  strychnine  or  nux  vomica. 

When  the  patient's  means  permit  him,  it  is  important  that  he  should  avoid 
extreme  climatic  changes.    High  altitudes  are,  of  course,  not  only  disadvan- 


EMPHYSEMA  OF  THE  LUNGS  419 

tageous,  but  even  dangerous  to  patients  suffering  from  pulmonary  emphy- 
sema, because  of  the  dyspnoea  which  such  altitudes  produce  and  because  of 
the  strain  which  is  thrown  upon  the  dilated  right  heart. 

In  cases  of  emphysema  suffering  from  an  unusually  severe  attack  of 
dyspnoea,  with  great  congestion  and  engorgement  of  the  venous  system,  it  is 
often  advantageous  to  resort  to  venesection,  removing  as  much  as  20  to  30 
ounces  of  blood ;  but  it  is  manifest  that  this  method  of  treatment  can  only 
be  resorted  to  on  a  few  occasions,  and  when  the  symptoms  of  dilatation  and 
distention  of  the  right  side  of  the  heart  and  of  the  liver  are  very  well  devel- 
oped. Sometimes  in  these  cases,  if  there  is  evidence  of  hypostatic  congestion 
of  the  lungs,  the  application  of  wet  or  dry  cups,  posteriorly,  near  the  bases 
is  advantageous. 

For  many  years  various  text-books  have  recommended  the  employment 
of  the  iodides  in  their  various  forms  in  the  treatment  of  pulmonary  emphy- 
sema, with  the  idea  that  they  distinctly  modify  the  pathological  process 
going  on  in  the  lungs,  and  to  a  certain  extent  arrest  the  destruction  of  the 
elastic  tissue  which,  by  its  failure,  results  in  the  coalescence  of  the  vesicles. 
It  must  be  manifest  that  even  that  wonderful  drug,  iodide  of  potassium, 
must  be  quite  useless  for  this  purpose  in  many  instances.  Any  advantage 
which  follows  its  employment  probably  depends  upon  its  influence  upon  the 
associated  bronchitis,  or  upon  the  effect  which  it  produces  upon  the  vascular 
system  by  diminishing  the  tendency  to  atheromatous  change,  and  by  reducing 
high  arterial  tension  if  it  is  present,  and  so  relieving  the  heart  of  unnecessary 
burden.  Still  another  advantage  in  the  iodides  may  be  that  in  some  cases 
they  act  as  a  diuretic  and  so  help  to  relieve  the  tissues  of  an  undue  quantity 
of  fluid  if  dropsy  be  threatened. 

Compensatory  or  Acute  Emphysema. — This  is  an  unfortunate  use  of 
the  word  emphysema,  as  the  condition  is  not  a  true  emphysema,  but  simply 
an  abnormal  distention  of  each  individual  air  vesicle  by  active  efforts  at 
forced  respiration,  so  that  the  entire  lung  may  be  increased  in  size  and  the 
areas  of  pulmonary  resonance  greatly  increased.  Usually  in  this  state  some 
high-pitched  rales  are  audible  in  the  chest.  The  condition  may  be  seen  in 
cases  which  have  suffered  from  stridor  due  to  laryngeal  obstruction,  or  more 
commonly  in  those  who  are  recovering  from  an  acute  asthmatic  attack.  It 
is  also  found  in  those  parts  of  the  lungs  which  have  endeavored  to  compen- 
sate for  other  parts  affected,  as,  for  example,  by  pneumonia. 

Interstitial  Emphysema. — In  interstitial  emphysema  the  pathological  con- 
dition is  not  like  that  of  ordinary  pulmonary  emphysema,  for  the  lung  is 
riddled  with  tiny  globules  of  air  which  find  their  way  between  the  lobules 
and  underneath  the  visceral  layer  of  the  pleura,  where  they  may  form  quite 
large  blebs.  The  condition  arises  whenever  air  escapes  into  the  pulmonary 
tissues,  as  after  tracheotomy,  when  it  extends  down  along  the  trachea  into 
the  lung  itself;  fractures  of  the  ribs  with  puncture  of  the  lung;  other  wounds 
of  the  lung;  rupture  of  air  vesicles  by  great  thoracic  compression,  as  in  sand 
crushes,  even  without  injury  to  the  skeleton,  and  occasionally  results  from 
violent  abnormal  respiratory  action,  as  in  whooping-cough,  strangling,  and 
sneezing.  It  has  been  observed  after  severe  convulsions  in  epileptics  and 
eclamptics. 


420  DISEASES  OF  THE  LUNGS 

Small-lunged  Emphysema. — Small-lunged  emphysema  is  sometimes 
called  senile  or  atrophic  emphysema,  or  senile  atrophy  of  the  lung.  It  resem- 
bles ordinary  emphysema,  as  just  described,  in  the  fact  that  there  is  a  wast- 
ing of  the  walls  of  the  air  vesicles,  so  that  several  vesicles  form  a  larger 
cavity;  but  instead  of  the  lung  being  larger  and  more  voluminous  than  normal, 
it  is  shrunken  and  small,  so  that  the  heart  is  uncovered,  the  diaphragm 
raised  in  well-marked  cases,  and  the  whole  thorax  distinctly  decreased  in 
size.  The  expansion  of  the  vesicles,  as  in  large-lunged  emphysema,  is  most 
marked  at  the  apices  and  the  edges  of  the  lung.  Inspection  of  the  chest  in 
such  a  case  shows  the  intercostal  spaces  obliterated  by  the  drawing  together 
of  the  ribs,  while  the  epiclavicular  and  episternal  spaces  are  exaggerated  and 
the  respiratory  movement  is  feeble  and  very  shallow.  On  percussion  the 
chest  is  found  to  be  hyperresonant  everywhere,  but  there  is  a  great  increase 
in  the  area  of  cardiac  dulness,  due  to  the  retraction  of  the  lung.  On 
auscultation  little  that  is  abnormal  is  heard,  save  that  expiration  may  be 
prolonged. 

Except  there  be  an  associated  bronchitis,  the  patient  with  this  type  of 
emphysema  rarely  suffers  from  much  inconvenience  as  a  result  of  the  pul- 
monary disease,  and  life  is  not  materially  shortened. 

Treatment. — There  is  no  curative  treatment  for  this  type.  The  physician 
can  only  order  rest,  good  food,  proper  clothing,  and  the  avoidance  of 
exposure. 

GANGRENE  OF  THE  LUNG. 

Etiology. — This  condition  arises  in  individuals  whose  general  vitality  is 
greatly  impaired  by  some  primary  disease,  with  the  result  that  various  micro- 
organisms, putrefactive  and  otherwise,  produce  death  of  part  of  the 
pulmonary  parenchyma,  and  so  a  slough  is  formed.  Manifestly,  the  causes 
of  gangrene  and  abscess  must  be  nearly  related,  and  why  gangrene  rather 
than  abscess  should  develop  in  any  particular  case  is  difhcult  to  determine. 
Infarction  of  the  lung,  or  pulmonary  hemorrhage,  may,  by  affording  a  nidus 
for  the  development  of  putrefactive  germs,  result  in  this  state,  and  so  may 
croupous  pneumonia ;  yet  it  is  a  curious  fact  that  bronchopneumonia,  which 
is  often  due  to  profound  debility  and  secondary  infection,  rarely  so  results. 
Equally  curious  it  is  to  note  that  pulmonary  tuberculosis  in  all  its  forms  is 
rarely  complicated  in  this  manner. 

The  most  common  cause  of  pulmonary  gangrene  is  embolism  and 
thrombosis,  after  this  croupous  pneumonia,  and,  thirdly,  injuries  to  the  lung 
through  the  chest  wall,  as  in  gunshot  injuries.  It  may  also  arise  from 
foreign  bodies  in  the  bronchi.  It  may  also  be  due  to  pressure  produced  by 
an  aneurysm,  or  tumor,  or  by  an  extension  of  an  infective  process  to  the 
lung  from  the  oesophagus,  pleura,  vertebrae,  mediastinum,  or  ribs.  It  may 
also  follow  the  inspiration  of  particles  of  food.  Rarely  it  is  due  to  pressure 
of  an  aneurysm  or  to  perforation  of  the  oesophagus  when  that  tube  is  affected 
by  cancer. 

Frequency. — Pulmonary  gangrene  most  frequently  attacks  males  in  middle 
life — ^that  is,  from  twenty  to  forty  years  of  age — and  is  undoubtedly  a  very  rare 


GANGRENE  OF  THE  LUNG  421 

affection.  In  a  large  hospital  service  only  a  single  case  may  be  met  with  in 
many  years. 

Pathology  and  Morbid  Anatomy. — No  description  of  pulmonary  gangrene 
is  better  than  that  given  by  Laennec,  who,  nevertheless,  in  an  experience  of 
twenty-four  years,  saw  only  2  cases.  He  divides  the  condition  into  three 
stages:  (1)  that  of  early  mortification,  in  which  the  pulmonary  tissue  is 
oedematous  and  of  dark-brown  or  greenish  hue,  the  sloughing  area  looking 
shreddy  and  water-soaked;  (2)  that  of  deliquescence  or  liquefaction,  the 
part  of  the  lung  affected  becoming  still  more  soft  and  flabby;  and  (3)  that 
of  excavation  or  abscess  formation,  in  which  the  lung  undergoes  the  separa- 
tion of  the  slough  and  the  formation  of  a  line  of  demarcation  to  limit  the 
pathological  process.  At  this  line  of  separation  a  consolidation  takes  place, 
the  sphacelus  breaks  down,  and  suppuration  rapidly  results  in  the  coughing 
up  of  the  dead  tissues.  As  a  matter  of  fact,  it  is  incorrect  to  speak  of  a  single 
sphacelus,  for  the  cavity  usually  contains  separate  masses  of  shred-like 
tissue. 

Finally  the  limiting  wall  may  undergo  fibroid  contraction,  as  it  does 
in  abscess,  and  the  area  be  more  or  less  closed,  a  focus  usually  remaining, 
from  which  more  or  less  foul  pus  is  constantly  discharged.  In  the  majority 
of  cases  this  reparative  process  does  not  occur,  and  the  patient  dies.  Over 
the  seat  of  the  process  the  pleural  membrane  is  usually  thickened  and  may 
be  covered  by  a  fibrinopurulent  exudate,  while  if  the  pleura  be  perforated  a 
putrid  empyema  may  develop.  In  such  cases  pyopneumothorax  may  also 
manifest  itself.    Extensive  suppuration  of  the  bronchial  glands  may  occur. 

Pulmonary  gangrene  affects  the  lower  lobes  oftener  than  the  upper. 

Symptoms. — The  symptoms  of  pulmonary  gangrene  in  the  early  stages  are 
not  very  definite.  They  depend,  to  some  extent,  upon  the  severity  of  the 
lesions  and  upon  the  micro-organisms  which  produce  it.  The  patient  is 
markedly  ^prostrated,  the  heart's  action  is  jeehle  and  rapid,  the  skin  leaky, 
the  jace  anxious  and  thin,  and  the  tongue  dry  and  coated.  The  temperature 
runs  the  typical  course  of  hectic  fever,  and  it  is  a  noteworthy  fact  that  the 
exhaustion  seems  out  of  proportion  in  its  severity  to  the  febrile  movement. 
Sometimes  these  symptoms  are  ushered  in  with  severe  chills,  which  recur  at 
irregular  intervals.  The  respirations  are  quickened,  and  there  may  be  cough 
and  expectoration,  but  until  the  break-down  goes  on  so  far  as  to  result  in 
suppuration  there  may  be  but  little  material  expectorated.  If  a  cavity  forms, 
the  ordinary  signs  of  excavation,  with  those  of  surrounding  consolidation, 
may  be  developed  upon  auscultation  and  percussion. 

One  of  the  most  characteristic  symptoms  of  pulmonary  gangrene  is  the 
odor  of  the  patient's  breath  and  of  the  materials  which  he  expectorates. 
There  is  probably  no  discharge  from  the  human  body  the  odor  of  which  is 
so  penetrating  and  disgusting  as  is  that  of  pulmonary  gangrene.  Not  only 
does  it  render  the  patient  disgusting  to  everyone  who  comes  near  him, 
but  it  penetrates  every  part  of  the  room  in  which  he  exists,  and  often  can 
be  smelled  throughout  the  whole  house.  On  some  days  it  is  worse  than 
others,  but  the  variation  of  the  quantity  of  expectoration  does  not  neces- 
sarily mean  a  variation  in  its  fetid  character.  The  quantity  of  material  which 
is  expectorated  does  not  give  any  very  definite  conception  of  the  size  of  the 


422  DISEASES  OF  THE  LUNGS 

lesion  of  the  lungs.  "West  quotes  a  case  of  Godlee  and  Williams  in  which 
the  patient  expectorated  a  quart  daily,  and  yet  the  autopsy  revealed  a 
gangrenous  ca\4ty  which  was  not  large  enough  to  contain  more  than  an 
ounce  of  fluid. 

The  sputum  is  peculiar,  in  that  on  standing  it  separates  into  three 
layers.  The  upper  layer  is  apt  to  be  yellowish-green  and  opaque;  the  middle 
layer  is  opalescent  and  turbid,  and  resembles  saliva  when  a  considerable 
quantity  is  gathered  in  a  glass.  The  lowest  layer  consists  in  a  mass  of 
greenish  or  brown-looking  material,  which  contains  considerable  quantities 
of  pus,  altered  red  blood  cells,  and  fragments  of  connective  tissue.  A  careful 
microscopic  examination  of  this  sputum  will  show  that  it  is  filled  with  an 
immense  number  of  micro-organisms,  and  crystals  of  leucin  and  t}Tosin  can 
be  seen  in  large  numbers.  Various  fatty  acid  crystals  are  also  present. 
The  sputum,  at  first  alkaline,  becomes  acid,  and  seems  to  exercise  a  peculiar 
digestant  or  disintegrating  influence  upon  the  shreds  of  connective  tissue 
which  it  contains. 

The  cough  in  a  case  of  pulmonary  gangrene  varies  greatly  according  to  the 
amount  of  material  which  is  expectorated,  and  also  with  the  degree  of  bronchial 
irritation  which  coexists.  Sometimes,  after  a  prolonged  spell  of  coughing, 
a  considerable  amount  of  material  from  the  gangrenous  area  comes  away  in 
a  gush.  Sometimes,  too^  the  fluid  which  is  expectorated  is  distinctly  blood- 
tinged,  due  to  the  ulceration  of  small  bloodvessels  in  the  part  surrounding 
the  affected  part.  Not  only  may  free  haemoptysis  develop,  but  septic  emboli 
may  be  carried  elsewhere,  as,  for  example,  to  the  brain  or  liver,  and  so  cause 
secondary  abscesses. 

If  by  chance  the  patient  swallows  any  of  the  sputum,  septic  diarrhoea  may 
be  established  and  the  stools  may  also  become  excessively  offensive.  The 
degree  of  exhaustion  gradually  increases,  the  heart  becomes  more  and  more 
feeble,  the  patient  more  and  more  emaciated,  and,  finally,  dies  of  asthenia. 

Diagnosis. — The  diagnosis  between  a  moderate  degree  of  pulmonary 
gangrene,  pulmonary  abscess,  and  bronchiectasis  may  be  almost  impossible, 
since,  if  bronchiectasis  exists,  the  fetor  of  the  sputum  may  be  very  marked. 
If  the  sputum  under  the  inicroscope  shows  a  large  amount  of  connective 
tissue,  the  diagnosis  is  largelv  in  favor  of  o-angrene.  The  absence  of  tubercle 
bacilli  in  the  sputum  and  the  presence  of  the  various  bodies  already  named 
as  appearing  in  this  fluid  will  also  aid  in  differentiation  of  the  case.  "When 
the  gangrene  cavity  is  small,  a  positive  antemortem  diagnosis  may  not  be 
possible,  the  more  so  because  of  the  presence  of  acid-resisting  bacilli,  which 
may  be  mistaken  by  the  novice  for  tubercle  bacilli. 

Treatment. — The  treatment  of  pulmonary  gangrene  is  not  promising.  It 
is  the  duty  of  the  physician  to  maintain  the  strength  of  the  patient,  as  far  as 
possible,bythe  administration  of  nutritious  food  given  at  frequent  intervals, 
in  small  quantities,  so  that  the  digestion  will  not  be  overloaded;  to  give 
stimulants,  as  alcohol;  and  occasionally,  if  the  circulation  becomes  feeble, 
to  administer  strychnine  hypodermically,  or  by  the  mouth.  Bitter  tonics 
may  also  be  prescribed  for  the  purpose  of  maintaining  digestive  activity. 
The  employment  of  antiseptic  inhalations,  as  suggested  in  the  treatment  of 
pulmonary  abscess,  may  also  be  resorted  to,  but  at  most  only  do  good  by 


PULMONARY  ABSCESS  423 

soothing  the  Irritation  of  the  bronchial  mucous  membranes  and  cannot,  of 
course,  influence  the  pulmonary  parenchyma  where  the  disease  exists. 

If  the  evidences  of  sepsis  are  marked  and  anoemla  Is  present,  the  tincture 
of  chloride  of  iron  is  to  be  administered,  and  the  heart  supported  by  alcohol, 
digitalis,  and  occasionally  by  caffeine.  The  internal  use  of  creosote,  car- 
bolic acid,  and  similar  substances,  with  the  idea  that  they  exercise  a 
beneficial  influence  upon  the  gangrenous  portion  of  the  lung,  is  futile. 

A  few  cases  of  gangrene  of  the  lung  have  been  treated  surgically,  with 
success,  by  incision  and  drainage.  For  these  methods  the  reader  is  referred 
to  surgical  treatises. 


PULMONARY  ABSCESS. 

Etiology. — Abscess  of  the  lung  Is  always  due  to  invasion  of  its  tissues  by 
one  or  more  forms  of  pyogenic  micro-organisms.  Single  large  abscess  occurs 
very  rarely,  but  it  is  met  with  as  a  sequel  of  lobar  pneumonia,  broncho- 
pneumonia, and  as  a  result  of  injury  to  the  lung  by  the  entrance  of  foreign 
bodies  through  the  chest  wall  or  by  the  respiratory  passages.  Most  commonly 
small  abscesses  are  the  result  of  sep^^c  emboli.  Abscess  may  be  due  to  the 
extension  of  a  septic  process  from  the  mediastinal  tissues  or  of  the  liver. 
So,  too,  a  suppurative  process  in  the  deep  tissues  of  the  neck  may  result 
in  secondary  infection  of  the  lung. 

When  pulmonary  abscess  ensues  after  an  attack  of  croupous  pneumonia 
or  bronchopneumonia,  it  is  usually  not  single,  but  multiple,  the  area  of  con- 
solidation being  the  seat  of  several  foci  of  purulent  material.  These  forma- 
tions are  not  by  any  means  so  rare  as  in  the  larger  variety.  Holt  states  that 
he  found  them  in  about  7  per  cent,  of  the  autopsies  of  young  children  dying 
of  pneumonia.  Such  foci  are  really  not  true  abscesses;  that  is  to  say,  they 
have  no  true  abscess  wall.  When  these  formations  are  numerous,  as  they 
usually  are,  and  of  considerable  size,  the  patient  may  maintain  a  high  tem- 
perature for  a  long  time  after  the  acute  primary  disease  has  passed  away, 
and  may,  by  causing  septic  absorption,  ultimately  produce  the  patient's 
death.  It  may  be  difficult,  even  at  autopsy,  to  state  positively  whether  the 
purulent  infiltration  of  the  later  stages  of  both  forms  of  pneumonia  is 
present,  or  if  there  is  a  true  suppurative  abscess  in  the  lung.  In  both  cases 
the  areas  of  softening  are  found  to  be  infected  by  the  streptococcus, 
staphylococcus,  or  other  pyogenic  organism. 

When  the  foci  are  of  large  size,  and  are  multiple,  the  prognosis  is  bad,  for 
widespread  suppuration  in  the  lung  is  always  fatal  when  the  breaking-down 
process  involves  the  exudation  of  pneumonia.  If  there  be  a  single,  large, 
localized  abscess  involving  the  area  of  pneumonic  exudate,  the  prognosis  is 
less  grave,  but  it  is  exceedingly  bad,  nevertheless.  To  sum  up,  therefore, 
we  find  that  suppuration  takes  place  in  the  lung  in  three  degrees  or  forms 
after  pneumonia:  (1)  as  a  mild  suppurative  process,  which  is  really  nothing 
more  than  a  rapid  breaking  down  of  the  exudate  of  the  disease;  (2)  as  a 
more  severe  process,  partaking  more  of  the  character  of  true  suppuration, 
in  which  multiple  and  large  foci  of  pus  form;  and  (3)  of  a  single  large  sup- 


424  DISEASES  OF  THE  LUNGS 

puratlve  process;  in  other  words,  a  single  abscess  of  the  lung.     As  already 
stated,  these  so-called  "abscesses"  rarely  have  a  true  abscess  wall. 

Abscess,  multiple  or  single,  when  it  arises  from  the  entrance  of  a  foreign 
body,  only  occurs  if  that  body  enables  infecting  micro-organisms  to  enter 
the  surrounding  tissues.  Thus,  a  marble,  or  small  stone,  entering  a  bronchus 
may  be  there  for  a  long  time  without  causing  abscess;  whereas,  the  entrance 
of  a  piece  of  food,  a  straw,  or  a  fragment  of  cork,  or  other  organic  matter 
may  speedily  cause  a  septic  suppurative  pneumonia  and  death.  Such  an 
abscess  may  follow  a  septic  infection  in  a  gunshot  injury. 

If  by  chance  the  patient  recovers  from  the  acute  illness,  there  may  be  left 
a  constantly  discharging  focus  of  pus. 

Again,  we  find  pulmonary  abscess  forming  as  the  result  of  a  septic  embolus 
entering  the  lung.  About  the  site  of  its  lodgement  an  inflammatory  exudate 
rapidly  forms,  and  this  speedily  proceeds  to  suppuration.  Pus  and  yellow 
elastic  tissue  are  expectorated,  and  the  patient  dies  of  septic  poisoning  and 
exhausion,  or  if  recovery  takes  place  there  is  formed  around  the  zone  of 
necrotic  tissue  a  wall  of  inflammatory  exudate,  which  prevents  further 
destruction  of  the  parts,  and,  with  recovery,  proceeds  to  organization,  finally 
developing  into  more  or  less  well-formed  fibrous  tissue,  which  gradually 
contracts  until  the  cavity  disappears  or  is  greatly  decreased  in  size.  We 
have  in  this  type  what  may  be  called  the  true  form  of  abscess  as  it  occurs  in 
other  tissues;  whereas,  the  ordinary  suppurative  foci  hitherto  described 
are  hardly  to  be  regarded  as  true  abscesses.  Occasionally  the  abscess 
cavity  persists  for  months,  and  we  have  then  a  chronic  pulmonary 
abscess. 

When  abscesses  elsewhere  than  in  the  lung  break  into  its  tissues  the  result 
is  not  always  a  pulmonary  abscess  by  any  means.  It  is  often  extraordinary 
how  much  foul  pus  may  pass  from  an  empyema  or  hepatic  abscess  through 
the  lung,  and  be  expectorated,  without  causing  any  severe  lesions  in  these 
organs. 

Sometimes  suppuration  takes  place  in  an  echinococcus  cyst  in  the  lung. 
Symptoms  and  Diagnosis.  —The  diagnosis  of  pulmonary  abscess  in  its  early 
stages  may  be  practically  impossible,  for  there  may  be  present  no  other 
signs  than  cough,  fever,  and  scanty  expectoration,  with  patches  of  impaired 
resonance  on  percussion.  In  unresolved  pneumonia  the  physical  signs  may 
be  identical,  but  the  leukocyte  count  is  rarely  above  15,000  or  20,000, 
whereas  in  abscess  from  30,000  to  50,000  white  cells  may  be  present.  As 
the  pus  is  freely  formed,  much  aid  may  be  gained  from  the  temperature 
chart,  which  may  show  the  long  sweeps  of  septic  absorption.  There  may  be 
sweats,  chills,  and  some  hectic  flushing ;  but  these  do  not  necessarily  point 
to  abscess  of  the  lung,  for  they  may  be  due  to  empyema  or  an  abscess  else- 
where, or  be  a  result  of  tuberculosis.  If  the  sputum  becomes  distinctly  puru- 
lent, and  the  microscope  shows  abundant  pus  and  masses  of  connective 
tissue  without  tubercle  bacilli,  the  diagnosis  is  readily  made.  About  this 
time  it  may  be  possible,  too,  to  discover  the  physical  signs  of  cavity. 

When  a  single  large  abscess  is  present  the  positive  diagnosis  may  be 
made  evident  by  the  sudden  rupture  of  its  contents  into  a  bronchus,  and 
the  expelling  through  the  mouth  of  a  considerable  quantity  of  pus.    I  had 


CONGESTION  OF  THE  LUNGS  425 

under  my  care  recently  a  young  woman,  aged  twenty  years,  who,  after  an 
attack  of  typical  croupous  pneumonia,  developed  a  more  and  more  septic 
temperature,  and,  finally,  expelled  at  one  time  nearly  a  pint  of  pus  from  the 
right  lung.  Constant  expectoration  of  pus  persisted  for  several  days,  and 
then  an  equally  large  amount  was  expelled,  nearly  causing  death  by  strangu- 
lation. After  a  long  convalescence  she  reached  perfect  health.  In  this  case 
the  fluoroscope  revealed  the  site  of  the  abscess  very  clearly.  Care  must  be 
taken  that  the  purulent  expectoration  and  fetid  breath  of  a  case  of  bron- 
chiectasis is  not  considered  an  indication  of  true  pulmonary  abscess. 

Prognosis. — ^The  prognosis  in  these  cases  is  always  very  grave.  Death  may 
ensue,  not  only  from  septic  absorption,  but  from  the  gradual  exhaustion 
due  to  prolonged  suppuration  or  from  the  ulceration  of  the  wall  of  a  blood- 
vessel, with  consequent  severe  haemoptysis.  Again,  a  secondary  pneumonia 
may  develop  from  the  primary  suppurative  process. 

Treatment. — The  treatment  of  abscess  of  the  lung  divides  itself  into  three 
parts :  the  support  of  the  patient's  strength  by  good  food  and  the  moderate 
use  of  stimulants ;  the  resort  to  as  much  fresh  air  and  sunshine  as  possible ; 
the  inhalation  of  gentle  antiseptic  balsams  which  do  not  really  influence 
the  abscess,  but  perhaps  benefit  the  associated  bronchitis;  and,  lastly, 
by  the  use  of  the  knife,  bone  forceps,  and  the  actual  cautery,  to  open  the 
abscess  through  the  chest  wall  and  lung. 

As  supporting  drugs,  iron  and  arsenic,  whiskey  and  port  wine,  are  par- 
ticularly valuable.  Easily  digested  semi-liquid  foods,  with  digestants  to  aid 
their  speedy  absorption,  are  valuable,  and  in  the  way  of  an  inhalation  equal 
parts  of  oil  of  eucalyptus,  oil  of  pine,  and  compound  tincture  of  benzoin 
may  be  added  to  the  water  in  a  croup  kettle,  and  so  dissipated  through 
the  air  of  the  room.  Codeine  and  cannabis  indica  may  be  used  to  relieve 
excessive,  painful  cough;  but  large  doses  of  these  drugs  should  not  be  used, 
because  they  prevent  the  expectoration  of  the  pus,  and  if  the  patient  sleeps 
soundly  while  under  their  effects,  rupture  of  the  abscess  may  cause  fatal 
asphyxia. 

CONGESTION  OF  THE  LUNGS. 

Definition. — Strictly  speaking,  there  is  a  congestion  of  the  lungs  when- 
ever severe  exercise  is  taken,  but  this,  of  course,  is  not  referred  to  here; 
nor  is  it  the  intention  to  consider  that  form  which  precedes,  or  rather  con- 
stitutes, the  early  stage  of  croupous  pneumonia,  and  which  ends  in  the  forma- 
tion of  a  croupous  exudate.  The  form  of  congestion  here  referred  to  is  that 
due  to  mechanical  causes  which  interfere  with  the  proper  passage  of  blood 
through  the  pulmonary  vessels  (passive  congestion),  or  that  due  to  intense 
irritation  caused  by  inhaling  irritant  vapors  or  fumes. 

Etiology  and  Pathology. — The  most  common  cause  of  pulmonary  conges- 
tion is  progressive  valvular  inadequacy  at  the  left  auriculoventricular  orifice, 
or,  in  other  words,  mitral  disease,  either  obstructive  or  regurgitant.  These 
lesions  dam  the  blood  back  into  the  lungs,  and  the  right  ventricle  undergoes 
hypertrophy  in  an  endeavor  to  drive  it  onward.  As  a  result  the  pulmonary 
capillaries  are  placed  under  abnormal  strain,  increased  hemolysis  occurs. 


426  DISEASES  OF  THE  LUNGS 

and  when  the  condition  becomes  chronic  there  is  produced  what  is  known 
as  brown  induration  of  the  lungs.  At  autopsy  they  appear  of  a  dull  red- 
dish-brown hue,  the  incised  surfaces  becoming  brighter  red  after  exposure 
to  the  air.  The  supporting  tissue  of  the  lung  is  thickened  and  less  elastic 
than  normal,  and  the  organ  is  heavy,  as  shown  by  the  fact  that  when  placed 
in  water  it  does  not  floa.t  so  high  as  normal  lung-tissue.  Microscopically 
the  connective  tissue  and  the  alveolar  epithelium,  some  of  which  is  desqua- 
mated, contain  granules  of  brownish  pigment  derived  from  the  hsemoglobin 
content  of  the  disintegrated  red  blood  cells. 

The  bloodvessels  are  tortuous,  and  the  capillaries  which  line  the  walls  of 
the  alveoli  project  in  loops  or  tufts  into  the  air  spaces.  Sometimes  haemop- 
tysis of  moderate  degree  arises  from  rupture  of  these  vessels  or  those  which 
are  in  the  bronchial  tubes.  It  can  be  readily  understood  why  it  is  that  a 
person  with  these  lesions  is  a  ready  victim  for  pneumonia,  hypostatic  con- 
gestion, and  infarction. 

Acute  pulmonary  congestion  resulting  from  sudden  failure  of  the  left 
ventricle  is  often  the  cause  of  sudden  death  in  the  course  of  an  attack  of 
sunstroke  or  after  the  inhalation  of  irritant  gases. 

Closely  connected  with  this  form  of  congestion  from  an  etiological  stand- 
point is  hypostatic  congestion  of  the  lungs.  In  this  state  the  lower  portions 
of  the  lungs  are  commonly  affected  because  the  patient  is  usually  in  the 
dorsal  decubitus  and  the  blood  accumulates  in  the  most  dependent  part  of 
the  organs.  Associated  with  this  accumulation  of  blood  in  the  vessels  of 
the  lung,  an  excess  of  serum  collects  in  the  intervesicular  structures,  pro- 
ducing oedema,  or,  passing  into  the  vesicles,  causes  the  affected  part  to  be- 
come essentially  airless. 

The  causes  of  hypostatic  congestion  are  not  very  different  from  those  of 
ordinary  congestion  as  just  described,  save  that  the  failure  of  the  right  side 
of  the  heart  is  more  marked  and  the  condition  is  more  frequently  met  with 
as  the  result  of  profound  asthenia  occurring  in  the  course  of  some  malady 
like  severe  typhoid  fever  or  advanced  renal  disease.  That  the  dorsal  decubi- 
tus is  not  the  chief  cause  is  proved  by  the  fact  that  many  persons  suffering 
from  certain  maladies  which  require  the  maintenance  of  this  posture  do 
not  suffer  from  hypostatic  congestion.  That  posture  exercises  some  influence, 
however,  is  shown  by  the  fact  that  if  the  patient  remains  on  one  side  the 
stasis  is  often  unilateral. 

iVutopsy  in  cases  of  hypostatic  congestion  reveal  the  involved  areas 
darkened  in  color,  often  black  or  purplish-black  in  hue.  They  may  be 
airless,  with  frothy  accumulations  in  the  bronchial  tubes,  loss  of  crepitation 
on  pressure,  and  a  doughy  condition  when  one  finger  is  pressed  upon  the 
lung,  resembling  the  sensation  produced  by  oedema  elsewhere.  In  some 
cases,  not  only  a  serous  exudation  takes  place  into  the  vesicles,  but  red 
and  white  blood  cells  are  extruded,  which  may  render  the  lung  so  red  that 
it  looks  somewhat  as  if  true  croupous  pneumonia  were  present.  To  this 
state  has  been  applied  the  term  "splenization,"  in  distinction  from  the  red 
solidification  in  true  pneumonia  cahed  "hepatization"  or  "hypostatic  pneu- 
monia." Still  less  frequently  actual  hemorrhage  into  the  lung  occurs  as 
the  result  of  giving  way  of  the  walls  of  small  vessels. 


CONGESTION  OF  THE  LUNGS  427 

The  causes  being  identical  on  both  sides  of  the  chest,  it  is  natural  that 
hypostatic  congestion  should  usually  be  found  to  be  bilateral.  It  begins  at 
the  bases  and  slowly  creeps  upward,  until  it  may  involve  the  lower  lobes  of 
each  side,  and  even  the  middle  lobe  on  the  right  side  and  part  of  the  upper 
on  the  left. 

Symptoms. — The  symptoms  of  that  form  which  is  due  to  valvular  disease 
at  first  are  those  of  shortness  of  breath,  with  repeated  attacks  of  bronchitis, 
which  may  become  chronic.  The  mucus  expectorated  may  contain  tiny 
clots  of  blood  arising  from  the  dilated  vessels  just  described.  If  the  hem- 
orrhage is  free  an  infarct  of  the  lung  may  develop  into  an  area  of  consolida- 
tion and  haemoptysis  may  occur.  Sometimes  this  accident  follows  an 
improvement  in  the  condition  of  the  heart,  which  is  produced  by  rest  and 
tonics,  because  the  renewed  strength  of  the  right  ventricle  ruptures  a  weak 
and  tortuous  vessel. 

The  symptoms  of  hypostatic  congestion  differ  greatly  with  the  rapidity 
with  which  the  condition  develops,  and  the  underlying  cause.  When  the 
exudation  rapidly  takes  place  evidences  of  respiratory  embarrassment 
develop  and  dyspnaa  and  cyanosis  are  often  marked.  If  the  condition  is 
slow  and  gradual,  as  in  most  instances,  when  it  complicates  some  state  of 
adynamia,  as  in  severe  typhoid  fever,  the  symptoms  are  so  gradual  in  onset 
that  not  until  the  lungs  are  seriously  involved  is  attention  called  to  respiratory 
disorder.  Cases  of  the  acute  type  are  seen  chiefly  as  the  result  of  renal 
disease  and  cardiac  failure,  whereas,  as  just  stated,  the  gradual  type  comes 
on  in  the  course  of  the  infectious  diseases. 

The  physical  signs  of  hypostatic  congestion  are  not  well  marked  in  the 
early  stages.  Careful  light  percussion  may  reveal  slight  impairment  of 
resonance,  and  auscultation  may  discover  a  few  7noist  rales,  which  are  chiefly 
bronchial,  forming  small  rhonchi  or  sibilant  sounds.  These  are  the  signs 
which  it  is  important  to  recognize,  since  it  is  at  this  time  that  the  physician 
can  do  much,  in  many  cases,  to  limit  or  even  prevent  the  spread  of  the  condi- 
tion which  is  beginning  to  develop.  Later  on  the  condition  is  so  well  marked 
that  the  merest  tyro  can  recognize  it  by  reason  of  the  bronchial  breathing, 
the  moist  rales,  and  the  absence  of  vesicular  sounds  which  have  been  put 
aside  by  the  exudation.  The  only  thing  to  be  done  at  such  a  late  hour  is  to 
endeavor  to  support  the  circulation,  so  that  the  lesions  will  not  spread  and 
so  that  the  patient  may  be  kept  going  till  absorption  or  resolution  occurs. 

The  presence  of  hypostatic  congestion  is  often  not  recognized,  because 
the  physician  does  not  carefully  examine  the  lungs.  In  many  cases,  too,  it 
is  agonal,  particularly  if  death  comes  slowly. 

Diagnosis. — Hypostatic  congestion  must  be  separated  from  catarrhal  and 
croupous  pneumonia,  and  from  pleural  effusion,  serous  or  purulent.  An 
important  point  in  the  difPerentiation  is  the  fact  that  in  both  forms  of 
pneumonia  the  temperature  is  usually  febrile,  and  if  they  complicate  some  pre- 
existing state  the  fever  is  usually  exacerbated  when  the  pulmonary  condition 
develops,  whereas  distinct  febrile  movement  is  unusual  in  hypostatic  con- 
gestion unless  it  is  in  turn  associated  with  a  true  pneumonic  process. 
The  sputum,  if  any  is  raised,  is  frothy  in  cases  of  congestion,  but  is  sticky 
and    rusty  in   croupous   pneumonia,   and   perhaps   mucopurulent  in    the 


428  DISEASES  OF  THE  LUNGS 

catarrhal  form.  The  cough  is  loose  and  productive  (juicy)  and  not  hard 
and  difficult  as  in  pneumonia.  Then,  too,  the  onset  of  congestion  is  not 
characterized  by  a  chill  nor  by  pain  in  the  chest.  Pleural  effusion  may  be 
separated  from  hypostatic  congestion  by  a  change  in  the  level  of  dulness 
on  percussion  when  the  patient  changes  his  posture,  by  the  fact  that  the 
percussion  note  in  congestion  is  rarely  as  flat  as  in  effusion,  by  the  fact 
that  pleural  effusion  is  rarely  bilateral,  and  if  at  all  profuse  usually  displaces 
the  heart  to  the  left  if  it  be  on  the  right  side  and  downward  if  it  be  on  the  left. 

Prognosis. — ^This  depends  largely  on  the  promptness  with  which  hypo- 
stasis is  discovered  and  treated,  the  cause  of  the  condition,  and  the  vitality 
of  the  patient.  When  due  to  renal  disease  and  associated  with  a  general 
tendency  to  oedema,  the  prognosis  is  bad.  So,  too,  if  it  ensues  in  a  prolonged 
exhausting  fever  the  prognosis  is  bad  because  it  indicates  great  feebleness. 
In  old  persons  and  in  young  children  it  is  very  often  the  cause  of  death 
during  the  course  of  other  diseases. 

Treatment. — ^This  consists  in  preventive  measures,  such  as  changing  the 
posture  of  the  patient  every  hour,  in  the  use  of  cold  sponging  if  fever  is 
present,  to  readjust  the  circulation,  and  in  the  proper  use  of  stimulants  if 
the  heart  seems  feeble.  As  soon  as  any  signs  of  the  malady  appear,  the 
patient  should  be  made  to  lie  on  one  side  and  then  on  the  other  and  not 
upon  the  back.  Two  or  three  dry  cups  should  be  apphed  to  the  chest  over 
the  base  of  each  lung  posteriorly,  or  in  their  place  a  mustard  plaster  may  be 
used.  If  the  heart  is  feeble,  strychnine,  digitalis,  and  belladonna  are  useful. 
It  may  be  wise  in  urgent  cases  to  give  strychnine  and  atropine  hypodermic- 
ally  and  to  use  Hoffmann's  anodyne  in  the  dose  of  a  drachm  every  hour 
for  several  doses.  Sometimes  if  the  patient  is  strong  enough  to  stand  active 
purgation  colocynth  or  elaterium  are  valuable  cathartics,  the  latter  being 
given  in  the  dose  of  ^  grain,  but  when  the  symptoms  are  urgent  and  the 
venous  system  is  engorged  free  venesection  should  be  practised. 

Manifestly  it  is  the  physician's  duty  in  all  these  cases  of  exhausting  disease 
to  carefully  listen  to  the  chest  at  every  visit  during  an  illness,  to  note  the 
first  sign  of  this  insidious  state. 

TUMORS  IN  THE  LtJNGS. 

Tumors  in  the  lungs  are  rarely  met  with.  They  may  be  benign  or  malig- 
nant, but  are  usually  the  latter,  and  occur  as  primary  or  secondary  growths ; 
tumors  secondary  to  growths  elsewhere  being  much  the  more  frequent. 
The  benign  tumors  are  chondroma,  fibroma,  osteoma,  and  dermoid  cyst. 
The  malignant  tumors  are  sarcoma,  carcinoma,  and  occasionally  endothe- 
homa.  The  sarcoma  and  carcinoma  usually  occur  as  nodular  masses  which 
as  they  grow  push  the  lung-tissue  aside,  or  more  rarely  they  occur  as  infil- 
trating growths  which  extend  along  the  bloodvessels  or  bronchial  tubes. 
If  the  tumors  are  placed  peripherally  or  are  primary,  it  may  be  difficult  to 
determine  whether  they  are  pleural  or  pulmonary.  In  cases  of  Hodgkin's 
disease  and  in  leuksemia  typical  masses  of  lymphomatous  tissue  are  quite 
frequently  found  infiltrating  the  lung,  and  they  may  cause  consolidation 
throughout  considerable  areas. 


TUMORS  IN   THE  LUNGS  429 

When  the  mahgnant  growths  are  secondary  they  are  usually  found  in 
both  lungs  unless  the  tumor  is  the  result  of  extensive  infection,  as  in  the  case 
of  tumor  in  the  chest  wall  directly  involving  the  lung  tissue  through  the 
pleura.  In  such  an  instance  the  growth  at  first  is  single,  whereas  when 
it  has  spread  by  metastasis  it  is  multiple.  Secondary  cancer  of  the  lung 
is  more  frequent  in  women  than  in  men  because  of  the  frequency  with  which 
women  suffer  from  carcinoma  of  the  breast. 

Symptoms. — The  symptoms  are  not  characteristic.  They  depend  largely 
upon  the  situation  of  the  growth  and  upon  the  degree  of  pressure  which  they 
exercise  upon  surrounding  tissues.  If  they  press  upon  nerve  trunks  they 
cause  severe  'pain;  if  upon  a  large  bronchus  they  produce  cough  and  expec- 
toration; and  if  a  considerable  area  of  lung-tissue  is  involved  they  cause 
dyspnoea,  particularly  if  the  growth  or  growths  press  upon  the  bloodvessels 
and  so  cause  pulmonary  congestion  or  stasis,  so  that  as  the  disease  ad- 
vances pulmonary  oedema  aids  in  decreasing  the  area  for  the  oxygena- 
tion of  blood.  Great  and  manifest  engorgement  of  the  superficial  veins 
of  the  neck  and  head  is  sometimes  present  as  the  result  of  pressure  on 
the  superior  vena  cava,  and  if  the  vagus  or  the  recurrent  laryngeal  nerves 
are  pressed  upon  cardiac  neuroses  and  laryngeal  spasm  or  paralysis  may 
ensue. 

Diagnosis.  — The  diagnosis  of  tumor  of  the  lung  when  no  primary  growth 
exists  elsewhere  is  extremely  difficidt.  The  presence  of  thoracic  pain, 
in  the  absence  of  signs  of  aneurysm,  and  inability  to  discover  cardiac 
disease,  aortitis,  or  disease  of  vertebrae  should  arouse  the  suspicion  of  the 
presence  of  a  growth,  which  may  be  confirmed  by  the  presence  of  dulness 
on  percussion  in  the  area  affected.  When  these  symptoms  develop  in  a 
patient  who  has  a  growth  elsewhere,  or  has  had  a  growth  elsewhere  which 
has  been  excised,  as  in  carcinoma  of  the  breast,  they  possess  much  more 
diagnostic  value.  Stokes  considered  that  prune-juice  sputum  was  a  very 
typical  sign  of  malignant  growth  in  the  lung.  Emaciation  may  be  a  marked 
symptom,  as  it  is  so  often  in  cases  of  malignant  growth  elsewhere  in  the 
body,  but  the  maintenance  of  flesh  by  the  patient  does  not  negative  malignant 
growth,  as  sometimes  little  weight  is  lost. 

It  is  hardly  necessary  to  add  that  the  malignant  tumors  are  more  fre- 
quently met  with  in  middle  life  or  in  advanced  age  than  in  youth. 

No  treatment  is  of  any  avail  so  far  as  cure  is  concerned.  The  most  that 
can  be  done  is  to  support  the  system  by  good  food  and  relieve  pain  by 
morphine. 


430 


DISEASES  OF  THE  PLEURA 


DISEASES  OF  THE  PLEURA. 

PLEURITIS. 

Definition. — The  term  pleuritis,  or  pleurisy,  is  applied  to  an  inflammation, 
either  acute  or  chronic,  of  the  serous  membrane  which  hues  the  thoracic 
cavity  and  in  its  reflections  covers  the  lung;  the  so-called  parietal  and 
visceral  layers  of  the  pleura.  This  inflammation  is  always  the  result  of 
an  infection  by  some  pathogenic  micro-organism.  It  occurs  in  four  forms, 
namely,  as  dry  or  fibrinous,  serofibrinous,  purulent,  when  it  is  called 
empyema,  and  that  due  to  tuberculosis,  or  tuberculous  pleurisy.  Sometimes 
malignant  disease  afi^ects  this  membrane,  and  this  may  be  considered  a  fifth 
form  of  pleural  inflammation  (Figs.  57  and  58). 


Fig.  57 


^:^  - 


Carcinomatosis  oi  the  costal  pleurse.     (Kast  and  Rumpler.) 

Etiology. — As  just  stated,  pleurisy  is  practically  always  due  to  an  infection 
by  some  micro-organism.  In  a  large  number  of  cases  it  arises  as  the  result 
of  an  invasion  of  the  lung  by  the  pneumococcus,  with  or  without  an  associ- 
ated pneumonia.  In  other  instances  it  is  due  to  the  entrance  of  pyogenic 
organisms  such  as  the  staphylococcus  and  streptococcus,  and  in  still  other 
cases  from  invasion  by  tubercle  bacilli.  Infection  of  the  pleura  may  also 
take  place  through  the  pericardium,  the  mediastinal  tissues,  the  vertebrae, 


PLEURITIS 


431 


and  the  diaphragm.  Sometimes,  though  rarely,  it  is  from  the  chest  wall 
itself,  after  injury  to  the  thorax  or  by  extension  of  infection  from  the  mammary 
gland.  Pulmonary  abscess  may,  by  the  extension  of  the  inflammatory  process, 
produce  pleuritis,  or  a  bronchopneumonia  may  cause  a  secondary  infection. 
In  some  cases,  however,  the  inflammation  of  the  pleura  is  a  primary  lesion 
without  any  pathological  change  in  the  lung  except  as  a  secondary  condi- 
tion. 

The  relative  frequency  with  which  acute  pleurisy  is  produced  by  each 
specific  micro-organism  is  unknown,  since  recovery  takes  place  in  mild 


Fig.  58 


Metastatic  carcinoma  of  the  visceral  pleura.     (Kast  and  Rumpler  ) 


cases  and  no  opportunity  of  determining  the  provoking  cause  presents 
itself.  The  pneumococcus  is,  however,  the  cause  in  the  majority  of 
cases. 

When  empyema  follows  pleurisy .  the  necessity  of  setting  free  the  pus 
enables  us  to  determine  the  character  of  the  infection  in  the  great  majority 
of  cases,  and  the  statistics  derived  from  this  source  give  us  some  conception 
of  the  relative  frequency  with  which  pleurisy  follows  infection  by  different 
organisms.     (See  Empyema.) 


432  DISEASES  OF   THE  PLEURA 

Frequency. — Pleurisy  is  most  commonly  met  with  between  the  ages  of  twenty 
and  forty,  but  it  is  by  no  means  confined  to  these  decades  of  life.  On  the 
contrary,  it  is  very  frequent  in  young  children — at  least,  as  a  complication 
of  pneumonia  in  its  various  forms — and  is  also  not  rarely  met  with  in  persons 
of  advanced  years.  In  adults  pleurisy  occurs  more  than  twice  as  often  in 
males  as  in  females,  but  in  early  childhood  this  predominance  does  not 
occur.  As  an  illustration  of  these  facts  it  is  interesting  to  note  that  in  651 
cases  in  St.  Bartholomew's  Hospital,  London,  465  were  in  males  and  only 
186  in  females.  The  distribution  of  these  cases  as  to  age  was  as  follows: 
five  years  and  under,  25;  ten  years,  59;  fifteen  years,  50;  twenty  years,  54; 
thirty  years,  179;  forty  years,  149;  fifty  years,  85;  sixty  years,  35;  over 
sixty  years,  15. 

Pleurisy  occurs  most  frequently  in  the  early  spring  and  late  autumn, 
when  great  changes  in  temperature  take  place.  This  does  not  mean  that 
exposure  to  cold  produces  pleurisy  directly,  but  rather  that  the  exposure 
reduces  vital  resistance  to  such  an  extent  that  infection  takes  place. 

So,  too,  a  number  of  acute  and  chronic  diseases  result  in  pleurisy,  not 
because  they  have  any  direct  effect  on  the  pleural  membrane,  but  because 
they  lower  vital  resistance  at  the  same  time  that  they  expose  the  pleura  to 
infection  by  their  specific  germ.  Thus,  pleurisy  may  be  indirectly  pro- 
duced by  the  acute  specific  fevers  and  by  Bright's  disease,  the  first  of 
which  provides  a  predisposing  cause  and  a  specific  germ,  while  the  latter 
lowers  vital  resistance  in  general.  So,  too,  it  is  possible  for  damage  to  the 
chest  wall  to  result  in  acute  pleuritis. 

It  is  to  be  constantly  borne  in  mind  that  of  all  specific  infections  that  by 
the  tubercle  bacillus  is  the  most  important,  because  of  the  prognosis,  because 
it  is  often  insidious,  and  because  it  is  probably  one  of  the  most  frequent 
causes  of  pleurisy. 

The  pathology,  morbid  anatomy,  symptomatology  and  treatment  of  the 
various  forms  of  pleurisy  are  best  considered  under  the  specific  description 
of  each  type. 

Dry  Pleurisy. — Dry  pleurisy,  as  its  name  indicates,  is  an  inflammation  of 
the  pleural  membrane  with  a  minimum  amount  of  serous  exudate.  It  may 
be  circumscribed  or  localized,  as  over  a  tuberculous  cavity,  or  may  be  dif- 
fused over  a  large  area,  as  in  croupous  pneumonia.  The  pathology  and 
morbid  anatomy  of  pleurisy  of  the  dry  type  may  be  described  as  follows :  As 
in  all  inflammations  of  serous  membranes,  there  is  an  acute  hyperaemia 
followed  by  infiltration  and  exudation  of  blood  cells,  fibrin,  and,  it  may  be, 
serum.  The  pleural  membrane  is  lustreless  in  appearance,  and  roughened 
or  granular,  and  is  somewhat  thickened,  partly  because  of  infiltration,  but 
chiefly  by  reason  of  the  fibrinous  exudate  on  its  surface.  This  exudate  is  a 
primary  factor  in  the  formation  of  adhesions  between  the  visceral  and 
parietal  layers  of  the  pleura.  Sometimes  the  exudate  is  remarkably  profuse 
or  perhaps  a  number  of  layers  are  formed,  so  that  the  pleura  may  exceed  a 
quarter  of  an  inch  in  thickness,  and  is  somewhat  reticulated  or  uneven  on 
the  surface.  Such  an  exudate  is  rarely  completely  absorbed  after  the  attack 
has  passed,  and  it  often  organizes  and  produces  impaired  resonance  on 
percussion  and  other  morbid  physical  signs  during  the  lifetime  of  the  patient. 


PLEURITIS  433 

Symptoms. — The  onset  of  acute  dry  pleurisy  is  characterized  by  a  severe 
pain,  or  "stitch,"  in  the  side  and  by  the  development  of  some  fever.  The 
pain  in  the  side  is  sharp  and  stabbing  in  character  and  the  patient "  catches  his 
breath,"  to  use  a  popular  expression,  when  he  endeavors  to  inspire.  Speaking, 
coughing,  or  any  movement  which  causes  increase  in  the  thoracic  movement, 
greatly  increases  the  pain,  which  can,  however,  be  markedly  relieved,  as  a  rule, 
by  strapping  the  side  of  the  chest  which  is  affected,  and  so  diminishing  its 
freedom  of  movement.  The  pain  which  is  developed  by  pressure  on  the 
chest  wall  is  sometimes  of  two  types,  namely,  severe  pain  produced  by  deep 
pressure,  and  exquisite  tenderness  of  the  skin  over  that  part  of  the  pleura 
which  is  inflamed.  In  the  great  majority  of  cases  the  patient  states  that 
the  greatest  pain  is  between  the  mammary  line  and  the  posterior  axillary 
line,  but  it  may  be  complained  of  in  many  other  parts  ox  the  chest,  particu- 
larly if  the  disease  be  due  to  tuberculosis.  Young  children  who  have  not 
been  trained  in  the  localization  of  pain  often  state  that  the  suffering  is  in 
the  epigastrium,  or  in  the  left  or  right  hypochondrium,  and  even  in  adults 
I  have  more  than  once  seen  physicians  misled  into  a  diagnosis  of  appendicitis 
because  of  the  pain  referred  by  the  patient  to  this  region,  when  in  reality 
the  cause  was  acute  pleuritis.  In  all  cases  of  pain  below  the  diaphragm  it  is 
a  good  rule  for  the  physician  to  examine  the  condition  of  the  thoracic  viscera 
before  asserting  that  abdominal  disease  is  present.  As  severe  stabbing 
pain  in  the  thorax  is  sometimes  due  to  aneurysm,  muscular  rheumatism, 
or  intercostal  neuralgia,  these  possibilities  must  be  excluded  before  we  can 
decide  that  the  cause  is  pleuritis. 

The  most  important  physical  sign  which  determines  the  diagnosis  of  this 
affection  is  the  so-called  "friction  sound"  produced  by  the  rubbing  of  the 
visceral  layer  of  the  pleura  upon  the  parietal  layer,  both  layers  being  rough- 
ened and  dried  by  the  early  stage  of  the  inflammation.  This  friction  sound 
is  usually  best  heard  just  below  and  just  back  of  the  nipple  on  the  side 
involved.  (See  Fig.  59.)  In  persons  who  have  very  thick  chest  walls  and 
who  breathe  superficially,  by  habit  or  because  of  the  pain,  it  is  often  necessary 
that  they  take  a  deep  breath  before  a  friction  sound  is  produced.  Sometimes 
the  friction  sound  is  so  creaking  and  loud  that  it  sounds  like  the  noise  made 
by  a  new  leather  saddle  when  it  is  first  used;  at  other  times  it  so  soft  that 
only  the  most  careful  auscultation  will  reveal  it,  and  it  may  resemble  the 
fine  rales  of  croupous  pneumonia.  In  other  cases  this  creaking  can  be  felt 
by  the  hand  of  the  physician.  If  the  pleurisy  be  situated  near  the  heart 
the  action  of  that  organ  may  cause  the  pleural  friction  sound  to  occur  as 
often  as  the  heart  beats,  and  so  lead  one  to  the  diagnosis  of  pericarditis. 
This  is  called  a  pleuropericardial  friction  sound,  and  may  also  depend  upon 
a  simultaneous  development  of  pericarditis  and  pleuritis. 

A  second  important  physical  sign  is  the  diminished  respiratory  movement 
on  the  side  of  the  chest  which  is  affected,  as  may  be  seen  by  the  eye  and 
recognized  by  the  feeble  respiratory  sounds  when  auscultation  is  performed, 
the  semi-fixation  of  the  chest  being  an  effort  to  decrease  the  thoracic  move- 
ment, and  so  limit  the  degree  of  pain.  My  colleague,  Coplin,  has  suggested 
that  the  fixation  is  in  part  due  to  changes  in  the  intercostal  muscles  them- 
selves. (See  article  on  Croupous  Pneumonia.)  This  fixation  may  extend  to 
28 


434 


DISEASES  OF   THE  PLEURA 


one  side  of  the  diaphragm,  and  so  result  in  decreased  abdominal  movement 
on  that  side.  The  rate  of  respiration  may  be  increased  in  order  to  com- 
pensate for  the  shallow  breathing,  but  it  is  never  the  hurried  or  urgent 
respiration  met  with  in  cases  of  real  dyspnoea. 

There  are  two  other  signs  of  pleurisy  which  are  of  some  diagnostic  value, 
namely,  the  suppressed  cough,  which  the  patient  attempts  to  stifle  in  order 
to  prevent  pain,  and  the  attitude  of  fixation  of  the  body  so  that  inadvertent 
movement  of  the  patient  himself,  or  change  in  his  position  made  by  his 

Fig.  59 


Area  in  which  a  right-sided  pleural  friction  sound  is  usually  heard  best. 


attendant  may  not  produce  pain.  Sometimes  if  the  skin  is  not  hyperajsthetic 
the  patient  lies  on  the  affected  side  to  render  it  fixed,  or  he  may  lie  on  the 
well  side  to  avoid  pressure  on  the  involved  pleura. 

The  fever  in  acute  pleurisy  is  rarely  high  in  adults,  although  it  may  be  in 
young  persons.  Often  it  never  rises  above  102°,  and  the  pulse  is  usually 
only  increased  by  reason  of  the  fever;  so  that  it  bears  no  direct  relation- 
ship to  the  disease. 

Diagnosis. — Dry  pleurisy  is  separated  from  muscular  soreness  due  to 
strain  by  the  facts  just  given  and  by  the  history  of  an  injury;  from  muscular 
rheumatism  by  the  fact  that  signs  of  this  malady  are  to  be  found  elsewhere; 
from  intercostal  neuralgia  by  the  inconstancy  of  that  affection,  and  by  the 
fact  that  ordinary  breathing  does  not  increase  the  pain  in  the  majority  of 
cases,  and,  further,  that  all  three  of  these  conditions  are  not  accompanied 


PLEURITIS  435 

by  any  febrile  movement  or  evidence  of  general  systemic  disturbance. 
Acute  pleurisy  of  the  dry  type  lasts  from  a  few  days  to  two  weeks.  A 
longer  attack  than  this  should  arouse  the  suspicion  of  the  presence  of  a 
more  persistent  disease,  such  as  tuberculosis. 

Prognosis. — Barring  complications  the  prognosis  is  favorable.  (See 
Empyema,  and  Pleurisy  with  Effusion.) 

Treatment. — ^The  treatment  of  dry  pleurisy  consists  in  applying  adhesive 
strips  two  inches  wide,  and  overlapping  one  another  one  inch,  from  the 
middle  line  of  the  vertebrae  to  the  middle  line  of  the  sternum,  not  following 
the  line  of  the  ribs,  but  passing  from  behind  forward  horizontally.  They 
should  be  applied  from  below  upward,  and  with  a  sufficient  degree  of  pressure 
to  produce  almost  complete  fixation  of  that  side  of  the  chest.  The  pain, 
if  it  is  extensive,  may  be  further  controlled  by  the  administration  of  3  grain 
doses  of  Dover's  powder  every  two  or  three  hours.  If  necessary,  a  hypo- 
dermic injection  of  morphine  may  be  given.  If  the  fever  is  high  an  ice-bag 
may  be  applied  to  the  head,  and  tepid  or  cold  spongings  over  the  entire 
body  may  be  employed.  An  ice-bag  may  also  be  applied  to  the  side  of  the 
chest  which  is  inflamed,  for  the  rehef  of  pain. 

In  the  earliest  stages  of  an  acute  dry  pleurisy,  in  a  strong,  healthy  indi- 
vidual of  a  plethoric  type  with  a  bounding  pulse,  there  can  be  no  doubt  that 
the  administration  of  sufficiently  large  doses  of  the  tincture  of  veratrum 
viride  or  the  tincture  of  aconite  is  advantageous,  as  it  may  diminish  the 
local  hypersemia  in  the  pleura  and  decrease  the  action  of  the  heart  so  that 
it  pumps  less  blood  into  the  inflamed  area,  thereby  causing  determination 
of  blood  to  the  peripheral  capillaries.  This  vascular  relaxation,  associated 
with  sweating,  tends  to  still  further  reheve  the  local  congestion,  and 
altogether  exercises  a  beneficial  influence  upon  the  local  lesion.  These 
depressant  drugs,  however,  are  distinctly  contraindicated  unless  the  patient 
is  strong  and  hearty,  and  after  the  first  twenty-four  hours  of  the  illness 
they  are  probably  useless.  Indeed,  after  this  time  they  may  do  harm.  If 
they  are  used  at  all,  they  should  be  given  freely.  Thus,  3  minims  of  the 
tincture  of  veratrum  viride  may  be  given  every  half-hour  until  the  patient 
is  very  slightly  nauseated  or  until  his  skin  becomes  moist,  when  the  drug 
should  be  stopped.  A  similar  method  of  employing  aconite  may  also  be 
practised. 

The  employment  of  a  poultice,  or  cotton  jacket,  in  the  treatment  of 
pleurisy  is  less  and  less  resorted  to  at  the  present  time.  There  is  no  reason 
to  believe  that  its  influence  is  advantageous,  and  it  very  greatly  increases 
the  discomfort  of  the  patient  because  of  the  heat  and  consequent  sweatings 
which  are  produced.  Further  than  this,  there  is  always  danger  of  the  patient 
taking  cold  by  the  poultice  becoming  chilled,  or  during  the  removal  of 
the  poultice  or  cotton  jacket  for  cleansing  purposes. 

It  is  important  to  remember  that  the  presence  of  a  moderate  pleural  effusion 
does  not  require  the  physician  to  institute  measures  for  its  immediate  relief, 
because  in  a  very  considerable  proportion  of  cases  absorption  will  take 
place  by  natural  processes,  and  so  nature  will  produce  a  cure. 

Finally,  all  patients  convalescing  from  an  attack  of  dry  pleurisy  should 
be  instructed  to  present  themselves  to  the  physician  several  times  at  intervals 


436  DISEASES  OF  THE  PLEURA 

of  a  few  days,  in  order  that  he  may  have  the  opportunity  of  determining 
whether  the  pathological  condition  has  entirely  disappeared.  It  happens, 
all  too  frequently,  that  such  patients  are  discharged  "cured"  at  the  end 
of  a  few  days,  when  they  actually  have  an  insidious  tuberculosis,  the  primary 
pleurisy  having  been  due  to  this  cause. 

Pleurisy  with  Effusion. — While  a  large  proportion  of  cases  of  acute 
pleurisy  are  dry,  in  the  sense  that  no  excess  of  serum  is  poured  out  by  the 
inflamed  serous  membrane,  it  is  not  to  be  forgotten,  on  the  other  hand, 
that  a  considerable  number  of  cases  of  pleural  inflammation  terminates  in 
more  or  less  profuse  outpouring  of  fluid  into  the  pleural  sac.  This  forms 
what  is  sometimes  called  "pleurisy  with  efi^usion,"  or  "pleuritic  exudation." 
While  the  dry  type  often  only  involves  a  patch,  or  small  part,  of  the  pleural 
membrane,  that  form  which  is  accompanied  by  effusion,  unless  limited  by 
adhesions,  usually  affects  the  entire  pleura  of  one  side,  and,  indeed,  it  may 
be  bilateral,  although  this  is,  fortunately,  a  rare  occurrence. 

The  exudate  is  composed  of  two  parts:  (1)  a  soHd  portion,  consisting  of 
fibrin  and  cells,  which  is  attached  to  the  surface  of  the  pleura  and  which  con- 
stitutes the  basis  by  which  adhesions  binding  the  two  layers  of  the  pleura 
together  may  be  formed,  and  (2)  serum  or  fluid  exudate,  which  may  be  so 
abundant  that  the  pleural  sac  is  completely  filled.  This  fluid  is  always 
turbid  or  cloudy  from  the  presence  of  degenerated  and  exfoliated  endothe- 
lial cells,  particles  of  fibrin  and  blood  cells,  particularly  leukocytes.  It  is 
worthy  of  note  that  the  pleura  in  cases  of  pleuritis,  accompanied  by 
serous  effusion,  is  usually  not  so  markedly  infiltrated  as  in  the  dry  type. 

These  effusions  are  usually  the  result  of  infection  by  the  pneumococcus, 
the  staphylococcus  pyogenes,  and  the  tubercle  bacillus.  The  latter  infection 
is  always  to  be  suspected  in  subacute  cases  with  much  fluid  and  little  plastic 
exudate. 

An  examination  of  the  literature  on  the  bacteriology  of  this  state 
shows  that  a  large  number  of  organisms  have  been  found  in  pleural  effusions 
and  also  that  in  many  cases  the  effused  fluid  is  sterile.  (See  Empyema.) 
For  example,  Lemoine  made  cultures  from  the  fluid  of  38  cases  of  serofibri- 
nous pleurisy,  and  found  it  sterile  in  28  instances. 

Recovery,  which  takes  place  in  the  majority  of  cases,  occurs  by  the 
absorption  of  the  serum  and  the  partial  absorption  and  shrinkage  of  the 
fibrin,  but  the  chief  change  in  the  plastic  exudate  is  organization  brought 
about  by  the  formation  of  granulation  tissue,  which  finally  becomes  dense 
and  cicatricial  in  character. 

There  is  probably  no  form  of  pleural  effusion  so  prone  to  confuse  the 
clinician  as  loculated  or  ensacculated  effusions.  These  may  form  between 
lobes,  between  the  base  of  the  lung  and  the  diaphragm,  or  on  the  mediasti- 
nal aspect  of  the  organ.  Their  localization  is  maintained  by  marginal 
adhesions  that  prevent  the  diffusion  of  fluid  throughout  the  pleural  cavity. 
Empyema,  similarly  limited,  offers  identical  difficulties  in  diagnosis. 

The  lung  may  be  markedly  distorted,  displaced,  or  compressed  by  the 
adhesions,  and  even  the  heart  may  be  forced  from  its  normal  position. 

Symptoms. — The  symptoms  of  pleurisy  with  effusion  are  not  very  char- 
acteristic, except  in  so  far  as  the  physical  signs  are  concerned,  but  these  are 


PLEURITIS  437 

typical,  and  some  of  them  pathognomonic.  If  the  onset  of  the  attack  of 
pleurisy  has  been  sharp  the  severe  pain  already  described  passes  away  as  the 
effusion  takes  place  and  so  separates  the  inflamed  layers  of  the  pleura,  at  the 
same  time  probably  depleting  them.  The  fever  often  diminishes  or  disap- 
pears when  the  stage  of  effusion  is  reached.  Dysyncea  may  or  may  not 
be  present,  according  to  the  size  of  effusion,  the  spaciousness  of  the  chest,  and 
the  ability  of  the  healthy  side  to  do  enough  work  to  compensate  for  the  part 
which  is  impaired  in  function.  Strong,  hearty  individuals  often  seem  to  be 
more  dyspnoeic  than  feeble  ones,  probably  because  in  the  former  case  the 
effusion  is  more  rapid  and  the  restricting  adhesions  are  more  firm.  Cough 
in  this  stage  of  effusion  is  usually  not  severe,  and  may  be  absent,  except  on 
exertion.     It  is  often  due  to  an  associated  bronchitis. 

The  posture  of  the  patient,  if  the  effusion  be  large,  is  usually  character- 
istic, in  that  he  persists  in  lying  on  the  affected  side,  in  order  to  permit  the 
healthy  lung  to  have  full  play.  Turning  him  on  the  affected  side  may 
cause  urgent  dyspnoea  and  a  sudden  change  to  the  erect  posture  may  do 
likewise,  since  the  pressure  of  the  fluid  on  the  diaphragm  interferes  with  its 
movements  or  with  the  action  of  the  heart. 

Physical  Signs. — ^The  physical  sighs  of  pleural  effusion  are  as  follows: 
Inspection  shows  decrease  in  respiratory  movement  on  the  affected  side, 
v/ith  increased  activity  on  the  healthy  side;  bulging  of  the  entire  chest  on 
the  diseased  side,  with  fulness  of  the  interspaces  and  some  fulness  it  may 
be  in  the  hypochondrium.  Palpation  reveals  an  absence  of  vocal  fremitus 
on  the  affected  side,  and  if  the  effusion  be  on  the  left  side  the  apex  beat  of 
the  heart  is  displaced  dbwnward  and  to  the  right. 

Percussion  elicits  flatness,  or  marked  dulness,  except  at  the  apex  above 
the  fluid,  where  the  percussion  note  is  peculiarly  high-pitched,  and  almost 
tympanitic — the  so-called  Skodaic  resonance.  Percussion  of  the  liver,  if 
the  effusion  be  on  the  right  side,  may  show  that  the  lower  margin  of  liver 
dulness  is  abnormally  low.  If  the  effusion  is  on  the  left  side,  percussion 
shows  dulness  in  Traube's  semilunar  space.     (See  Fig,  60.) 

Auscultation  discovers  that  there  is  an  absence  of  breath  sounds  in  the 
area  where  percussion  gives  flatness,  except  it  may  be  for  distant  and 
transmitted  bronchial  breathing.  Along  the  vertebral  column  and  near  the 
inner  edge  of  the  scapula  on  the  affected  side  segophony,  or  the  "bleating 
voice"  sound,  may  be  heard  if  the  patient  speaks,  while  vocal  resonance  in 
the  apex  of  the  lung,  where  Skodaic  resonance  is  present,  is  greatly 
increased,  even  to  the  degree  of  pectoriloquy.  At  this  place  above  the 
effusion  bronchial  or  tubular  breathing  may  be  very  marked.  Sometimes 
the  breath  sounds  are  even  amphoric  in  character. 

Occasionally,  as  the  result  of  the  formation  of  adhesions,  pleural  effusion 
is  circumscribed  within  narrow  limits,  and  the  presence  of  an  inflammatory 
exudate  produces  an  area  of  dulness  which  is  much  larger  than  that  space 
occupied  by  the  fluid.  The  introduction  of  an  aspirating  needle  for  diag- 
nostic purposes  may,  therefore,  readily  mislead  the  physician,  since  a  dry 
tap  will  often  occur  unless  the  needle  happens  to  enter  that  portion  of  the 
area  of  dulness  which  actually  contains  the  fluid.  The  mere  introduction  of 
the  needle  into  the  centre  of  the  area  of  dulness  is  not  necessarily  followed 


438 


DISEASES  OF  THE  PLEURA 


by  the  withdrawal  of  fluid,  since  it  not  infrequently  happens  that  a  consider- 
able mass  of  inflammatory  exudate  lies  to  one  side  of,  or  above  or  below,  the 
fluid.  These  loculated  effusions  are  more  common  in  cases  of  empyema  than 
in  ordinary  cases  of  pleurisy  with  effusion.     (See  Empyema.) 

The  rate  at  which  effusion  takes  place  varies  very  greatly.  Rarely  the 
chest  may  become  filled  in  a  few  days;  more  commonly  it  takes  a  week  or  even 
three  weeks.  Rapid  effusion  is  more  dangerous  than  the  delayed  type, 
because  the  thoracic  viscera  in  the  former  case  do  not  have  time  to  adjust 
themselves  to  the  altered  conditions.  I  have  seen  a  case  of  rapidly  fornaing 
pleural  effusion  in  which  sudden  death  followed  the  turning  of  the  patient 
on  his  well  side. 


Fig.  60 


Showing  at  x  mark  the  so-called  area  called  Traube's  semilunar  space,  where,  in  health,  percussion 
gives  a  tympanitic  note,  which  becomes  flat  in  left-sided  pleural  eflfusion.  The  solid  block  represents 
hepatic  and  cardiac  dulness. 

The  duration  of  pleural  effusion  varies  very  greatly.  Small  effusions  are 
often  absorbed  with  surprising  speed  within  a  few  days,  but  large  ones  are 
often  very  slowly  absorbed  and  may  not  be  absorbed  at  all  until  some  of  the 
pressure  is  removed  by  aspirating  the  chest. 

Diagnosis. — It  is  a  noteworthy  fact  that  while  the  diagnosis  of  pleural 
effusion  is  very  readily  made  in  some  cases,  in  other  instances  it  is  so  difficult 
as  to  baffle  the  most  experienced  clinician. 

Pleurisy  with  effusion  is  to  be  separated  from  pneumonia,  from  tuberculous 
consolidation,  from  pulmonary  oedema   and    hypostatic   congestion,  from 


PLEURITIS  439 

new-growths   in   the   lung,  pleura,   and    mediastinum,  and  from  pleurisy 
with  great  fibrinous  exudation  and  thickening. 

If  on  examining  one  side  of  the  chest  it  is  found  to  present  impaired  move- 
ment, impaired  percussion  resonance,  and  absence  of  breath  sounds,  it  is 
fair  to  suppose  that  the  cause  is  effusion,  if  in  addition  we  find,  in  disease  of 
the  right  side,  displacement  of  the  apex  beat  to  the  left,  or,  if  it  be  left-sided, 
obliteration  of  Traube's  semilunar  space.  This  opinion  is  still  further 
confirmed  if  the  area  of  dulness  on  percussion  varies  with  a  change  in  the 
posture  of  the  patient,  and  if  Skodaic  resonance  is  present  above  the  area 
in  which  resonance  is  impaired.  On  the  other  hand,  it  is  not  to  be  forgotten 
that  high-pitched  resonance  is  often  met  with  in  that  part  of  the  lung  which 
is  over  an  area  consohdated  by  pneumonia.  In  pneumonia  distinct  bronchial 
or  tubular  breathing  is  usually  heard  throughout  the  consolidated  area,  and 
this,  of  course,  is  not  the  case  in  effusion;  but  if  the  bronchial  tubes  become 
plugged  by  secretion  in  pneumonia,  this  important  differential  point  is 
destroyed.  Again,  it  sometimes  happens  that  if  the  physician  auscults  the 
chest  with  the  unaided  ear  he  can  readily  hear  bronchial  breathing  even  if 
an  effusion  be  present,  although  if  he  uses  a  stethoscope  bronchial  breath- 
ing seems  absent.  In  pneumonia,  however,  bronchial  breathing  is  usually 
associated  with  rales  which  are  absent  in  effusion. 

Very  useful  in  the  differentiation  of  the  two  affections  is  the  history  of 
the  patient,  in  whom  the  early  symptoms  of  the  two  diseases  are  usually 
quite  at  variance,  unless  the  case  has  been  one  of  primary  pleuropneumonia. 

In  cases  of  tuberculous  consolidation  the  appearance  of  the  patient  and  the 
history  of  onset  may  be  valuable  differential  points,  and  if  loss  of  flesh  or 
fever  is  present  these  facts  are  still  further  emphasized. 

When  pulmonary  oedema  is  present  the  presence  of  moist  rales,  the 
feeble  heart  action,  and  the  discovery  of  some  prolonged  preceding  illness, 
or  of  renal  disease  predisposing  to  pulmonary  oedema,  and  bilateral  dulness, 
are  the  points  of  value  in  making  a  diagnosis. 

In  cases  of  acute  pleurisy  with  great  thickening  of  the  pleural  membrane 
there  may  be  marked  impairment  of  resonance  on  light  percussion,  and  a 
friction  sound  may  be  heard,  but  deep  percussion  may  elicit  normal  pul- 
monary resonance. 

Growths  in  the  lung,  or  pulmonary  abscess,  usually  are  so  peculiarly  placed 
and  surrounded  by  healthy  tissue  that  careful  examination  of  the  chest  and 
a  study  of  the  patient's  history  will  be  sufficient  to  make  the  differentiation. 

Pneumothorax  is  separated  from  pleural  effusion  by  its  high-pitched 
resonance  on  percussion  and  the  other  physical  signs  of  that  condition  which 
are  only  partly  modified  if  the  pleura  is  chronically  thickened. 

There  still  remain  two  important  diagnostic  points  in  these  cases  which 
have  to  be  studied  before  diagnosis  can  be  reached,  viz.:  Are  the  physical 
signs  due  to  the  possible  presence  of  subphrenic  abscess,  which,  pushing  the 
diaphragm  upward,  encroaches  upon  the  thoracic  space,  or  are  they  due  to 
abscess  or  hydatid  cyst  in  the  liver?  These  conditions  become  manifest  if 
the  patient  is  carefully  examined  for  them.  Further,  their  rarity  is  a  point 
against  their  presence. 

Lastly,  it  is  important  to  determine  the  size  of  the  effusion  in  order  that 


440  DISEASES  OF  THE  PLEURA 

the  danger  to  the  patient  may  be  appreciated.  It  is  not  possible  to  even 
approximate  the  actual  quantity,  because  the  capacity  of  the  chest  varies 
greatly  in  different  cases,  but  the  extent  of  the  effusion  can  be  decided  by 
the  line  at  which  percussion  dulness  first  changes  to  impaired  resonance, 
and  higher  to  high-pitched  resonance. 

After  a  diagnosis  of  pleural  effusion  has  been  made,  the  question  which 
arises  is  whether  the  effusion  is  serous  or  purulent,  and  if  serous  whether 
it  is  the  result  of  inflammation  or  transudation.  This  is  a  most  important 
question,  since  the  treatment  is  quite  different  in  each  instance. 

This  may  be  determined  by  performing  paracentesis  thoracis  and  to  a 
great  extent  by  an  examination  of  the  fluid  after  it  is  withdrawn  by 
aspiration.  Its  specific  gravity,  if  the  cause  be  of  an  inflammatory  nature, 
varies  from  1.010  to  1.018,  and  it  contains  large  amounts  of  fibrin  and 
albumin.  On  the  other  hand,  the  fluid  due  to  transudation  in  dropsy 
shows  a  specific  gravity  of  only  about  1.008  and  contains  little  fibrin  and 
albumin.  (See  Hydrothorax.)  When  the  effusion  is  due  to  tuberculosis 
the  specific  gravity  is  very  high  (1.012  to  1.024).  The  symptoms  and 
diagnosis  of  empyema  will  be  found  discussed  below. 

Cytoscopy  in  Pleural  Effusion. — In  1900  Widal  and  Ravaut  called 
attention  to  the  cytological  examination  of  the  fluid  of  pleural  effusion, 
asserting  that  the  nature  of  the  pleurisy  can  be  determined  by  the  organized 
elements  held  in  suspension  in  the  exudate.  According  to  their  observations, 
the  fluid  of  tuberculous  pleurisy  is  characterized  by  the  presence  of  lympho- 
cytes, that  of  the  acute  infective  pleurisies  by  polymorphonuclear  leukocytes, 
and  that  of  the  pleurisies  dependent  upon  new-growths  and  the  aseptic  pleu- 
risies accompanying  renal  and  cardiac  disease,  by  shreds  of  endothelium. 
Further  investigations  have  not  confirmed  these  results,  for  Naunyn  found 
that  the  effusions  complicating  Bright's  disease  often  contain  lymphocytes 
instead  of  endothelium  shreds,  and  Tarchetti  and  Rossi  found  lymphocytes 
in  only  a  portion  of  the  tuberculous  effusions  which  they  examined.  More- 
over, Patella's  investigations  convinced  him  that  lymphocytes  are  not  char- 
acteristic of  primary  tuberculous  effusions.  On  the  other  hand,  Barjone  and 
Cade,  and  Gemelli,  of  Milan,  have  found  lymphocytes  in  the  fluid  of  all 
tuberculous  pleurisies.  From  what  has  been  said,  it  is  evident  that  the  sub- 
ject is  yet  in  its  experimental  stage,  but  the  discovery  of  a  marked  lympho- 
cytosis in  the  fluid  is  certainly  of  some  value  as  indicating  tuberculosis, 
particularly  if  it  is  associated  with  other  signs.  So  too  high  a  count  (60  to 
90  per  cent.)  of  polymorphonuclear  cells  is  indicative  of  an  infection  by 
the  pneumococcus. 

Prognosis. — ^The  prognosis  in  cases  of  pleural  effusion  is  favorable,  except 
in  two  conditions.  If  the  formation  of  the  fluid  is  very  rapid  and  very  copious, 
pressing  upon  the  heart  and  lungs  and  seriously  impairing  their  action  so 
that  dyspnoea  becomes  urgent,  the  prognosis  is,  of  course,  grave,  unless  relief 
is  given  by  thoracentesis.  Again, if  the  effusion  is  primarily  due  to  tuberculosis, 
or  to  nephritis,  which,  by  decreasing  vitality,  has  permitted  infection  to  take 
place,  the  prognosis  must  be  correspondingly  grave  as  to  ultimate  recovery. 

Treatment. — ^The  early  stages  of  pleurisy  with  effusion  are,  of  course, 
treated  in  a  manner  identical  with  that  already  described  for  a  dry  pleurisy. 


PLEURITIS  441 

It  is  only  when  the  effusion  has  formed  and  is  in  such  large  quantity  that  it 
produces  pressure  upon  a  vital  organ,  or,  again,  when  it  remains  un- 
absorbed  for  a  considerable  period  of  time,  that  the  physician  should 
undertake  measures  for  its  removal. 

The  only  measure  of  any  value  when  the  pressure  is  sufficiently  great  to  be 
producing  serious  symptoms  is  "tapping"  the  chest  by  means  of  an  aspi- 
rator. The  skin  over  the  affected  side  should  be  first  thoroughly  cleansed, 
as  if  for  the  performance  of  a  minor  surgical  operation.  A  hollow  needle 
having  a  moderately  wide  calibre,  and  attached  to  a  rubber  tube  three  feet 
long,  which  is  filled  with  fluid,  is  then  pushed  into  the  pleural  cavity  in  the 
sixth  or  seventh  interspace  in  the  midaxillary  line.  Care  should  be  taken 
that  the  aspirating  needle  should  be  kept  well  down  on  the  upper  surface 
of  the  nether  rib,  in  order  to  avoid  injurmg  the  intercostal  artery,  and  the 
physician  should  grasp  the  needle  with  his  thumb  and  forefinger  not  far 
from  its  point,  so  that  after  it  pierces  the  skin  it  will  not  suddenly  plunge 
into  the  chest  for  several  inches,  and  so,  perhaps,  do  damage  to  deep-lying 
tissues.  No  sooner  does  the  needle  enter  the  pleural  cavity  than  the  end  of 
the  rubber  tube  is  lowered  to  a  level  with  the  floor  and  the  contents  of  the 
pleura  is  in  this  way  siphoned  out  of  the  chest.  The  advantage  claimed  for 
this  method  of  treatment  is  that  the  degree  of  suction  is  at  no  time  great, 
and,  furthermore,  it  is  constant.  Again,  there  is  no  danger  of  the  fluid  being 
withdrawn  with  too  great  rapidity. 

A  very  much  more  frequently  resorted  to  measure  of  performing  'paracen- 
tesis thoracis  is  to  attach  a  large  needle,  or  trocar  and  cannula,  to  a  piece  of 
rubber  tubing,  which,  in  turn,  is  attached  to  a  tube  running  through  the 
cork  of  a  bottle  in  which  a  vacuum  has  been  produced  by  a  small  hand- 
pump.  The  entrance  to  the  bottle  is  guarded  by  a  small  stopcock.  After 
the  needle  has  been  placed  in  the  chest,  the  trocar  is  withdrawn,  the  stop- 
cock is  turned,  and  the  fluid  is  drawn  by  the  vacuum  from  the  chest  into 
the  bottle.  It  is  rarely  if  ever  proper  to  completely  empty  the  chest  by 
this  means  at  one  sitting,  particularly  if  the  effusion  has  been  a  large  one. 
Too  rapid  withdrawal  of  the  pressure  in  the  thorax  may  cause  serious 
disturbance  of  the  action  of  the  heart,  or  too  rapid  an  expansion  of  that 
portion  of  the  lung  on  the  affected  side  which  has  been  compressed  by  the 
fluid,  with  the  result  that  damage  is  done  to  the  pulmonary  tissue,  or  that  a 
peculiar  form  of  gelatinous  exudation  into  the  lungs  takes  place,  which  is 
only  relieved  by  constant  and  exhausting  cough,  and  sometimes  results 
fatally. 

Should  constant  cough  develop  during  paracentesis,  it  is  best  to  discon- 
tinue the  operation  at  once. 

It  is  also  important  to  remember  that  not  infrequently  the  withdrawal  of 
a  small  quantity  of  the  effusion,  by  the  relief  of  pressure  and  the  establish- 
ment of  normal  lymphatic  and  blood  circulation  in  the  chest  wall,  may 
result  in  the  natural  absorption  of  the  remaining  fluid  with  a  very  consider- 
able degree  of  rapidity,  so  that  even  if  the  chest  is  not  emptied  by  the 
aspiration  it  may  become  so  in  a  few  days  by  a  natural  process.  This  holds 
true  with  particular  force  in  those  cases  of  large  pleural  effusion  which  do 
not  require  interference  because  of  pressure  symptoms,  but  which  do  not 


442  DISEASES  OF  THE  PLEURA 

undergo  absorption  by  natural  means  until  after  absorption  has  been 
stimulated  by  the  performance  of  paracentesis. 

It  is  necessary  that  the  physician  should  exercise  care  in  inspecting  his 
needle  before  he  employs  it.  Experienced  clinicians  have  frequently  been 
infected  by  a  dry  tap  when  they  were  skilful  enough  to  diagnose  an  effusion, 
but  careless  enough  not  to  notice  that  their  needle  was  plugged. 

A  pleural  effusion  should  not  be  permitted  to  remain  too  long  in  the  chest, 
since  its  presence  tends  to  increase  the  organization  of  the  inflammatory 
process  on  the  surface  of  the  lung,  or  results  in  the  formation  of  such 
firm  adhesions  that  decortication  of  the  lung  by  the  surgeon  is  necessary  if 
recovery  is  to  ensue. 

The  employment  of  purges,  diuretics,  or  diaphoretics  in  cases  of  pleurisy 
with  effusion,  with  the  object  of  causing  an  absorption  of  the  fluid,  is,  for 
very  good  reasons,  futile  in  almost  every  instance.  It  has  already  been 
pointed  out  that  in  this  disease  the  pleura  is  almost  invariably  covered  by  a 
dense  fibrinous  exudate,  which  is  plastic  in  character  and  mechanically 
interferes  with  the  absorption  of  the  exudate.  Even  if  the  physician  is  able, 
by  the  administration  of  powerful  hydragogue  cathartics,  to  cause  a  concen- 
tration in  the  blood,  this  concentration  does  not  result  in  the  absorption 
of  the  pleural  effusion,  because  of  the  obstruction  just  spoken  of,  and  also 
because  absorption  takes  place  from  the  pleura  chiefly  by  the  lymphatic 
vessels,  and  not  by  the  bloodvessels.  The  only  result  of  administering  pow- 
erful diaphoretics  and  cathartics  to  patients  suffering  with  effusion  following 
pleurisy  is  to  exhaust  their  vitality  without  materially  influencing  the  local 
condition. 

The  application  of  blisters  to  the  chest,  with  the  hope  that  they  will 
stimulate  absorption,  is  probably  quite  as  futile  as  the  employment  of 
purgatives,  although  they  may  indirectly  result  in  the  absorption  of  fluid 
by  stimulating  the  removal  of  the  film  of  plastic  exudate  which  covers  the 
pleural  membrane. 

The  condition  in  pleural  transudations  following,  or  accompanying,  car- 
diac or  renal  dropsy  is  quite  a  different  one  from  that  due  to  inflammation. 
In  the  letter  condition  there  is  not  any  fibrinous  exudate,  and  the  effusion 
takes  place  by  a  process  of  transudation  from  the  vessels,  the  fluid  being 
quite  different  in  its  character  from  that  found  after  the  acute  inflammatory 
process  just  discussed.     Purgatives  may  therefore  do  good. 

Aside  from  the  operative  measures,  which  are  necessary  in  about  one- 
half  the  cases  of  pleurisy  with  effusion,  the  physician  should  administer 
mild  tonics,  with  the  object  of  aiding  digestion,  and  he  should  support 
the  system  by  the  administration  of  proper  quantities  of  nutritious  food. 
If  after  tapping  the  fluid  it  recurs,  it  should  be  withdrawn  a  second  time. 
Such  a  recurrence  rarely  takes  place  in  the  effusion  following  pleurisy, 
although  it  is  not  infrequently  met  with  in  cases  of  ordinary  transudation 
into  the  pleural  cavity  in  other  pathological  states. 


PURULENT  PLEURAL  EFFUSION,  OR  EMPYEMA 


443 


PURULENT  PLEURAL  EFFUSION,  OR  EMPYEMA. 

Definition  and  Etiology. — By  empyema  we  mean  a  condition  in  which  pus 
has  accumulated  in  the  pleural  space  or  spaces.  It  was  taught  at  one  time 
that  such  an  effusion  might  primarily  be  serous  and  by  infection  become 
purulent,  but  at  present  this  view  is  not  generally  held.  Empyema  occurs 
as  a  sequel  to  infection  from  the  lung  in  the  great  majority  of  cases,  but  it 
may  arise  from  primary  infection  of  the  pleura.  The  condition  is  far  more 
common  in  children  than  in  adults  (Fig.  61).  In  children  it  is  generally 
the  result  of  the  presence  of  the  pieumococcus,  which  commonly  causes  a 

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Chart  showing  morbidity  percentage  of   empyema  due  to  all  causes  at  different  ages,  based  on  403 
cases  occurring  in  five  hospitals  in  tlie  United  States  and  England. 


444 


DISEASES  OF  THE  PLEURA 


bronchopneumonia  or  a  croupous  pneumonia  first  and  an  empyema  after- 
ward, but  in  adults  the  streptococcus  is  usually  the  exciting  cause.  The 
condition  occurs  much  more  frequently  in  boys  than  in  girls. 

In  69  cases  of  empyema  in  children,  P.  S.  Blaker  found  the  pneumococcus 
in  62  cases;  the  streptococcus  in  3;  the  pneumococcus  and  streptococcus  in 
3,  and  the  staphylococcus  in  1.  In  40  cases  in  children  reported  by  Bythell, 
26  were  due  to  the  pneumococcus  and  9  to  the  pneumococcus  and  some  other 
organism  (Fig.  62). 


Fig. 

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Chart  showing  morbidity  percentage  of  empyema  due  to  the  pneumococcus  at  different  ages,  based 
on  286  cases  collected  by  Netter.    Large  percentage  in  childhood. 

Empyema  is  sometimes  due  to  infection  by  the  Bacillus  tuberculosis,  and 
it  is  a  fact  worthy  of  note  that  the  pus  in  such  cases  is  usually  sterile,  only 
revealing  the  presence  of  tubercle  bacilli,  when  by  chance  some  of  the  exudate 
which  lines  the  pleura  is  obtained  through  the  aspirator.  In  other  words, 
sterile  pus  from  an  empyema  raises  a  suspicion  of  tuberculous  infection. 
Bacteriological  examination  of  pus  from  311  cases  of  empyema,  occurring  in 
hospitals  in  the  United  States,  Canada,  England,  France,  Germany,  Austria, 
and  Italy,  showed  that  the  pneumococcus  was  the  infecting  organism  in  92 


PURULENT  PLEURAL  EFFUSION,   OR  EMPYEMA  445 

cases,  the  streptococcus  in  58;  the  tubercle  bacillus  in  30.  In  the  remaining 
cases  the  pus  was  sterile,  or  more  than  one  micro-organism  was  found.  If 
children  are  excluded  from  these  statistics,  the  streptococcus  becomes  the 
most  common  infectious  agent. 

When  no  pulmonary  lesion  can  be  discovered  in  a  case  of  empyema,  it 
must  be  recalled  that  a  very  small  and  insignificant  lesion  in  the  lung,  and, 
therefore,  one  which  is  easily  overlooked,  may  be  the  focus  for  a  very  severe 
pleural  infection,  and,  therefore,  the  inability  of  the  physician  to  find  a 
primary  pulmonary  lesion  does  not  prove  that  it  has  not  existed. 

The  character  of  the  pus  found  in  cases  of  empyema  varies  considerably 
in  different  cases,  the  variation  depending  in  part  upon  the  micro-organism 
which  has  produced  the  condition,  and  upon  the  duration  of  the  malady  at 
the  time  the  effusion  is  examined.  Usually  it  is  creamy  and  homogeneous; 
in  other  cases  it  is  thin  and  separates  on  standing  into  a  thick  and  thin  layer. 
When  the  effusion  is  an  old  one,  the  pus  may  be  quite  thick  and  curdled  in 
its  appearance,  containing  clot-like  masses  or  shreds  of  fibrin,  which  plug 
the  aspirating  needle  and  make  aspiration  impossible.  While  the  color  is 
commonly  a  creamy  yellow,  it  is  sometimes  slightly  pinkish  in  appearance, 
and  may  be  greenish  in  hue,  and  in  still  other  cases,  when  a  considerable 
amount  of  blood  has  been  extravasated  into  the  effusion,  it  is  a  dirty,  pale- 
cocoa  color.  In  some  instances,  as  in  cases  due  to  infection  by  the  pneu- 
mococcus,  the  pus  is  almost  odorless,  while  in  others,  particularly  if  the 
empyema  has  ruptured  into  a  bronchus,  it  is  fetid. 

Purulent  effusion  in  the  pleural  space  is  usually  profuse.  Indeed,  it  has 
been  taught  that  as  a  class  these  collections  are  larger  than  are  serous  effu- 
sions, which  is  not,  however,  always  true  by  any  means.  On  the  other  hand, 
they  are  very  much  more  likely  than  are  serous  effusions  to  be  walled  off  and 
encysted  by  reason  of  adhesions,  thereby  forming  a  small  pocket  of  pus. 

Symptoms. — If  after  an  attack  of  pneumonia  the  temperature  does  not  fall, 
or  if,  after  it  has  been  normal  or  near  normal,  it  begins  to  rise  again,  and 
the  patient  has  cliills  or  chilly  sensations,  empyema  should  be  sought  for. 

The  symptoms  of  empyema  in  general  are  those  of  impaired  health.  The 
patient  is,  as  a  rule,  fale  and  ill-looking,  suffers  from  loss  of  weight,  and 
sweats,  which  are  particularly  prone  to  come  on  when  he  sleeps. 

A  moderate  fever  may  be  present,  and  suppressed  or  even  well-developed 
chills  may  recur.  It  is  important,  however,  to  remember  that  in  some  cases 
none  of  these  constitutional  symptoms  are  manifest,  the  fever  in  particular, 
being  so  mild  that  they  fail  to  attract  attention,  so  that  the  condition  of 
empyema  is  suspected  only  when  some  shortness  of  breath  calls  attention  to 
the  thorax. 

The  pus  in  cases  of  empyema  sometimes  becomes  so  completely  walled  off 
from  the  surrounding  tissues  that  it  remains  for  weeks  without  producing 
any  signs  of  its  presence,  but  in  other  cases,  and  these  are  the  more  numerous 
it  causes  such  severe  pressure  symptoms  or  so  much  evidence  of  sepsis  that 
relief  is  demanded  by  the  patient.  In  other  cases — and  these  are  often  those 
in  which  the  empyema  has  not  been  recognized — the  pus  burrows  its  way  out, 
rupturing  into  a  bronchus  or  perforating  the  chest  wall.  Very  much  more 
rarely  it  empties  into  the  pericardium,  or  even  into  the  oesophagus.    In  other 


446  DISEASES  OF   THE   PLEURA 

instances  it  has  perforated  the  diaphragm,  although  this  process  is,  curiously, 
much  more  rare  than  the  rupture  of  a  subdiaphragmatic  abscess  into  the 
pleural  cavity. 

Statistics  as  to  the  relative  frequency  v^ith  which  rupture  into  a  bronchus 
takes  place  are  not  in  accord.  Thus,  of  195  cases  of  empyema  occurring  in 
St.  Thomas^  Hospital,  London,  and  in  the  Leeds  General  Infirmary,  11 
ruptured  into  the  lung,  a  percentage  of  5.64;  while  an  analysis  of  a  large 
number  of  cases  of  empyema  collected  by  Netter  gave  a  percentage  of  26.2 
rupturing  into  the  lung.    These  latter  figures  certainly  must  be  far  too  high. 

The  physical  signs  of  empyema  have  already  been  discussed  when  describ- 
ing those  of  serous  effusion,  for  in  both  states  they  are  practically  the  same. 
Sometimes  the  presence  of  pus  may  be  shown  by  an  oedema  of  the  superficial 
tissues,  which  is  often  met  with  over  deep-seated  suppurations.  Empyema 
is  also  apt  to  produce  more  bulging  of  the  intercostal  spaces  than  is  serous 
effusion,  perhaps  because  there  is  more  wasting,  and  so  the  bulging  is  more 
readily  observed.  In  some  instances  of  empyema,  however,  the  contrac- 
tion of  the  thickened  pleura  draws  the  edges  of  the  ribs  so  closely  to  one 
another  that  bulging  of  the  interspaces  is  obliterated. 

When  pulsation  is  transmitted  to  the  purulent  effusion,  so  that  the  impulse 
is  manifest  through  the  interspaces,  it  is  called  "  empyema  necessitatis." 

Complications. — The  chief  complications  of  empyema  have  already  been 
named,  viz.,  sepsis  and  perforation.  The  signs  of  sepsis  are  similar  in  this 
state  to  those  produced  by  accumulations  of  pus  elsewhere,  and  require  no 
further  discussion.  The  symptoms  of  perforation  into  a  bronchus  consist 
of  an  attack  of  violent  coughing,  during  which  the  patient  expels,  in  large,  or 
sometimes  in  small  amount,  a  quantity  of  almost  pure  pus.  After  the  pus 
first  appears,  it  is  commonly  brought  up  in  mouthfuls  several  times  a  day, 
and  more  rarely  in  such  large  quantities  as  to  threaten  the  patient  with 
suffocation.  This  drainage  of  pus  through  the  lung,  curiously  enough, 
rarely  causes  serious  permanent  damage  to  the  lung,  which  may  ultimately 
entirely  recover  if  the  physician  will  but  provide  an  opening  in  the  chest  wall 
for  proper  drainage. 

When  the  pus  escapes  externally  by  burrowing,  it  most  frequently  does  so 
about  the  sixth  intercostal  space  in  the  axillary  area,  but  it  sometimes  bur- 
rows a  great  distance  and  escapes  by  way  of  numerous  openings.  In  other 
instances  it  burrows  far  down  the  trunk  and  discharges  as  low  down  as  the 
pelvis.  Indeed,  Barton  has  reported  a  pulsating  empyema  in  the  left  lumbar 
region.  These  openings  may  persist  for  many  years,  and  if  the  suppurative 
process  persist,  amyloid  disease  of  the  liver  and  kidneys  may  ensue. 

Diagnosis. — The  differentiation  of  empyema  from  serous  effusion  is  to  be 
made  by  the  presence  of  the  septic  symptoms  just  named,  and  by  the  use  of 
an  aspirating  needle  to  determine  the  character  of  the  fluid.  The  localized 
types  of  empyema  are  those  which  offer  real  difficulty  in  diagnosis,  since  the 
pus  may  be  between  two  lobes  of  the  lung,  or  at  the  base  of  the  lung  next 
the  diaphragm,  or  be  extended  over  a  considerable  area  while  very  shallow, 
or,  again,  the  inflammatory  process  in  the  adjacent  lung  tissue  causes  the 
presence  of  the  physical  signs  of  consolidation  of  the  lung  or  of  large  effusion, 
when  in  reality  the  purulent  collection  is  a  small  one.     In  these  cases  the 


PURULENT  PLEURAL  EFFUSION,  OR  EMPYEMA  447 

introduction  of  the  aspirating  needle  may  fail  to  reveal  the  presence  of  pus, 
because  the  instrument  does  not  happen  to  exactly  strike  the  purulent  focus. 

When  the  pus  is  localized  by  adhesions  in  the  neighborhood  of  the  heart, 
this  organ  may  be  displaced  by  the  pressure  and  transmit  its  impulse  to  the 
effusion,  so  giving  rise  to  the  belief  that  a  purulent  pericarditis  is  present; 
the  absence  of  this  more  serious  state  being  revealed  only  when  the  pus  is 
set  free. 

A  still  more  difficult  condition  to  discover  is  interlobar  pleurisy  with 
effusion.  In  such  cases  if  the  accumulation  is  pus,  it  may  rupture  into  the 
bronchi  and  give  rise  to  the  belief  that  the  patient  has  true  pulmonary 
abscess. 

Prognosis. — The  prognosis  in  empyema  in  children,  over  three  years  of 
age,  if  the  condition  is  due  to  the  pneumococcus,  and  if  the  pus  is  allowed  to 
escape  before  it  has  done  much  damage,  is  surprisingly  good,  both  as  to  rapid 
and  complete  recovery.  Not  only  do  many  of  these  cases  soon  cease  to  form 
any  more  pus,  but  the  compressed  lung  expands  with  remarkable  rapidity, 
and  may,  in  the  course  of  a  few  months,  fill  the  pleural  cavity  so  well  that 
nearly  all  traces  of  the  disease  may  disappear.  When  the  disease  affects 
infants  the  outlook  is  bad,  because  of  their  susceptibility  to  wasting  processes 
and  their  low  vital  resistance. 

In  streptococcus  infection  the  prognosis  is  not  so  favorable,  nor  is  it  good 
in  tuberculous  empyema,  for  in  the  first  type  the  formation  of  pus  is  persistent 
and  the  deformity  of  the  chest  is  very  apt  to  be  great,  while  in  the  second 
type  a  primary  infection  elsewhere  is  usually  present. 

It  has  been  stated  by  some  authors  that  an  empyema  may  undergo  absorp- 
tion. While  a  decrease  in  the  size  of  the  efl'usion  may  result  from  the  absorp- 
tion of  some  of  its  fluid  constituents  true  disappearance  of  pus  from  the 
thorax  does  not  take  place  unless  it  is  let  out  or  escapes  spontaneously.  It 
may,  however,  become  inspissated  and  encysted. 

Treatment. — ^There  is  but  one  thing  to  be  done  in  cases  of  empyema, 
and  that  is  to  let  out  the  pus,  treating  the  case  as  one  of  ordinary  abscess. 
If  the  quantity  of  the  fluid  is  sufficiently  large  to  compress  and  displace 
adjacent  organs,  particularly  the  heart,  it  is  better  to  first  relieve  some  of  this 
pressure  by  aspiration,  as  in  a  case  of  serous  effusion,  removing  enough  of 
the  pus  to  permit  the  heart  and  vessels  to  slowly  regain  their  normal  position. 
As  the  pus  in  these  cases  is  often  under  great  pressure,  so  that  it  squirts 
several  feet  when  an  incision  is  made,  I  am  confident  that  this  preliminary 
modification  of  the  pressure  is  wise  in  most  cases.  On  the  following  day 
or,  if  need  be,  immediately  after  aspiration,  an  incision  should  be  made 
between  the  sixth  and  seventh,  or  seventh  and  eighth,  ribs  in  the  middle 
axillary  line,  and  this  opening  should  be  maintained  by  the  insertion  of  a 
doubled,  or  extra-large,  drainage  tube  or  by  a  gauze  drain.  If  the  ribs  have 
been  drawn  so  closely  together  by  the  contraction  of  the  parietal  pleura 
that  free  drainage  cannot  be  obtained,  then  the  upper  surface  of  the  lower 
rib  should  be  cut  away  until  drainage  is  free,  or,  if  need  be,  several 
inches  of  the  rib  or  of  several  ribs  should  be  resected.  This  is  usually 
necessary  in  streptococcus  infection.  As  a  rule,  the  milder  measures  suffice 
in  children,  but  if  the  formation  of  pus  persists  resection  should  always  be 


448  DISEASES  OF  THE  PLEURA 

performed.     For  the  details  as  to  the  exact  technique  of  these  operative 
procedures  reference  should  be  made  to  a  surgical  work. 


CHRONIC  PLEURISY. 

Definition. — Chronic  inflammation  of  the  pleura  may  be  nothing  more 
than  a  sequence  of  some  of  the  acute  conditions  already  discussed.  If  a 
fluid  accumulation,  serofibrinous  or  purulent,  be  allowed  to  remain  within 
the  chest  cavity,  important  alterations  take  place  in  the  serous  membrane. 
With  the  subsidence  of  infection  reparative  efforts  lead  to  the  production  of 
fibrous  tissue,  which  greatly  thickens  both  parietal  and  visceral  layers  and 
ensheaths  the  collapsed  lung,  eventually  forming  such  a  dense  investing 
membrane  that  re-expansion  becomes  impossible.  In  other  cases  the  fluid 
is  absorbed  and  the  pleural  surfaces  coated  by  inflammatory  products  come 
in  contact,  coalesce,  and  become  fused  by  permanent  organization  of  the 
exudate.  In  the  latter  group  of  cases  the  pleural  cavity  may  be  obliterated, 
or  partial  adhesions  only  may  form.  In  some  cases  unattended  by  frankly 
expressed  acute  inflammation,  hyperplastic  thickening  of  large  or  small  , 
areas,  usually  with  adhesions,  occurs.  In  such  cases  the  newly  formed 
inflammatory  tissue  may  attain  a  thickness  of  1  cm.  or  more  and  not  in- 
frequently contains  calcareous  plaques. 

The  third  form  is  called  "primitive  dry  pleurisy"  in  the  sense  that  it 
begins  without  effusion  and  often  without  pain,  and  is  not  associated  with 
fever.  The  patient  may  himself  feel  the  pleural  friction.  Finally,  limited 
adhesions  occur  between  the  layers  of  the  pleura,  but  they  do  not  cause 
marked  interference  with  the  lung  nor  deformity  of  the  chest. 

The  fourth  type  is  the  so-called  ^''primitive  dry  pleurisy"  described  by 
Sir  Andrew  Clarke,  in  which  the  layers  of  the  pleura  become  adherent  and 
thickened  as  in  the  forms  just  described.  From  the  visceral  layers  of  the 
pleura  bands  of  connective  tissue  penetrate  and  traverse  the  lung  almost 
as  if  they  were  true  trabeculse.  The  effect  of  these  bands  as  they  contract 
is  to  produce  bronchiectasis  and  some  distortion  of  the  lung  in  its  lower 
lobe,  where  the  process  is  nearly  always  situated.  The  condition  is  really 
a  pleurogenous  interstitial  pneumonia.  These  cases  are  not  identical  in 
character  with  those  due  to  old  empyema. 

Occasionally  in  chronic  pleurisy  large  calcareous  or  even  bony  plates  are 
developed  in  the  newly  formed  inflammatory  tissues. 


HYDROTHORAX. 

This  condition  is  to  be  clearly  separated  from  ordinary  pleural  effusion 
due  to  inflammatory  changes.  Pleural  effusion  due  to  inflammation  is 
usually  unilateral,  but  hydrothorax  is  generally  bilateral.  The  fluid  in  the 
pleural  cavities  is  present  as  a  result  of  transudation  in  cases  of  renal  disease, 
cardiac  disease,  profound  anaemia,  or  any  cause  which  tends  to  impede  cir- 
culation or  to  increase  the  readiness  with  which  the  serum  can  escape  from 


PNEUMOTHORAX,   HYDROPNEUMOTHORAX,   PYOPNEUMOTHORAX  '  449 

the  bloodvessels.  Thus  it  may  develop  in  cases  of  thrombosis  of  the  vena 
azygos  during  the  course  of  typhoid  fever.  While  it  is  true,  as  already 
stated,  that  hydro  thorax  is  usually  bilateral,  it  sometimes  happens  that  it  is 
unilateral,  if  perchance  the  obstruction  to  the  flow  of  blood  or  lymph  is  pro- 
duced by  some  lesion  which  affects  only  one  side  of  the  chest.  This  occurs 
much  more  frequently  on  the  right  side  than  on  the  left,  in  those  cases  in 
which  the  cause  is  cardiac  disease.  Many  years  ago  Jaccoud  pointed  out 
that  this  is  due  to  pressure  upon  the  major  azygos  vein  by  the  dilatation 
of  the  inferior  vena  cava  and  the  right  auricle,  and  more  recently  Steele 
and  Stengel  have  called  attention  to  this  class  of  cases. 

When  it  is  present  in  the  course  of  cirrhosis  of  the  liver  it  is  probably 
due  to  the  presence  of  associated  pulmonary  tuberculosis.  Osier  asserts 
that  such  an  effusion  may  occasionally  occur  in  what  he  designates  as 
"perfectly  healthy  men." 

The  fluid  in  hydrothorax  is  usually  of  low  specific  gravity  (see  Pleurisy 
with  Effusion),  and  clear  or  but  slightly  opalescent,  yellowish  or  straw- 
colored.  It  is  not  rich  in  cells,  and  those  cells  that  are  present  consist 
largely  of  relatively  voluminous  flat  endothelial  cells.  Fibrin  is  usually 
absent.  If  an  injury  or  obstruction  of  the  thoracic  duct  is  present,  the  fluid 
may  be  chylous  in  character. 

Again,  if  such  a  patient  is  given  iodide  of  potassium  and  the  fluid  is 
withdrawn  by  aspiration  iodine  will  be  found  in  it,  whereas  if  the  fluid  is 
due  to  inflammation  iodine  is  absent.  The  fluid  is  placed  in  a  test-tube, 
a  few  drops  of  fuming  nitric  acid  are  added,  and  then  it  is  shaken  with  some 
chloroform,  when  if  iodine  is  present  a  red  color  will  appear,  which  sinks  to 
the  bottom  of  the  tube  with  the  chloroform. 

Hydrothorax  can  often  be  relieved  by  the  free  use  of  a  saline  purgative, 
such  as  half  an  ounce  of  magnesium  sulphate  given  every  morning  before 
breakfast  and  by  cardiac  tonics  if  they  are  needed.  If  it  causes  symptoms 
by  pressure  it  must  be  removed  by  aspiration.    (See  Pleurisy  with  Effusion.) 

Bloody  effusion  into  the  pleura  is  met  with  in  cases  of  cancer  of  the  pleura 
and  of  Bright's  disease.  It  is  more  indicative  of  the  presence  of  the  former 
malady.  I  have  more  than  once  seen  a  simultaneous  pleural  and  abdominal 
bloody  effusion  due  to  a  general  carcinomatosis. 

When  pleural  effusion  is  tapped  a  second  time,  or  when  the  needle  has 
been  introduced  more  than  once  in  the  search  for  fluid,  it  not  infrequently 
happens  that  the  liquid  obtained  is  blood-stained,  owing  to  wounding  of  a 
bloodvessel  by  the  instrument.  Of  course,  this  possibility  must  be  remem- 
bered when  a  bloody  effusion  is  found.  Sometimes  a  true  hsemothorax 
arises  from  this  cause,  or  it  is  due  to  a  leakage  from  an  eroded  bloodvessel. 


PNEUMOTHORAX,  HYDROPNEUMOTHORAX,  PYOPNEUMOTHORAX. 

Definition, — Pneumothorax — that  is,  the  presence  of  air  in  the  pleural 

spaces — is  rarely  present  as  the  result  of  disease  unless  it  is  associated  with 

fluid  (hydropneumothorax)  or  pus   (pyopneumothorax).     As  the  result  of 

injuries  to  the  chest  and  to  the  lungs  it  not  rarely  appears  as  true  hydro- 

29 


450  DISEASES  OF  THE  PLEURA 

pneumothorax,  as  after  the  fracture  of  a  rib,  or  as  the  result  of  a  stab 
wound. 

History. — As  long  ago  as  the  time  of  Hippocrates  a  succussion  sound  on 
shaking  a  patient  suffering  from  empyema  or  pleural  effusion  was  recognized, 
but  it  was  not  until  the  time  of  Laennec,  about  2200  years  later,  that  the 
value  of  this  sign  was  appreciated  as  indicating  the  presence  of  both  fluid 
and  air  in  the  chest. 

Etiology. — The  most  common  cause  of  pneumothorax  is  pulmonary  tuber- 
culosis, and  it  arises  as  a  result  of  the  perforation  of  the  pleura  by  the  rupture 
of  a  cavity  through  the  visceral  layer;  in  order  that  air  may  enter  the  pleura 
the  tuberculous  cavity  must  directly  or  indirectly  communicate  with  a 
patulous  bronchus,  thereby  affording  a  communication  between  the  lung 
and  the  thoracic  cavity.  West  believes  that  fully  90  per  cent,  of  the 
cases  are  due  to  this  cause.  In  many  cases  this  accident  is  prevented 
by  an  acute  or  subacute  pleurisy  occurring  at  the  area  diseased,  so  that  the 
pleura  is  thickened  or  the  two  layers  glued  together.  This  is  particularly 
prone  to  be  the  case  when  a  cavity  has  formed;  and  were  it  not  for  this 
protective  process  the  condition  of  pneumothorax  would  be  commonly  met 
with.  In  still  other  cases,  however,  these  very  adhesions  result  in  pneumo- 
thorax, for  during  some  severe  exertion  they  are  torn,  and  so  the  air  finds 
an  opening  through  which  to  escape. 

As  a  rule,  the  perforation  occurs  in  the  lower  part  of  the  upper  lobe,  or 
in  the  upper  part  of  the  middle  lobe.  Pneumothorax  develops  on  the  left 
side  nearly  twice  as  often  as  on  the  right.  West,  however,  beheves  that  the 
two  sides  are  nearly  equally  affected.  At  times  the  opening  through  which 
the  air  escapes  is  so  small  that  it  cannot  be  found.  Sometimes  there  is 
more  than  one  perforation. 

Very  much  more  rare  as  causes  of  pneumothorax  are  bronchiectasis, 
pulmonary  abscess,  and  pulmonary  gangrene.  So  rare  are  they  that  when 
cases  of  this  kind  occur  they  should  be  reported.  This  holds  true  as  well 
of  cases  which  develop  from  rupture  of  a  vesicle  in  cases  of  emphysema  of 
the  lungs.  Pneumothorax  has  arisen  in  the  course  of  whooping-cough, 
diphtheria,  and  typhoid  fever. 

Pneumothorax  occurs  three  times  as  often  in  men  as  in  women. 

Sjrmptoins. — ^The  onset  of  pneumothorax  is  often  very  sudden  and  severe, 
but  at  times  it  develops  so  insidiously  that  no  signs  of  its  presence  are  noted 
by  the  patient  until  he  attempts  to  make  some  exertion,  when  dyspnoea 
ensues.  In  cases  of  sudden  onset  there  is  not  only  urgent  dyspnoea,  but 
sometimes  syncope  to  the  point  of  unconsciousness.  These  severe  symptoms 
are  much  more  prone  to  develop  in  a  patient  who  has  slight  pulmonary 
disease  than  in  one  who  has  well-advanced  lesions,  because  in  the  latter 
case,  the  lung  being  already  partly  useless,  the  other  lung  is  ready  to  com- 
pensate for  the  inactivity  of  the  diseased  part.  When  the  accident  occurs 
on  the  comparatively  healthy  side  death  may  speedily  ensue.  In  some 
instances  the  pain  may  be  so  severe  that  angina  pectoris  is  thought  to  be 
present. 

Physical  Signs. — ^The  physical  signs  in  these  cases  of  pneumothorax 
consist  in  bulging  of  the  interspaces  on  the  affected  side,  and  at  times  the 


PNEUMOTHORAX,   HYDROPNEUMOTHORAX,   PYOPNEUMOTHORAX      451 

development  of  subcutaneous  emphysema.  There  is  also  in  many  cases  a 
distinct  increase  in  the  size  of  the  chest  on  that  side.  If  the  air  escapes  on 
the  right  side  the  liver  is  markedly  depressed  and  the  heart  is  displaced  to 
the  left.  In  left-sided  cases  the  heart  may  be  pushed  to  the  right  of  the 
median  Hne. 

Percussion  reveals  hyperresonance  unless  there  has  been  an  old  pleurisy 
with  secondary  pleural  thickening.  If  the  lung  is  adherent  to  the  chest  wall 
and  collapsed  by  pressure,  or  consolidated  by  tuberculosis,  a  dull  note  may 
be  present.  In  a  case  of  this  character  recently  under  my  care,  in  a  patient 
whose  general  health  seemed  to  negative  the  possibility  of  tuberculosis,  this 
state  was  confirmed  at  autopsy,  much  relief  being  given  before  death  by 
frequently  permitting  the  air  to  escape  from  the  chest,  over  part  of  the  chest 
wall  through  a  hollow  needle. 

Auscultation  reveals  an  absence  of  vesicular  murmur  over  the  area  of 
hyperresonance,  and,  perhaps,  loud  amphoric  breathing  over  the  lung, 
particularly  if  it  contain  a  cavity  which  freely  communicates  with  the 
pleural  space. 

When  hydropneumothorax  is  present  the  lower  part  of  the  chest  is  flat 
on  percussion  as  in  ordinary  pleural  effusion,  above  this  is  an  area  of  hyper- 
resonance, and  above  this  again  is  the  Skodaic  resonance  due  to  the 
compressed  lung.  On  shaking  the  patient  a  succussion  sound  is  heard, 
and  when  the  patient  is  at  rest  auscultation  reveals  "metallic  tinkling," 
which  is  supposed  to  be  due  to  the  dropping  of  fluid  into  the  liquid  at  the 
base  of  the  chest.  Succussion  and  metallic  tinkling  are  the  most  important 
signs  of  hydropneumothorax.  Another  valuable  sign  is  the  so-called  "coin 
sound"  produced  by  striking  a  large  coin,  held  against  the  chest  wall,  with 
another  coin.  The  physician  listens  to  the  back  of  the  chest  as  the  percussion 
is  done,  by  an  assistant,  on  its  anterior  surface,  and  closes  his  unoccupied 
ear  with  his  finger-tip.  If  the  coin  be  struck  so  that  the  sound  has  to  be 
transmitted  through  the  chest  at  the  level  of  the  fluid  the  sound  is  very 
indistinct.  At  the  level  of  the  air  it  is  transmitted  with  startling  clearness, 
and  at  the  level  of  the  lung  its  transmission  is  again  impaired. 

Diagnosis. — In  considering  the  possible  presence  of  pneumothorax  in  the 
type  which  is  insidious  the  following  conditions  must  be  included :  A  large 
cavity  may  give  somewhat  similar  physical  signs,  but  the  limited  area  over 
which  they  are  manifested  or  demonstrable  separates  the  two  states.  Emphy- 
sema of  the  lungs  is  excluded  by  the  universal  presence  of  breath  sounds 
and  the  fact  that  the  condition  is  bilateral.  Rupture  of  the  diaphragm  with 
diaphragmatic  hernia  should  be  considered  if  some  injury  has  been  suffered, 
and  pyopneumothorax  subphrenicus  must  be  excluded  by  study  of  the  pul- 
monary signs  above  the  area  involved  and  of  the  condition  of  the  epihepatic 
and  epigastric  areas. 

Prognosis. — ^The  prognosis  of  pneumothorax  depends  largely  upon  the 
cause  of  the  condition  and  the  associated  states  of  effusion  and  empyema. 
Much  depends  upon  the  suddenness  of  onset.  I  have  seen  death  occur  in 
twelve  hours  in  cases  with  sudden  onset,  and  cases  are  on  record  of  death 
in  twenty  minutes.  On  the  other  hand,  if  the  dyspnoea  is  not  severe  the 
pulmonary  condition  may  be   actually  benefited  by  the  temporary  rest 


452  DISEASES  OF  THE  PLEURA 

enforced  by  the  collapse  of  the  lung.  West  has  placed  the  mortality  at 
70  per  cent.,  and  of  these  fatal  cases  75  per  cent,  died  within  two  weeks 
and  90  per  cent,  within  a  month.  In  those  cases  which  do  not  die  soon 
after  the  onset  of  this  condition  death  may  result  either  from  empyema  and 
exhaustion,  or  from  the  progress  of  the  underlying  disease.  If  the  heart  is 
feeble,  if  the  other  lung  is  far  advanced  in  disease,  and  if  the  strength  of 
the  patient  is  badly  impaired  the  prognosis  is,  of  course,  bad.  Recovery 
takes  place  in  about  10  per  cent,  of  the  cases  of  simple  pneumothorax 
without  fluid. 

Treatment. — The  treatment  of  pneumothorax  consists  in  the  relief  of 
pain,  if  it  be  very  severe,  by  a  small  dose  of  morphine — say,  |^  of  a  grain 
given  hypodermically.  If  the  dyspnoea  is  marked  a  large  hollow  needle,  or 
aspirating  cannula,  should  be  introduced  into  the  chest,  but  not  attached  to 
the  aspirator.  The  pressure  in  the  chest  will  cause  more  air  to  escape  than 
will  flow  in,  and  as  the  lung  is  already  collapsed  any  damage  caused  by  its 
entrance  is  done.  To  prevent  the  air  from  entering,  the  finger  may  be  tem- 
porarily used  as  a  valve  on  each  inspiring  movement  until  a  wash-bottle  can 
be  so  arranged  that  the  air  will  escape  through  the  water  it  contains  and  then 
cannot  return.  If  the  air  constantly  re-accumulates  the  case  should  be  treated 
by  a  drainage  tube  inserted  as  in  the  treatment  of  empyema.   (See  Empyema.) 

If  oedema  of  the  other  lung  is  threatened,  dry  cups  should  be  applied  over 
its  base. 

When  serous  effusion  is  present,  or  when  empyema  is  a  complication,  the 
conditions  should  be  treated  as  described  when  discussing  these  conditions. 

A  most  exhaustive  study  of  this  subject  has  been  made  by  West  in  London, 
and  more  recently  by  Emerson  in  Baltimore  during  1903. 

DISEASES  OF  THE  MEDIASTINUM. 

Under  this  heading  are  considered  diseases  of  the  mediastinum  other  than 
those  of  the  heart  and  aorta.  In  my  Fothergillian  Prize  Essay  I  collected 
520  cases  of  mediastinal  disease,  and  the  facts  there  presented  form  the  basis 
for  the  following  views.  The  statistics  on  their  face  show  that  there  were 
134  cases  recorded  as  carcinoma,  98  as  sarcoma,  21  as  lymphoma  or  lymph- 
adenoma,  and  115  as  abscess.  In  other  words,  a  large  proportion  of  cases 
of  disease  in  this  area  are  due  to  malignant  growths,  for  the  remaining 
lesions  were  non-malignant  or  inflammatory.  The  statistics  apparently 
indicate  that  cancer  is  by  far  the  most  frequent  form  of  individual  growth. 
While  we  have  no  right  to  go  "behind  the  returns,"  in  the  sense  that  cases 
reported  as  cancer  may  be  regarded  as  sarcoma,  it  is  nevertheless  probable 
that  sarcoma  is  really  the  most  frequent  growth  in  the  mediastinum,  because 
tissues  favorable  to  its  growth  are  found  there  in  great  abundance  and 
tissues  susceptible  to  carcinomatous  growth  are  scanty.  Again,  it  is  well 
known  that  up  to  the  middle  of  the  last  century,  and  later,  little  distinction 
was  made  between  cancer  and  sarcoma,  and  so  many  cases  of  sarcoma  were 
probably  reported  as  cancer.  Finally,  lymphoma  and  lymphadenoma  are  so 
nearly  allied  to  sarcoma  that  it  is  fair  to  add  them  to  the  so-called  sarcoma- 
tous cases,  making  the  total  119  reported  as  sarcoma. 


DISEASES  OF  THE  MEDIASTINUM  453 

The  non-malignant  tumors  of  the  mediastinum  are  fibroma,  teratoma, 
dermoid  cyst,  and  hydatid  cyst. 

Notwithstanding  the  fact  that  the  middle  and  posterior  mediastinal  spaces 
are  more  richly  provided  with  lymphoid  tissues  than  the  anterior  mediastinum, 
the  statistics  prove  that  maUgnant  growth  is  more  common  in  the  latter  space 
than  in  the  other  spaces.  Thus,  of  the  cases  reported  as  sarcoma  and  cancer, 
in  which  the  space  affected  was  stated,  81  were  in  the  anterior  space  as 
against  28  in  the  posterior  space,  and  only  5  in  the  middle  space  alone, 
although  in  many  other  instances  the  entire  mediastinum  was  invaded. 

For  this  reason  we  should  expect  to  find  that  sarcoma  in  a  very  large  pro- 
portion of  cases  occurred  as  a  secondary  growth  in  the  mediastinum ;  but  an 
examination  of  the  literature  of  the  subject,  both  as  regards  general  opinion 
and  reports  of  cases,  shows  such  a  conclusion  to  be  erroneous.  Indeed, 
the  mediastinum  seems  to  rarely  suffer  from  any  form  of  this  disease  save 
the  primary,  and  even  in  those  cases  in  which  the  lesions  were  scattered  all 
through  the  body  from  head  to  foot,  this  space  seems  to  have  escaped 
secondary  contamination.  Should  the  growth  appear  in  the  mediastinum, 
secondarily,  it  generally  affects  the  posterior  or  middle  spaces,  owing  to 
the  large  number  of  lymphatic  glands  and  like  tissues  which  are  found  in 
these  cases. 

It  is  a  curious  fact  that  mediastinal  growths  are  twice  as  common  in  men 
as  in  women,  although  women  so  much  more  frequently  have  malignant 
growths  in  nearby  tissues,  and  in  them,  as  already  stated,  malignant  growth 
of  the  lung  is  said  to  be  more  common. 

The  average  age  affected  by  mediastinal  tumors  is  about  thirty-seven 
years. 

Symptoms. — The  symptomatology  of  mediastinal  tumor  is  by  no  means 
clear  and  well  defined,  since  so  many  other  conditions  may  produce  signs 
of  the  same  character,  and  it  has  been  stated  very  positively  by  certain 
writers  that  such  a  growth  cannot  be  diagnosticated  during  life. 

Although  this  assertion  seems  rather  sweeping,  there  is,  nevertheless, 
some  truth  in  it,  and  in  many  cases,  where  we  have  no  history  to  guide 
us  and  no  evidence  of  a  growth  elsewhere,  the  diagnosis  may  be  well-nigh 
impossible. 

Large  tumors  are  found,  in  the  anterior  mediastinum,  which  have 
not  been  diagnosticated  or  suspected  until  a  postmortem  has  been 
made,  not  from  any  lack  of  ability  on  the  part  of  the  physician,  but 
because  the  symptoms  of  mediastinal  disease  have  either  been  entirely 
absent  or  masked  by  others  of  more  importance  elsewhere.  Thus,  in 
a  case  reported  by  Bruen,  an  old  woman,  aged  seventy  years,  entered  the 
Philadelphia  Hospital  with  decided  symptoms  of  renal  disorder,  which  in 
a  few  days  caused  her  death.  Although  an  examination  was  made  of 
the  chest,  as  a  matter  of  routine  duty,  no  special  physical  signs  were 
discovered,  and  the  disease,  which  was  sarcoma  in  the  anterior  mediastinum, 
was  not  discovered  until  the  body  was  placed  on  the  postmortem  table. 
The  only  symptoms  of  such  a  condition  of  affairs  before  death  consisted 
in  slight  dyspnoea  and  cough,  both  of  which  were  supposed  to  arise  from 
the  renal  lesions;  and  this  is  the  more  remarkable,  since  the  growth  weighed 


454 


DISEASES  OF   THE  PLEURA 


Fig.  63 


fourteen  ounces,  was  six  inches  long  by  five  inches  broad  and  four  inches 
in  diameter,  or,  in  other  words,  was  about  the  size  of  a  normal  adult  heart. 
No  signs  of  sarcoma  existed  elsewhere  in  the  body  from  which  one  might 
suspect  any  malignant  disease. 

The  first  symptoms  complained  of  by  the  patient  vary  quite  as  much  as 
do  the  later  ones,  and  depend,  as  do  their  successors,  upon  the  parts  most 
involved.  By  far  the  largest  number  of  sufferers  notice  some  interference 
with  respiration,  particularly  on  exertion,  which  soon  increases,  so  that 
there  may  be  constant  dyspnoea,  and  even  attacks  of  partial  suffocation. 

The  dyspnoea  and  other  disturbances  of  respiration  are,  in  many  instances, 
due  to  several  rather  than  any  single  cause,  since,  in  addition  to  the  mechanical 
pressure  by  the  growth  on  the  air-passages,  we 
may  also  have  such  interference  with  the  circula- 
tion of  the  blood,  particularly  in  the  thoracic  veins, 
that  pleural,  pericardial,  or  mediastinal  effusions 
of  serum  may  occur. 

Effusions  into  the  abdomen  may  occur,  owing 
to  involvement  of  the  ascending  vena  cava,  but 
such  a  condition  is  rather  rare,  probably  owing 
to  the  fact  that  the  ascending  cava  more  frequently 
escapes  than  does  the  descending.  Dropsy  of  the 
lower  extremities,  without  abdominal  effusion,  some- 
times comes  on. 

In  still  another  class  of  cases  the  pulmonary 
vein  may  be  obstructed,  and  oedema  of  the  lung 
may  develop.  Hypostatic  congestions  are  by  no 
means  rare,  the  patient  often  being  forced,  by  car- 
diac weakness,  pleural  effusion,  or  pressure  on  the 
trachea,  to  lie  in  one  position.  In  some  cases  loud 
venous  murmurs  can  be  heard  in  the  jugular  and 
other  large  superficial  veins,  and  care  has  to  be 
exercised  as  to  the  diagnosis  of  the  true  cause  of 
the  distress.  The  ribs  and  sternum  may  undergo 
gradual  erosion  and  destruction  from  pressure,  and 
the  growth  appear  on  the  surface  of  the  body. 

In  a  certain  number  of  cases  the  nerves  of  the 

thorax  seem  to  be  more  affected  than  the  rest  of 

its  contents,  and  involvement  of  the  vagi  or  the  recurrent  laryngeal  nerves 

may  bring  on   a   long  train  of   obscure   and  dangerous  symptoms,  both 

as  regards  the  circulation,  respiration,  digestion,  speech,  and  swallowing. 

Tumors  of  the  mediastinum  invading  the  lungs  have  frequently  been 
mistaken  for  chronic  and  even  acute  pneumonia,  growing,  as  they  do,  along 
the  larger  bronchial  tubes  and  bloodvessels. 

Without  doubt,  in  a  certain  number  of  cases,  either  hypostatic  pneumonia, 
or  pneumonia  due  to  pressure  on  the  bronchial  vessels,  develops  as  the  tumor 
invades  the  lung,  and  in  such  cases  it  is  absolutely  impossible  to  make  a 
diagnosis  unless  there  are  symptoms  of  pressure  in  the  mediastinum. 
Walsh  has  stated  that  if  the  lesion  be  due  to  a  tumor,  the  affected  side  will 


Kronlein's  case  of  retro- 
tracheal  tumor  of  the  medi- 
astinum. 


DISEASES  OF  THE  MEDIASTINUM  455 

increase  in  bulk  rather  than  diminish,  and  that  dyspnoea  out  of  proportion 
to  the  degree  of  consohdation  points  to  a  mediastinal  disorder  rather  than 
one  confined  to  the  lungs. 

In  a  very  large  proportion  of  cases  of  mediastinal  disease  the  condition 
is  one  of  abscess.  There  were  115  cases  in  my  collection  of  520  of  medias- 
tinal disease.  The  proportion  of  acute  and  cold  abscess  in  79  cases  in  which 
the  differentiation  was  made  was  48  to  31. 

The  most  constant  and  severe  symptom  is,  in  nearly  all  cases,  the  deep- 
seated  pain,  which  increases  in  severity  from  first  to  last,  seldom  remitting 
until  suppuration  has  taken  place  and  the  pus  has  found  some  outlet.  If 
the  case  be  one  of  cold  abscess,  these  painful  symptoms  may  be  masked  by 
other  more  pressing  ones,  such  as  dyspnoea  and  oedema  from  pressure; 
although  it  should  not  be  forgotten  that  such  symptoms  may  appear  with 
equal  severity  in  both  varieties  of  the  disease.  In  the  acute  variety  all  the 
symptoms  of  ordinary  inflammation  appear,  such  as  rigors  and  periodical 
or  constant  fever. 

As  recovery  took  place  in  about  40  per  cent,  of  the  cases  of  mediastinal 
abscess  according  to  the  statistics  of  preantiseptic  days,  it  ought  to  occur 
much  more  frequently  now. 

Mediastinal  growths  are  usually  of  such  a  nature  as  to  be  beyond  either 
medicinal  or  surgical  treatment,  but  abscess,  dermoid  cysts,  and  teratomata 
are  sometimes  operable. 


DISEASES  OF  THE  CIBCULATOEY  SYSTEM. 


DISEASES  OF  THE  PERICARDIUM. 

PERICARDITIS. 

Acute  Pericarditis.  Definition. — Acute  pericarditis,  sometimes  called 
acute  fibrinous  or  acute  serofibrinous  pericarditis,  is,  as  its  name  implies, 
an  acute  inflammation  of  the  pericardium,  the  serous  membrane  which 
envelopes  the  heart. 

Etiology. — Acute  pericarditis  is  practically  always  due  to  the  presence  of 
some  infecting  micro-organism,  although  certain  conditions  existing  simul- 
taneously may  predispose  to  the  infection  by  lowering  vital  resistance.  In 
the  great  majority  of  cases  it  is  due  to  acute  articular  rheumatism,  in  com- 
paratively few  it  develops  as  a  complication  of  croupous  pneumonia,  the 
pneumococcus  being  its  cause,  and  it  also  develops  as  a  complication  of 
scarlet  fever,  in  which  disease  the  streptococcus  associated  with  this  malady 
is  probably  the  provoking  factor.  Acute  pericarditis  is  also  frequently 
associated  with  renal  disease,  and  is  often,  under  these  circumstances,  a 
form  of  terminal  infection.  So,  too,  it  may  develop  in  the  course  of  various 
infectious  diseases,  such  as  smallpox,  erysipelas,  typhoid  fever,  and  even  in 
measles.  Septic  infections,  such  as  general  septicaemia  and  ulcerative  endo- 
carditis, may  cause  it.  In  diabetes  it  occurs  as  a  terminal  infection.  Of 
course,  tuberculosis  and  syphilis,  diseases  which  affect  every  tissue,  may 
also  affect  this  one. 

Acute  pericarditis  also  develops  by  direct  extension  from  inflammation  in 
neighboring  parts,  in  distinction  from  infection  which  takes  place  through 
the  blood.  Thus,  inflammation  of  the  mediastinal  tissues  may  produce  it, 
as  in  diseases  of  the  bronchial  glands,  of  the  sternum,  or  of  the  vertebrae. 
So,  too,  pneumonia  and  pleurisy  affecting  nearby  portions  of  the  lung  may 
cause  inflammation  of  the  pericardium.  In  infections  involving  the  myo- 
cardium the  overlying  serosa — that  is,  the  visceral  layer  of  the  pericardium — 
rarely  escapes.  So,  too,  pericarditis  may  be  the  first  indication  of  impending 
rupture  of  that  part  of  the  aorta  covered  by  pericardium. 

Pericarditis  may  also  be  due  to  injury  to  the  chest  wall  or  to  the  mem- 
brane itself. 

It  is  evident,  therefore,  that  acute  pericarditis  is  nearly  always  a  condi- 
tion secondary  to  some  other  affection,  and  that  it  is  very  rarely  primary. 
When  it  is  primary  it  is  usually  due  to  tuberculosis.  (See  articles  on- 
Croupous  Pneumonia,  Acute  Rheumatic  Fever,  and  Typhoid  Fever.) 

(457) 


458 


DISEASES  OF  THE  PERICARDIUM 


Frequency. — The  frequency  of  pericarditis  as  a  primary  disease  is  very 
limited,  but  as  a  secondary  affection  it  is  great.  Very  many  cases  present 
no  sign  of  it  during  life,  yet  the  condition  is  found  at  autopsy.  It  occurs 
almost  as  frequently  in  children  as  in  adults,  although  at  one  time  this  class 
of  patients  was  supposed  to  be  not  so  commonly  attacked  as  older  persons. 
Sturges  found  it  present  in  94  out  of  100  cases  of  fatal  heart  disease  in  chil- 
dren. Of  these  cases  54  were  of  rheumatic  origin.  Indeed,  it  is  probable 
that  the  disease  is  less  prevalent  after  than  before  puberty.  It  occurs  far 
more  frequently  in  males  than  in  females,  and  this  is  particularly  true  after 


Fig.  64 


Heart  and  pericardium,  acute  serofibrinous  (pneumococcal)  pericarditis.  Most  of  the  anterior 
parietal  layer  of  the  pericardium  has  been  cut  away,  showing  the  villous  (shaggy)  irregular  projec- 
tions of  the  fibrin.  To  the  left,  where  the  parietal  pericardium  is  reflected  over  the  right  auricle  and 
great  vessels,  cohesion  of  the  layers  may  be  seen;  later,  had  the  patient  recovered,  such  fusion  of  the 
layers  would  have  constituted  the  basis  from  which  organized  fibrous  adhesions  would  have  formed. 


puberty,  when  the  greater  exposure  and  activity  of  males  become  domi- 
nant factors  in  causing  rheumatism  and  other  infections.  At  this  time  the 
proportion  is  from  4  to  1  to  6  to  1. 

Pericarditis,  as  we  would  expect,  develops  more  commonly  in  severe  cases 
of  acute  rheumatism  than  in  mild  cases,  but,  on  the  other  hand,  it  is  to  be 
borne  in  mind  that  even  in  those  cases  with  very  mild  joint  symptoms  severe 
pericardial  involvement  may  occur.  Prior  attacks  of  rheumatism  seem  to 
increase  the  frequency  of  pericarditis  in  subsequent  attacks.  The  condi- 
tion usually  comes  on  during  the  first  week  of  the  disease.     This  is,  how- 


PERICARDITIS  459 

ever,  by  no  means  always  the  case,  and  it  may  appear  as  late  as  the  sixtieth 
day  of  the  illness  or  during  a  relapse. 

Pericarditis  due  to  renal  disease,  the  Pericardite  Brightique  of  the  French, 
is  distinctly  a  state  of  advanced  years,  occurring  most  commonly  after  forty- 
five  or  fifty  years  of  age.  It  is  more  commonly  met  with  in  patients  sufi'ering 
from  contracted  kidney  than  in  those  that  present  the  parench}Tnatous 
form  of  renal  disease. 

Pathology. — As  in  inflammation  of  the  pleura,  so  in  inflammation  of  the 
pericardium,  it  is  well  to  recognize  three  forms  of  acute  pericarditis,  viz., 
the  acute  dry  or  fibrinous,  the  acute  exudative  (serofibrinous),  and  the  puru- 
lent type.  In  the  first  stage  of  all  these  forms  of  pericarditis  the  lining  sur- 
face of  the  pericardium  is  lustreless,  opaque,  and  somewhat  roughened 
by  a  delicate  fibrinous  exudate.  It  is  also  hypersemic  and  may  be  dotted 
with  petechise.  It  is  the  rubbing  together  of  the  two  layers  of  the  pericardium 
at  this  stage  that  causes  the  characteristic  friction  sound  of  the  disease. 
As  the  inflammation  progresses  the  membrane  becomes  completely  covered 
by  the  exudation  of  fibrin,  which  may  assume  a  villous  formation.  Adhesions 
between  the  layers  of  the  pericardium  also  take  place. 

In  the  serofibrinous  form  a  considerable  quantity  of  serum  is  poured  out 
into  the  sac,  and  particles  of  fibrin  and  leukocytes  are  found  in  it.  The 
quantity  may  be  so  large  as  greatly  to  distend  the  sac,  displace  the  heart, 
and  interfere  with  its  function,  particularly  by  pressure  upon  the  auricles  and 
cavse.  In  many  cases  as  much  as  three  pints  have  been  found  in  the  sac. 
West  quotes  cases  in  which  the  pericardial  sac  contained  no  less  than  five 
pints  (due  to  scurvy),  yet  recovery  occurred  after  aspiration. 

In  the  purulent  form  (pyopericardium)  the  serum  and  fibrin  are  mixed 
with  pus  cells  and  erythrocytes.  Pyopericardium  may  arise  as  a  primary 
purulent  pericarditis  or  be  converted  from  the  serous  form  by  infection 
with  the  Streptococcus,  Pneumococcus,  or  Staphylococcus  pyogenes  aureus. 
Sometimes  the  tubercle  bacillus  acts  as  a  pyogenic  organism  in  this  space. 

There  is  some  difference  of  opinion  as  to  the  frequency  of  pyopericardium. 
Two  opinions  which  represent  the  two  sides  of  this  question  are  as  follows : 
Samuel  West  speaks  of  it  as  "one  of  the  rarest  of  clinical  rarities,"  but 
Battin  says  "it  is  a  disease  seldom  suspected,  still  more  rarely  diagnosed, 
and  hardly  ever  treated,  and  yet  it  is  one  that  is  present  in  3  per  cent,  of  the 
deaths  in  the  records  of  the  Children's  Hospital." 

That  the  latter  view  is  correct  is  shown  by  the  fact  that  Breitung  in  324 
cases  of  pericarditis  found  that  108  were  serofibrinous,  30  hemorrhagic, 
and  20  purulent,  or  6.1  per  cent.  In  769  autopsies  collected  by  Still  24 
instances  of  pyopericardium  were  found,  and  11  were  due  to  infection  by 
the  pneumococcus.  Scott  found  it  in  no  less  than  16  cases  out  of  40  (40 
per  cent.),  and  in  38  cases  of  croupous  pneumonia  the  same  reporter  found 
pyopericardium  in  17,  or  44.7  per  cent. 

Symptoms  of  Acute  Fibrinous  Pericarditis. — The  symptoms  of  acute  fibrinous 
pericarditis  are  often  not  pronounced.  Pain  would  supposedly  be  a  well- 
marked  symptom,  but  it  is  not  present  in  all  cases,  although  when  it  is  present 
it  may  be  severe.  Fortunately  pain  from  this  cause  is  rare  in  children. 
When  it  occurs  it  is  usually  felt  from  the  right  edge  of  the  sternum  to  the 


460 


DISEASES  OF  THE  PERICARDIUM 


left  nipple  and  is  fairly  constant,  although  it  has  sharp  exacerbations.  In 
other  cases  the  pain  is  chiefly  situated  in  the  epigastrium,  or  a  sense  of 
prcecordial  distress  develops,  and  the  breathing  may  be  oppressed.  The 
action  of  the  heart  is  rapid,  often  reaching  100  or  120  and  even  160  beats  per 
minute  in  severe  cases.  The  temperature  is  usually  increased,  but  seldom 
rises  above  102°  or  103°.  In  some  cases  it  is  not  abnormal.  Nervous 
symptoms  are  sometimes  notable  and  great  restlessness  or  even  active  de- 
lirium may  ensue,  resembling  that  of  delirium  tremens.  Vomiting  is  a 
common  symptom. 


FiG.  65 


Area  in  which  pericardial  friction  sound  is  best  heard. 


Physical  Signs. — The  physical  signs  of  acute  fibrinous  pericarditis 
are  as  follows:  Palpation  over  the  base  of  the  heart  at  the  third  inter- 
space may  reveal  friction  fremitus  in  well-marked  cases,  and  auscultation 
will  show  a  distinct  friction  sound  in  the  same  area  when  the  disease  is 
established.  This  sound  is  creaking  and  dry  and  has  been  called  the 
"saddle-leather  sound,"  in  that  it  resembles  the  creaking  of  an  ordi- 
nary English  leather  saddle  when  it  is  first  used.  It  dift'ers  from  the  fric- 
tion sound  of'  pleurisy  in  that  it  is  to  and  fro  and  does  not  occur  with  the 
respirations.  At  times  it  has  a  gallop  rhythm  with  a  triple  sound  as  of  a 
horse  galloping.  If  the  stethoscope  be  pressed  against  the  chest  the  sound 
can  usually  be  intensified.  These  sounds  vary  with  the  severity  of  the  in- 
flammation of  the  pericardium  and  the  action  of  the  heart,  being  more 
sharply  defined  when  the  action  is  violent  than  when    it    is    depressed. 


PERICARDITIS  461 

Indeed,  variation  in  the  action  of  the  heart  may  cause  a  loud  friction 
sound  at  one  visit  and  a  lack  of  it  at  the  next.  As  a  rule  the  pericardial 
friction  sound  is  limited  to  the  area  of  the  cardiac  base  about  the  third 
or  fourth  interspaces,  but  it  may  be  heard  at  the  apex  or  along  the  sternum. 

Diagnosis  of  Acute  Fibrinous  Pericarditis. — Acute  dry  pericarditis  can 
scarcely  be  confused  with  any  other  state,  but  several  conditions  resemble 
it  somewhat.  Thus  in  cases  of  early  phthisis  there  is  occasionally  heard, 
near  the  apex  of  the  left  lung,  a  cardiopulmonary  murmur  or  puffing  sound 
during  inspiration,  occurring  with  each  beat  of  the  heart,  and  persisting  if 
the  patient  holds  his  breath  on  a  full  inspiration,  but  disappearing  on  expira- 
tion. Another  similar  condition  is  the  so-called  "  pleuropericardial  friction 
sound,"  which  is  apparently  due  to  the  beating  of  the  heart  against  the 
margin  of  the  lung.  Both  of  these  sounds  are,  however,  more  in  the  nature 
of  murmurs  than  friction  sounds. 

Symptoms  of  Serofibrinous  Pericarditis. — ^With  the  development  of  effusion, 
in  cases  which  go  on  to  that  state,  symptoms  of  cardiac  embarrassment  begin 
to  show  themselves.  The  evidences  of  cardiac  disturbance  are  not  always, 
however,  in  direct  proportion  to  the  amount  of  fluid,  for  in  some  instances 
large  accumulations  of  fluid  cause  so  little  inconvenience  as  to  be  over- 
looked, while  in  others  in  which  the  fluid  is  moderate  in  quantity  they  are 
severe.  It  is  important  that  these  variations  in  the  severity  of  the  symptoms 
be  remembered,  because  it  is  humiliating  in  the  extreme  to  find  after  some 
time  that  an  unsuspected  pericardial  effusion  is  present.  Probably  the  most 
constant  symptoms  are  dyspnoea,  a  dusky  skin,  an  anxious  fades,  and  a  rapid 
pulse,  which  varies  in  volume  and  speed  with  the  respirations.  The  voice 
is  somewhat  husky,  and  active  delirium  may  be  present  as  in  the  dry  form. 

Diagnosis  of  Pericardial  Effusion. — When  the  pericardium  is  well  filled 
with  fluid  the  sac  presents  a  peculiar  pear-shaped  swelling  which  consists 
of  two  spheres  superimposed,  the  smaller  one  above  the  larger  one.  It 
extends  across  the  middle  zone  of  the  chest  from  a  little  to  the  left  of  the 
right  nipple  to  a  little  to  the  left  of  the  left  nipple,  and  from  the  central 
tendon  of  the  diaphragm  nearly  to  the  top  of  the  sternum.  The  pressure 
of  this  fluid  upon  the  heart  and  its  great  vessels  may  very  markedly  inter- 
fere with  their  proper  movement,  but  it  does  not  greatly  change  its  position. 

Physical  Signs. — The  physical  signs  of  pericardial  effusion  are  as  follows: 
On  inspection  the  apex  beat  is  absent  and  in  many  cases  it  cannot  be  found  on 
palpation  unless  the  patient  is  turned  on  his  face.  The  chest  over  the  heart 
may  be  slightly  bulging,  and  palpation  may  reveal  the  fact  that  the  first  rib  can 
be  felt  projecting  more  prominently  from  beneath  the  clavicle  than  in  health. 
So,  too,  inspection  may  reveal  some  prominence  of  the  epigastrium,  and 
there  may  be  unusual  tenderness  on  palpation  of  this  area. 

The  heart  sounds,  on  auscultation,  are  distant  and  feeble  and  the  area  of 
cardiac  dulness  is  greatly  enlarged.  Thus  it  extends  to  the  right  of  the 
sternum  to  a  level  below  that  which  forms  the  base  of  the  cardiac  triangle, 
and  to  the  left  of  the  nipple.  There  is  also  enlargement  of  the  area  of  cardiac 
dulness  at  the  base  toward  the  left.  The  presence  of  dulness  in  the  fifth 
interspace,  to  the  right  of  the  sternum  (Rotch's  sign),  of  dulness  as  high 
as  the  second  cartilage  or  second   interspace   (Sansom's  sign),   combined 


462  DISEASES  OF  THE  PERICARDIUM 

with  dulness  over  the  sternum  between  these  points,  are  pretty  sure  signs 
of  pericardial  effusion,  particularly  if  at  the  left  infrascapular  angle  there  is 
dulness  on  percussion  (E wart's  sign).  The  area  of  dulness  is  that  of  a  flat- 
tened cone,  or,  as  Ewart  has  well  said  "it  is  that  of  a  bag  of  fluid  spreading 
out  at  the  base."  This  view  has  been  combated  by  Dr.  Frederick  Shattuck, 
but  the  distended  sac  does  undoubtedly  take  this  shape,  although  ina- 
bility to  demonstrate  its  outline  does  not  exclude  effusion  by  any  means. 

In  doubtful  cases,  resort  to  the  rs-ray  may  aid  greatly  in  deciding  the 
question  of  the  presence  of   effusion. 

The  most  important  states  to  be  differentiated  from  pericardial  effusion 
are  cardiac  dilatation  and  hypertrophy,  and  aneurysm  of  the  aorta  with 
some  leakage  into  the  pericardial  sac.  The  flrst  is  the  condition  most  apt 
to  mislead  the  physician.  I  have  seen  this  occur  several  times  and  I  have 
seen  the  heart  punctured  on  two  occasions  in  an  endeavor  to  aspirate  the 
pericardial  sac  in  the  belief  that  effusion  was  present  when  in  reality  the 
condition  was  one  of  great  cardiac  dilatation  with  pericardial  adhesion. 
The  presence  of  feeble  and  distant  heart  sounds,  the  absence  of  a  definite 
apex  beat,  and  the  manifest  cardiac  embarrassment  all  aided  in  producing 
an  erroneous  view  in  these  cases.  In  such  a  case  the  history  of  old  valvular 
difficulty  and  the  diffuse  character  of  the  apex  beat  should  help  us  to  a 
clear  view  of  the  condition.  In  cardiac  hypertrophy  the  distinct  apex  beat, 
the  strong  action  of  the  heart,  and  its  clear  sounds  separate  the  two  con- 
ditions. An  aneurysm  of  the  root  of  the  aorta  with  some  pericardial  effu- 
sion may  be  most  misleading.  In  a  case  of  this  kind,  seen  by  me,  aspira- 
tion of  the  pericardial  sac  caused  rupture  of  the  aorta  and  instant  death. 

Very  large  pericardial  effusions  have  been  taken  for  left-sided  pleural 
effusions,  and  an  encapsulated  pleural  effusion  has  been  taken  for  an  effusion 
into  the  pericardium. 

Prognosis  of  Acute  Pericarditis  with  and  without  Effusion. — This  is  good  in 
cases  in  which  the  heart  is  not  seriously  crippled  by  the  effusion  or  by 
associated  endocardial  changes.  The  outlook  is  favorable  in  proportion  to 
the  smallness  of  the  effusion  and  the  benignity  of  the  disease  causing  it. 
In  pneumonia  and  renal  disease  the  prognosis  is  worse  than  it  is  in  rheuma- 
tism, in  which  disease  it  is  good. 

In  the  great  majority  of  cases  pericardial  effusion  undergoes  absorption. 
This  happens  in  this  sac  far  more  frequently  than  in  the  pleural  sacs,  perhaps 
because  of  the  constant  action  of  the  heart.  When  the  effusion  persists  it 
must  be  removed.  (See  Treatment.)  Life  is  sometimes  prolonged  for  many 
weeks  even  after  pyopericardium  develops.  Coutts  has  recently  reported 
the  case  of  a  child  of  four  years  that  lived  seventeen  weeks  and  died  only 
after  operation.     Nevertheless,  pyopericardium  is  a  very  fatal  condition. 

Treatment. — ^In  the  early  stages  of  acute  pericarditis,  if  the  heart  is  over- 
acting and  irritated,  tincture  of  aconite  may  be  given  with  advantage  to 
quiet  its  action  and  to  diminish  friction.  An  ice-bag  may  be  placed  over 
the  preecordium  in  cases  of  pneumonia  with  this  complication,  and  in  rheu- 
matism several  flying  blisters  may  be  used.  Later  if  the  heart  becomes 
feeble  the  best  stimulants  are  the  aromatic  spirit  of  ammonia,  Hoffmann's 
anodyne,  and  alcohol.    Digitalis  except  in  small  doses  is  rarely  of  any  value, 


PERICARDITIS  463 

and  may  be  prevented  from  acting  properly  by  reason  of  the  fever  or 
because  there  is  not  room  in  the  pericardial  sac  for  full  diastole  to  take 
place  under  its  influence. 

If  the  quantity  of  effusion  be  very  great  it  must  be  removed  by  aspira- 
tion or  incision.  The  latter  operation  is  always  essential  if  pus  is  present, 
and  even  if  serum  is  present  incision  is  safer  because  it  is  by  no  means  easy 
to  diagnosticate  the  presence  of  fluid  beyond  a  doubt  and  more  difficult 
still  to  be  sure  of  the  part  of  the  sac  farthest  away  from  the  heart.  Aspira- 
tion may  be  therefore  in  the  nature  of  a  plunge  in  the  dark.  Incision  care- 
fully made  is  safer.  The  best  spot  for  operative  interference  depends  upon 
the  individual  conditions  and  the  position  of  the  apex  beat.  The  usual 
areas  of  election  are  in  the  fourth  interspace  at  the  left  edge  of  the  sternum 
and  at  the  fifth  right  interspace  at  the  edge  of  the  sternum. 

When  incision  is  practised  for  pyopericardium  the  mortality  is  high,  but 
nevertheless  it  must  be  performed  if  recovery  is  to  occur.  Out  of  51  cases 
collected  by  Porter  20  recovered  and  31  died. 

The  use  of  purgatives,  diuretics,  and  diaphoretics  to  cause  the  removal 
of  the  fluid  is  almost  useless.  If  any  drug  is  of  value  for  this  purpose  it  is 
iodide  of  sodium  in  doses  of  20  grains  three  times  a  day. 

Chronic  Pericarditis  (Adhesive  Form).  Definition  and  Pathology. — By 
chronic  adhesive  pericarditis  is  meant  a  condition  in  which  one  or  all  of  the 
following  pathological  conditions  arise  as  a  result  of  an  inflammatory  process, 
which  involves  the  pericardium  and  often  the  tissues  that  surround  it: 

(1)  There  may  develop  a  state  in  which  partial  or  localized  adhesions  take 
place  between  the  visceral  and  parietal  layers  of  the  pericardium.  Several 
such  adhesions  may  be  present  in  the  pericardium  at  the  same  time.  These 
adhesions  may  be  immediate  or  consist  in  long  strings  of  fibrous  tissue 
stretching  across  the  pericardial  sac.  They  are  commonly  found  near  the 
base,  but  also  occur  at  the  apex. 

(2)  In  the  second  class  of  cases  the  two  layers  of  the  pericardium  are 
closely  adherent,  and  the  walls  of  the  sac  in  some  cases  are  much  thickened. 
Here  again  the  adhesion  may  not  be  universal,  but  in  patches,  although 
at  times  the  entire  sac  is  obliterated  so  that  the  heart  is  surrounded  by  a 
thick  and  tough  capsule  composed  of  the  two  layers,  which  cannot  be  separated. 

(3)  In  still  a  third  class  the  inner  surfaces  of  the  pericardium  are  not  so 
much  involved  as  the  outer  surface,  and  as  a  consequence  we  find  adhe- 
sions to  the  chest  wall  or  to  the  pleura.  It  is  perhaps  hardly  fair  to  class 
this  type  with  those  already  named,  because  the  pericarditis  in  these  instances 
is  usually  the  result  of  a  spread  of  inflammation  from  neighboring  parts, 
as  from  the  pleura  or  mediastinal  tissues. 

(4)  Another  type,  and  the  most  serious  of  all,  is  that  in  which  the  internal 
and  external  layers  are  glued  together,  and  the  external  layer  is  adherent  to 
neighboring  tissues  so  that  the  heart,  its  membranes,  and  adjacent  parts 
are  bound  up  in  an  inflammatory  mass  or  mat.  If  the  mediastinal  tissues 
are  not  affected  the  condition  is  called  "pericarditis  externa  et  interna," 
but  if  the  mediastinal  tissues  are  included  it  is  given  the  name  of  "  indurative 
mediastinopericarditis."  In  some  cases  the  tissues  for  nearly  the  whole 
length  of  the  left  edge  of  the  sternum  may  be  involved. 


464 


DISEASES  OF  THE  PERICARDIUM 


(5)  Finally,  a  form  of  chronic  pericarditis  occurs  which  affects  the 
visceral  layer  of  the  pericardium  almost  solely,  and  encloses  the  heart  in 
a  thickened  inner  layer. 

Related  to  the  latter  condition  is  the  so-called  "multiple  serositis" 
or  the  "  pericarditic  pseudocirrhosis  of  the  liver"  of  Pick,  to  v^hich  the 
name  "iced  liver"   has  been    given  by  Curschmann.     In  such  cases   the 


Fig.  66 


Heart,  left  ventricle.     Adherent  pericardium,  with  lipomatosis  of  the  adhesions  and  slightly  fatty 
infiltration  of  the  myocardium. 

pericardium  suffers  from  a  chronic  hyperplastic  or  fibroid  inflammatory 
process,  which  likewise  affects  the  serous  membranes  elsewhere,  whence  the 
name  "  multiple  serositis."  In  other  words,  in  this  diseased  state  all  serous 
membranes  of  the  thoracic  and  upper  abdominal  zones  are  involved  in  a 
hyperplastic  process  which  is  prone  to  affect  the  pericardium  in  particular. 
In  some  instances  the  pericardial  sac  contains  fluid,  but  in  others  it  is 


PERICARDITIS  465 

closed  by  the  adhesions  between  its  walls  and  even  go  on  to  calcification. 
When  the  condition  is  well  developed  the  pericardium  and  pleurae  are 
adherent  to  one  another  and  to  all  adjacent  tissues,  and  the  peritoneum  is 
also  thickened  and  adherent  to  nearby  organs.  The  liver  is  adherent  to 
the  diaphragm  and  even  to  the  stomach,  colon,  omentum,  and  belly  wall. 
It  is  the  profuse  hyperplasia  of  the  peritoneum  which  causes  the  organs  it 
covers  to  look  as  does  a  cake  which  has  been  "  iced." 

The  two  symptoms  of  this  condition  which  are  most  constant  and  char- 
acteristic are  large  ascites  and  a  gradually  increasing  failure  of  cardiac  power. 
The  cause  of  the  excessive  ascities  is  the  perihepatitis  and  the  compression 
of  the  abdominal  vessels  by  the  newly  formed  connective  tissue.  Beyond 
these  two  symptoms  the  manifestations  of  the  process  are  practically 
identical  with  those  of  adherent  pericardium,  as  will  be  described  below. 
The  malady  is  a  very  slow  and  chronic  process  lasting,  it  may  be,  for 
years. 

The  result  of  these  adhesions  is  enlargement  or  hypertrophy  and  dilatation 
of  the  heart.  This  change,  however,  does  not  occur  in  all  cases  and  it  is 
chiefly  present  in  cases  in  which  valvular  lesions  coexist.  The  pressure 
produced  by  the  thickened  membranes  results  in  some  obstruction  to  the 
flow  of  blood  in  the  great  veins  at  the  cardiac  base,  and  this  causes  jugular 
distention. 

Symptoms  of  Adhesive  Pericarditis. — The  symptoms  of  the  milder  forms 
just  described  are  so  moderate  that  no  thought  of  their  existence  is  had  till 
autopsy  reveals  them.  It  is  in  the  well-developed  types  that  the  condition 
may  cause  symptoms  which  are  definite,  although  they  may  be  very  indefi- 
nite. Indeed,  in  some  cases  it  may  be  impossible  to  correctly  diagnosticate 
even  the  most  severe  forms.  The  subjective  symptoms  are  fain  in  the  prcE- 
cordium  or  a  sense  of  constriction.  This  pain  may  be  dull  and  constant  or 
paroxysmal,  arousing  the  suspicion  of  true  angina  pectoris.  Palpitation  is 
another  common  symptom  and  in  some  instances  the  action  of  the  heart  is 
irregular  and  hobbling.  Shortness  of  breath  on  exertion  is  also  present  and 
at  times  the  right  ventricle  becomes  engorged  and  secondary  engorgement  of 
the  liver  and  lungs  ensue.  Finally,  what  is  taken  for  ordinary  cardiac 
dropsy  due  to  valvular  disease  develops.  In  other  cases  pleural  effusion 
develops  from  this  cause. 

Diagnosis  of  Adhesive  Pericarditis. — The  physical  signs  to  be  searched  for 
in  making  a  diagnosis   are  as  follows: 

Inspection  may  reveal  depression  of  the  precordial  area  and  a  drawing 
together  of  the  ribs  so  that  the  intercostal  spaces  are  narrowed.  In  place 
of  this  condition  in  this  part  of  the  chest,  there  may  be  distinct  bulging. 
Again,  the  apex  beat  is  often  much  displaced  and  as  the  pericardium  is 
adherent  to  the  chest  wall  changes  in  posture  do  not  alter  its  position.  The 
usual  displacement  of  the  apex  is  upward  and  outward.  In  other  instances 
the  apex  l^eat  cannot  be  seen  or  felt  in  its  usual  place,  but  a  transmitted 
impulse  can  be  found  in  the  epigastrium.  Perhaps  the  most  important  diag- 
nostic symptom  is  retraction  of  the  chest  wall  at  systole.  This  retraction 
may  be  at  the  apex  or  along  the  left  edge  of  the  sternum  in  the  third, 
fourth,  and  fifth  interspaces.  Roberts  states  that  if  the  right  ventricle  is 
30 


466  DISEASES  OF   THE  PERICARDIUM 

greatly  enlarged  the  impulse  can  be  seen  to  the  right  of  the  sternum. 
Broadbent  has  called  attention  to  the  fact  that  in  many  of  the  well-marked 
cases  of  adherent  pericardium  marked  systolic  retraction  of  the  lower  ribs 
on  the  posterolateral  aspect  of  the  chest  is  visible,  if  the  patient  is  in  a  good 
light  and  the  physician  regards  his  back  and  side  from  a  distance.  This 
retraction  is  in  the  nature  of  a  tug  at  systole.  It  is  emphasized  by  a  deep 
inspiration.  Again,  if  the  physician  will  place  his  head  directly  against  the 
chest  in  this  area  he  may  have  transmitted  to  it  a  shock  at  the  time  of  systole. 
In  some  cases  the  adhesions  between  the  pericardium  and  the  diaphragm 
may  prevent  the  normal  epigastric  respiratory  movements. 

Percussion  may  reveal  in  some  cases  an  increase  in  the  area  of  cardiac 
dulness,  but  it  is  not  constant.  Auscultation  may  show  reduplication  of 
the  pulmonary  second  sound,  and  a  rough  and  widely  distributed  friction 
sound,  and  a  somewhat  prolonged  presystolic  murmur  at  the  apex  which  is 
not  necessarily  due  to  mitral  stenosis. 

The  pulse  often  presents  irregularities,  particularly  at  the  time  of  the 
inspiratory  movements,  the  so-called  pulsus  paradoxus.  Sudden  collapse 
of  the  cervical  veins  on  diastole  may  also  be  present. 

It  must  be  distinctly  understood  that  these  signs  are  often  absent  or  are 
difficult  to  discover.  There  is  perhaps  no  more  difficult  diagnosis  than 
that  of  some  cases  of  adherent  pericardium.  The  history  of  a  severe  or 
repeated  attacks  of  acute  rheumatic  fever  is  an  important  point  in  judging 
of  the  likelihood  of  its  presence,  particularly  if  there  is  also  a  history  of 
pericarditis.  Progressive  cardiac  weakness  without  valvular  lesions  in  a 
young  person  should  raise  the  suspicion  of  the  presence  of  this  state, 
particularly  if  an  insidious  ascites  and  dropsy  of  the  lower  extremities 
develop. 

Prognosis  of  Adhesive  Pericarditis. — The  prognosis  is  of  course  very  grave 
if  the  symptoms  are  severe  and  if  the  occupation  is  strenuous.  With 
adequate  rest  life  may  in  some  cases  be  prolonged  for  years  if  the  inflam- 
matory state  is  stationary. 

Treatment  of  Adhesive  Pericarditis. — The  treatment  cannot  be  curative 
for  obvious  reasons.  It  can  only  be  palhative,  by  rest,  good  food,  and  the 
relief  of  dropsy  by  purges  and  diuretics.  Digitalis  usually  cannot  act  use- 
fully because  the"  heart  is  too  firmly  bound  down  to  permit  of  increased 
diastole. 

HYDROPERICARDIUM. 

This  is  a  state  of  fluid  in  the  pericardium  due  to  transudation  from  vessels 
which  are  pressed  upon  by  growths,  or  it  results  from  hsemic  or  vascular 
changes  due  to  renal  disease.     It  is  not  an  inflammatory  effusion. 

Symptoms. — Symptoms  and  physical  signs  are  absent  except  when  the 
fluid  becomes  copious  enough  to  cause  cardiac  embarrassment,  when  the 
condition  of  the  patient  is  found  to  be  like  that  produced  by  an  ordinary 
serous  pericardial  effusion  due  to  true  pericarditis. 

Prognosis. — The  prognosis  depends  upon  the  cardiac  state  and  the  under- 
lying cause.    It  is  usually  grave,  because  of  the  underlying  malady. 


PNEUMOPERICARDIUM  467 

Treatment. — The  treatment  consists  in  free  purgation,  if  the  patient  is  able 
to  stand  it  and  the  use  of  diuretics.  Otherwise  it  is  that  of  general  dropsy. 
(See  Chronic  Parenchymatous  Nephritis.) 


H^MO  PERICARDIUM. 

Blood  in  the  pericardial  sac  arises  from  stab  and  other  wounds,  and  it  is 
also  present  in  cases  of  purpura  and  of  profound  diseases  of  the  blood.  In 
other  cases  it  arises  from  aneurysm  of  the  aorta  early  in  its  upward  course, 
and  finally  it  may  be  due  to  rupture  of  the  heart  or  aneurysm  of  one  of  the 
coronary  arteries.  Even  in  these  cases  death  may  be  postponed  a  number 
of  days.  If  a  large  amount  of  blood  escapes  into  the  pericardium  the  heart 
is  stopped  by  the  pressure  on  its  surface  and  on  the  great  veins  at  its 
base,  so  death  is  not  due  to  actual  loss  of  blood.  This  result  is  what  one 
would  expect,  and  I  proved  its  truth  some  years  ago  in  an  experimental 
research. 

When  the  condition  is  due  to  disease  it  usually  is  hopeless.  When  due 
to  injury  the  pericardium  should  be  opened,  the  blood  removed,  and  if  a 
wound  in  the  heart  exists  it  should  be  closed.  There  are  many  cases  of 
this  sort  on  record  in  which  operation  has  been  performed  and  in  which 
life  has  been  saved. 

PNEUMOPERICARDIUM. 

Air  or  gas  in  the  pericardium  appears  as  the  result  of  injury,  whereby  air 
enters  the  sac,  or  again  as  the  result  of  a  cavity  in  the  lung  perforating, 
through  adhesions,  into  this  space.  It  also  may  develop  in  cases  of  cancer 
or  other  ulcerative  lesions  of  the  oesophagus,  with  adhesions  between  this 
tube  and  the  pericardium,  followed  by  perforation  of  the  growth.  Again, 
it  occurs  rarely,  as  the  result  of  perforation,  in  pneumopyothorax.  Cases 
are  on  record  in  which  a  gastric  ulcer  has  caused  adhesions  to  the  diaphragm 
followed  by  perforation,  and  so  pneumopericardium  has  developed.  In  still 
other  instances  the  gas  which  is  present  is  due  to  the  presence  of  the  Bacillus 
aerogenes  cafsulatus  or  other  gas-producing  organisms. 

The  mere  presence  of  air,  or  gas,  in  this  cavity  is  such  an  abnormal  state 
that  some  serous  effusion  nearly  always  takes  place  within  a  few  hours; 
so  that  all  cases  of  pneumopericardium  are  really  to  be  considered  as 
hydropneumopericardium  primarily,  and  as  they  speedily  become  purulent 
by  infection  they  are  usually  instances  of  pyopneumopericardium. 

Symptoms. — ^The  symptoms  resemble  those  of  pericarditis  with  effusion, 
except  that  a  considerable  part  of  the  area  of  cardiac  dulness  may  give  a 
high-pitched  resonant  note  on  percussion.  This  area  of  resonance  varies 
greatly  with  the  posture  of  the  patient,  being  larger  when  he  is  recumbent 
than  when  he  is  erect.  Another  symptom  which  is  quite  characteristic,  if  it 
can  be  discovered,  is  a  pecuHar  crackling  sound  due  to  the  action  of  the  heart 
in  stirring  up  the  fluid  and  the  air.  Sometimes  these  sounds  are  gurgling 
or  churning  in  character.     They  have  been  compared  to  the  splashing  of 


468  DISEASES  OF   THE  HEART 

water  on  a  mill-wheel.  There  is  but  one  condition  which  can  produce 
s}Tnptoms  like  these,  and  that  is  a  large  cavity  in  the  lung  near  the  heart 
in  which  the  fluid  contents  are  disturbed  by  the  movements  of  the  heart. 

Prognosis. — The  prognosis  is,  of  course,  very  grave,  but  recovery  has 
occurred. 

Treatment. — The  treatment  depends  largely  upon  the  cause.  If  the  case  is 
one  of  perforated  oesophageal  cancer  it  is  of  course  hopeless;  in  an  instance 
of  traumatism  with  perforation  surgical  interference  may  give  good  results. 


PYOPERICARDIUM. 

(See  Pericarditis  with  Effusion.) 


DISEASES  OF  THE  HEAET. 

HYPERTROPHY  AND  DILATATION  OF  THE  HEART. 

Definition. — Hypertrophy  of  the  heart  is  a  condition  in  which  there  is 
a  growth  above  normal  of  its  muscular  fibres  resulting  in  an  increase  in  the 
size  and  particularly  in  the  muscular  power  and  weight  of  the  viscus. 

In  dilatation  one  or  more  of  the  cardiac  cavities  is  more  capacious  than 
normal;  the  wall  may  be  normal,  increased  or  decreased  in  thickness, 
with  a  cardiac  power  less  than  its  muscular  development  would  indicate. 

These  conditions,  which  at  first  glance  seem  diametrically  opposed  to 
one  another,  are  in  reality  nearly  always  present  simultaneously  in  varying 
degree.     For  this  reason  I  consider  them  side  by  side. 

^Vhen  the  wall  of  the  ventricle  is  increased  in  thickness  wdthout  any 
alteration  in  the  size  of  its  cavity  the  condition  is  called  simple  hyper- 
trophy. ^Mien  the  cavity  is  larger  than  normal  it  is  called  eccentric  hyper- 
trophy, or  hypertrophy  with  dilatation,  and  when  the  cavity  is  decreased 
in  size  it  is  known  as  concentric  hypertrophy. 

When  dilatation  is  combined  with  hypertrophy  it  is  called  active  dilatation. 
"When  there  is  no  hypertrophy,  but  thinning  of  the  walls  alone,  it  is  called 
passive  dilatation. 

Hypertrophy  of  the  Heart. — The  existence  of  concentric  hypertrophy 
has  been  denied.  It  certainly  is  very  rare.  Simple  hypertrophy  is  also  rare, 
but  eccentric  hypertrophy  is  one  of  the  most  common  of  secondary  patho- 
logical changes 

A  large  number  of  causes  produce  cardiac  hypertrophy  with  dilata- 
tion. Sometimes  they  act  singly,  but  not  rarely  several  of  them  are 
associated.  The  most  common  cause  is  valvular  disease,  which  by  its 
resulting  regurgitation  or  obstruction  increases  the  labor  of  the  heart.  The 
second  cause  of  importance  is  a  state  of  the  bloodvessels  which  renders  the 


HYPERTROPHY  AND  DILATATION  OF   THE  HEART  469 

propulsion  of  the  blood  more  difficult  than  in  health.  This  obstruction  to 
the  free  flow  of  blood  may  be  general,  as  in  cases  of  arteriocapillary  fibrosis; 
or  localized,  as  when  there  is  roughening  or  narrowing  of  the  aorta,  or  when 
a  tumor  presses  upon  the  aorta;  or,  again,  in  cases  of  aneurysm.  Other 
localized  causes  of  hypertrophy  are  emphysema  of  the  lungs  or  chronic 
phthisis  and  adherent  pericardium. 

The  increase  in  the  size  of  the  heart  in  cases  of  hypertrophy  is  sometimes 
very  great.  Thus,  this  organ,  which  in  the  healthy  man  weighs  about 
nine  ounces,  or  270  grams,  and  in  the  healthy  woman  about  eight  ounces 
(240  grams),  may  weigh  as  much  as  53  ounces  (1590  grams).  Usually, 
however,  the  increase  does  not  go  beyond  fifteen  ounces    (450   grams). 

A  heart  which  has  undergone  hypertrophy  is  broadened  or  widened 
at  its  apex,  but  the  actual  increase  in  the  size  of  this  organ  at  this  point 
depends  largely  upon  the  part  of  the  heart  which  is  chiefly  affected. 
Thus,  in  cases  in  which  the  right  ventricle  is  chiefly  involved,  this  part 
of  the  heart  is  often  far  larger  than  that  part  formed  by  the  left  ventricle, 
which  seems  small  by  contrast.  AMien  a  hypertrophied  heart  is  incised,  its 
walls  are  found  to  be  much  thickened  and  the  columnse  carnese  and  papillary 
muscles  larger  than  normal.  The  enlargement  is  due  to  both  an  increase 
in  the  number  and  size  of  the  muscle  fibres. 

Symptoms  and  Physical  Signs  of  Cardiac  Hypertrophy. — The  chief  symptom 
of  ordinary  eccentric  hypertrophy,  when  it  is  adequate  to  compensate  for 
the  valvular  lesion,  or  to  overcome  resistance,  may  be  said  to  be  the 
maintenance  of  a  comfortable  life  and  a  normal  circulation.  Many  persons 
develop  this  state  without  any  knowledge  of  there  being  present  any  valvular 
disease,  and  remain  in  perfect  health  for  years. 

If  the  physician  chances  to  examine  such  a  case  he  may  find  a  cardiac 
murmur  and  then,  on  closer  study,  discover  the  following  physical  signs, 
provided  the  process  is  well  developed.  On  inspection  the  prsecordium  is 
bulging,  but  the  impulse  transmitted  to  the  chest  wall  is  regular  and 
deliberate  in  distinction  from  the  cardiac  hurry  and  irregularity  present 
when  compensation  is  ruptured.  The  apex  beat  is  more  diffuse  than 
is  normal  and  is  often  in  the  sixth  or  seventh  interspace  instead  of  in  the 
fifth,  and  it  is  farther  toward  the  axilla  than  in  health.  On  'palpation  the 
apex  beat  is  found  to  be  forcible  and  it  may  be  heaving,  but  if  the  patient 
be  a  full-chested  individual  these  local  signs  may  not  be  present.  If  em- 
physema of  the  lungs  causes  these  enlarged  organs  to  overlap  the  heart 
they  may  hide  much  of  the  hypertrophy.  Percussion  may  reveal  increase 
of  the  area  of  cardiac  dulness  to  the  left,  to  the  right,  and  downward. 
Auscultation,  instead  of  revealing  an  exaggeration  of  the  first  sound,  reveals 
that  it  is  more  distant,  perhaps  because  the  thickness  of  the  heart  walls 
muffles  the  sound,  but  the  aortic  sound  is  accentuated  unless  the  aortic 
valves  are  diseased. 

If  the  patient  takes  violent  exercise  he  may  complain  of  palpitation  and 
the  thumping  of  his  heart. 

When  hypertrophy  begins  to  fail  the  patient  complains  of  shortness  of 
breath  on  exertion,  of  palpitation  and  oppression,  and  if  he  persists  in 
keeping  on  his  feet  the  symptoms  of  cardiac  failure  (see  Valvular  Disease) 


470  DISEASES  OF   THE  HEART 

develop.  The  first  physical  signs  of  the  failure  will  be  some  reduplication 
of  the  first  sound  and  diminution  in  its  clearness.  This  reduplication  is 
best  heard  just  inside  the  apex  beat  when  it  first  develops,  but  later  it  can 
be  heard  over  a  large  area.  The  period  between  the  first  and  second  sound 
is  prolonged  as  if  the  ventricle  was  able,  only  with  the  greatest  endeavor,  to 
slowly  expel  its  blood.  This  means  diminution  of  the  period  in  which  the 
heart  muscle  can  obtain  nourishment  through  its  coronary  vessels. 

The  causes  for  this  failure  are  various.  In  some  instances  the  degenerative 
changes  in  the  myocardium  and  in  the  bloodvessels  which  are  incident  to 
old  age  are  the  determining  factors.  In  others  some  acute  illness — as  typhoid 
fever,  influenza,  pneumonia,  or  renal  disease — may  be  the  cause ;  or,  again, 
severe  exercise  may  produce  so  much  exhaustion  of  the  heart  muscle  and 
acute  dilatation  that  the  cardiac  power  is  impaired  for  all  time. 

Diagnosis. — Cardiac  hypertrophy  must  be  separated  from  several  im- 
portant conditions  which  are  by  no  means  rare.  From  dilatation  hyper- 
trophy is  differentiated  by  the  facts  that  the  impulse  in  the  former  is  feeble, 
in  the  latter  it  is  strong,  and  by  the  feeble  heart  sounds  in  the  former  as 
compared  to  the  stronger  ones  in  hypertrophy.  So,  too,  palpation  of  the 
apex  in  dilatation  reveals  a  diffuse  and  feeble  impulse  and  in  hypertrophy  a 
forcible  beat. 

From  pericardial  effusion  it  is  differentiated  by  the  fact  that,  though  the 
area  of  cardiac  dulness  is  increased  in  both  states,  the  cardiac  impulse  and 
cardiac  sounds  are  muffled  in  effusion  and  exaggerated  in  hypertrophy. 
From  displacement  of  the  heart  it  can  be  differentiated  by  the  fact  that 
though  the  apex  beat  is  displaced  the  general  area  of  cardiac  dulness  is  not 
increased  in  cases  of  displacement. 

Again,  in  certain  cases  in  which  the  chest  wall  is  thin  and  the  lung  is 
retracted  so  that  it  fails  to  cover  the  heart  as  in  health,  the  heart  may  be 
so  close  to  the  chest  wall  that  its  area  of  dulness  will  be  abnormally  large 
and  its  apex  beat  unduly  forcible  and  diffuse.  In  such  a  case  the  careful 
study  of  the  state  of  the  lung  and  pleura  will  make  the  condition  clear. 

Of  the  functional  disorders  that  produce  overaction  of  the  heart  and 
so  cause  apparent  but  not  real  hypertrophy,  "tobacco  heart,"  the  irritable 
heart  of  exophthalmic  goitre,  and  that  of  neurotic  individuals  must  be 
remembered. 

Prognosis. — As  cardiac  hypertrophy  in  its  common  form  is  compensatory 
in  character,  and  as  it  very  rarely  becomes  excessive,  in  the  sense  that  it  is 
beyond  the  needs  of  the  patient,  the  prognosis  in  a  case  in  which  it  is  present 
deals  not  with  the  question  of  how  much  greater  will  hypertrophy  become, 
but  rather  how  much  longer  will  hypertrophy  enable  the  heart  to  supply  the 
bloodvessels  with  blood  in  satisfactory  quantities.  Unlike  most  alterations 
from  the  normal  as  the  result  of  disease  this  change  is  distinctly  advantageous 
to  the  patient. 

The  question  as  to  how  long  the  hypertrophy  will  be  maintained  can 
only  be  answered  after  its  provoking  cause  or  causes  have  been  determined. 
If  the  hypertrophy  following  valvular  disease  of  the  heart  is  adequate, 
if  the  patient  is  a  young  and  otherwise  healthy  adult,  and  if  the  valvular 
lesion  is  not  progressive,  the  prognosis  as  to  the  maintenance  of  the  con- 


HYPERTROPHY  AND  DILATATION  OF   THE  HEART  471 

dition  is  usually  good,  but  will  depend  upon  the  good  habits  of  the 
patient,  particularly  as  to  alcohol,  hard  work  and  exposure,  and  upon  the 
particular  valve  which  is  diseased.  (See  Prognosis  of  Valvular  Lesions.)  If 
the  hypertrophy  is  the  result  of  arteriocapillary  fibrosis  with  its  associated 
renal  changes,  the  duration  of  life  except  under  the  most  favorable  conditions 
is  brief,  because  the  arterial  obstruction  is  constantly  increasing  and  the 
heart  is  constantly  exposed  to  increasing  strain,  increasing  toxsemia,  and  is 
poorly  nourished  by  its  own  coronary  arteries. 

Treatment. — There  is  no  treatment  for  compensatory  hypertrophy  except 
to  maintain  it  by  care  as  to  manner  of  life,  and  the  use  of  digitalis  and  rest 
if  its  integrity  or  maintenance  is  threatened.  I  have  seen  a  few  cases 
of  aortic  regurgitation  with  great  hypertrophy  in  which  rest  in  bed  and 
moderate  doses  of  tincture  of  aconite  have  given  better  results  than  rest 
and  digitalis,  but  in  these  cases  the  patient  had  been  accustomed  to  severe 
toil,  and  when  he  was  put  at  rest  seemed  to  have  excessive  cardiac  power, 
as  shown  by  throbbing  and  oppression.  On  the  other  hand,  when  hyper- 
trophy seems  excessive,  it  is  not  rarely  in  reality  lacking,  and  the  violence 
of  the  heart  movements  may  be  abortive  efforts  at  circulation.  Often  the 
use  of  nitroglycerin  at  such  times  will  be  advantageous  if  the  arterial 
pressure  is  high. 

Dilatation  of  the  Heart. — Passive  dilatation  (without  hypertrophy)  may 
be  caused  by  valvular  lesions,  as  the  result  of  which  the  cavities  of  the 
heart  become  distended,  but  hypertrophy  does  not  develop.  Of  these  the 
chief  cause  is  sudden  and  prolonged  strain,  and  the  feebleness  often  due  to 
myocardial  disease.  Obstruction  to  the  flow  of  blood  in  the  pulmonary 
vessels  may  cause  dilatation  of  the  right  side  of  the  heart,  as  in  cases  of 
pneumonia,  in  cases  of  pleurisy  with  effusion,  and  in  cases  of  acute  pul- 
monary oedema  complicating  uraemia. 

A  common  cause  in  men  over  fifty  years  is  sudden  effort,  as  in  lifting  a 
heavyweight  or  climbing  rapidly  a  steep  flight  of  steps.  In  the  young  and 
vigorous  sudden  strain  may  be  followed  by  rapid  return  of  the  dilated  heart 
to  its  normal  size,  but  in  those  further  on  in  years,  or  who  have  valvular 
or  myocardial  disease,  an  acute  strain  often  results  in  permanent  dilata- 
tion. It  is  very  common  for  old  men  to  try  to  prove  that  they  are  "as 
young  as  they  used  to  be,"  and  to  attempt  athletic  feats  which  are  followed 
by  acute  dilatation  and  perhaps  immediate  death  or  death  in  a  few  days  or 
weeks.  In  other  instances  the  heart  suffers  from  a  gradual  dilatation  from 
prolonged  strain,  as  in  soldiers  on  the  march.  Not  rarely  dilatation  de- 
velops during  the  course  of  one  of  the  acute  infectious  diseases  or  during 
convalescence. 

When  the  strain  is  very  gradual,  instead  of  meeting  the  increased  demand 
by  increased  effort,  the  heart  slowly  dilates  and  is  perhaps  never  able  to 
empty  its  cavities  of  blood. 

The  intrinsic  causes  of  dilatation  are  myocarditis,  fatty  degeneration, 
fatty  infiltration,  and  serous  infiltration  from  pericarditis.  In  some  cases, 
however,  no  adequate  intrinsic  or  extrinsic  cause  can  be  found. 

Symptoms  of  Cardiac  Dilatation. — The  symptoms  and  physical  signs  of 
passive  dilatation  are  usually  such  that  a  diagnosis  is  readily  made.    When 


472  DISEASES  OF   THE  HEART 

it  is  sudden  in  onset  an  acute  or  partial  syncope  with  labored  respiration 
and  thoracic  oppression  may  be  present. 

When  the  onset  is  more  gradual  the  main  symptoms  are  impaired  circula- 
tion, a  tendency  to  syncope  on  suddenly  standing  or  sitting  up,  congestion 
of  the  kidneys  causing  albuminuria,  and  the  poor  capillary  circulation  which 
causes  the  skin  of  the  hands  to  remain  pallid  long  after  pressure.  Many 
persons  so  afflicted  cannot  lie  down  without  urgent  dyspnoea  and  cardiac  dis- 
tress. The  pulse  is  small  and  irregular,  and  the  arterial  tension  low.  In 
other  cases  the  pulse  wave  may  be  voluminous,  but  feeble. 

An  inspection  of  the  prsecordium  shows  that  the  apex  beat,  if  visible  at 
all,  is  diffuse  and  displaced  outward  and  downward.  On  placing  the  finger- 
tip on  the  spot  where  the  apex  beat  seems  most  marked,  the  examiner  is 
surprised  to  find  no  impulse  or  one  which  is  very  slight.  There  is  often 
visible,  but  rarely  palpable,  pulsation  near  the  ensiform  cartilage  or  in  the 
epigastrium.  Care  must  be  taken  that  overlying  lung  does  not  lead  to  an 
erroneous  belief  as  to  the  presence  of  cardiac  feebleness.  If  the  whole  hand 
is  placed  over  the  disturbed  surface  of  the  prsecordium  it  is  remarkable  how 
little  impulse  is  discernible.  Percussion  shows  an  increase  in  the  area  of 
cardiac  dulness  to  the  left,  to  the  right,  and  downward.  Often  it  is  also 
increased  upward. 

On  auscultation  the  first  sound  of  the  heart  may  be  short  and  small, 
valvular  and  flapping,  though  fairly  loud,  and  if  the  heart  is  strong  enough 
there  may  be  a  systolic  murmur  at  the  apex,  due  to  mitral  regurgitation 
arising  from  stretching  of  the  mitral  orifice.  As  in  ruptured  compensatory 
hypertrophy  the  sounds  of  the  heart  may  be  equalized  and  the  space  between 
them  may  be  altered  so  that  the  sounds  are  like  those  of  the  fetal  heart 
or  like  the  ticking  of  a  watch.  In  other  cases  the  first  and  second  sounds 
may  occur  close  together  and  the  diastolic  pause  be  prolonged.  Very  often 
great  arhythmia  is  present.  If  in  addition  to  these  signs  there  is  a  history 
of  acute  strain  near  or  remote,  or  symptoms  of  cardiac  feebleness,  and 
particularly  if  the  onset  has  been  sudden,  without  the  presence  of  an  acute 
infection  to  cause  valvular  disease,  the  diagnosis  of  dilatation  may  be  made. 

Prognosis. — ^The  prognosis  depends  upon  the  degree  of  the  dilatation,  the 
state  of  the  vessels  and  of  the  heart  muscle  and  of  the  kidneys,  and  last, 
but  not  least,  the  lungs.  When  the  latter  are  filled  with  rales  the  state  is 
alarming,  and  if  the  vessels  and  kidneys  are  diseased  the  outlook  is  hopeless 
for  much  betterment.  If  the  state  of  the  vessels  and  the  general  condition 
of  the  patient  indicate  fatty  myocardial  degeneration  the  prognosis  is  also 
bad.  If  these  states  are  absent,  and  rest  can  be  maintained,  distinct  improve- 
ment can  be  hoped  for,  but  a  complete  cure  in  the  sense  of  old-time  vigor  is 
rarely  reached. 

Treatment, — The  treatment  is,  first  of  all,  rest  in  bed,  or  in  an  easy  chair 
if  bed  is  impossible  because  of  orthopnoea.  The  second  object  to  be  gained 
is  the  removal  of  the  cause  of  the  dilatation,  if  that  be  possible,  as  the  reduc- 
tion of  high  arterial  tension  by  the  use  of  nitroglycerin.  Third,  the  employ- 
ment of  digitalis  and  strychnine  for  effect,  recalling  the  fact  that  once  this 
drug  has  produced  its  action  smaller  doses  will  maintain  its  influence,  and 
also  bearine;  in  mind  the  additional  fact  that  when  it  is  in  full  effect  sudden 


DISEASE   OF   THE  MYOCARDIUM  473 

changes  of  posture  are  dangerous,  and  that  it  may  cause  so  much  ventricular 
stimulation  as  to  overdistend  the  auricles,  which  are  poorly  protected  by 
the  relaxed  mitral  ring. 

When  the  lungs  and  kidneys  are  engorged,  the  application  of  several  dry 
cups  over  them  is  useful,  and  if  jugular  distention  and  hepatic  congestion  is 
marked,  the  patient  may  be  freely  bled  if  he  is  plethoric.  So,  too,  hydra- 
gogue  cathartics,  such  as  jalap  and  compound  extract  of  colocynth,  may 
be  used  to  unload  the  bowels  and  liver,  but  care  must  be  taken  that  the 
patient  is  not  exhausted  by  purging.  Blue  mass  in  the  dose  of  8  grains 
once  a  week  is  useful,  and  the  pill  of  calomel,  squill,  and  digitalis  men- 
tioned under  Endocarditis  may  be  used.  If  ascites  is  a  pressing  symp- 
tom tapping  is  indicated,  while  for  general  anasarca  the  formula  given 
under  Endocarditis,  or  apocynum  cannabinum  may  be  used,  or  the  digi- 
talis given  more  liberally. 

The  diet  should  be  light  and  nutritious,  and  often  it  is  well  to  give  pan- 
creatized  foods  or  starches  with  taka-diastase.  Great  care  must  be  taken 
that  the  stomach  is  not  distended  by  food  or  drink,  and  if  gas  accumulates 
in  the  stomach  it  should  be  expelled  by  the  use  of  Hoffmann's  anodyne  in 
drachm  doses,  and  by  the  employment  of  a  turpentine  stupe.  When  dyspnoea 
is  urgent  morphine  and  strychnine  are  useful  drugs. 

High  altitudes  should  be  carefully  avoided  and  only  gentle  exercise  on 
level  ground  be  allowed. 


DISEASE  OF  THE  MYOCARDIUM. 

Disease  of  the  myocardium  may  be  divided  into  two  classes,  viz.,  degenera- 
tive and  inflammatory. 

Degenerative  Changes.  Etiology  and  Pathology. — The  degenerative  con- 
ditions are  as  follows:  In  the  granular  form,  sometimes  called  "parenchy- 
matous degeneration,"  there  develops  in  the  protoplasm  of  the  cardiac 
muscle  fibres  albuminous  granules  which  differ  in  size  and  in  number, 
and  may  be  present  in  such  an  excess  as  to  obscure  the  nuclei  and  striae. 
The  affected  muscle  is  cloudy,  softened,  and  paler  than  in  health,  its  strength 
decreased,  and  the  circulation  is  proportionately  depressed.  In  a  later  stage 
some  degree  of  fatty  degeneration  may  also  be  present. 

This  type  of  degeneration  is  observed  in  the  course  of  acute  infectious 
diseases,  as  diphtheria,  typhoid  and  typhus  fever,  the  pyaemias,  and  even 
as  a  result  of  severe  burns,  and  in  debilitating  conditions  associated  with 
severe  cardiac  work  or  the  presence  of  toxic  bodies  in  the  blood. 

In  fatty  degeneration  of  the  heart  the  affected  fibres  contain  fat-globules, 
which,  in  marked  cases,  replace  the  structural  elements,  both  the  nuclei  and 
protoplasm.  In  some  instances  this  degenerative  process  is  restricted  to  a 
single  focus,  or  it  may  be  scattered  about  or  diffuse;  in  others  it  is  universal. 
When  the  heart  is  examined  at  autopsy  it  is  seen  to  be  mottled  and  the 
papillary  muscles  in  particular  will  reveal  the  fatty  areas,  the  so-called 
"Tiger  Herz"  of  the  Germans. 

Diffuse  fatty  degeneration  is  caused  by  prolonged  nutritional  disorders. 


474  DISEASES  OF   THE  HEART 

Pernicious  anaemia  and  leukgemia  may  also  cause  it,  as  may  poisoning  by 
arsenic,  phosphorus,  and  antimony.  Less  commonly  it  is  a  sequence  of 
various  acute  infectious  diseases  like  diphtheria  and  scarlet  fever  or  typhoid 
fever,  and  by  degenerative  or  atheromatous  changes  in  the  coronary  arteries. 
The  local  or  circumscribed  forms  follow  embolism  or  other  types  of  rapidly 
developed  coronary  occlusions. 

It  is  important  that  fatty  degeneration  be  clearly  separated  from  fatty 
infiltration,  in  which  state  the  muscle  fibres  are  not  altered,  but  have  been 
separated  by  the  projection  of  fatty  masses  between  them.  This  may  cause 
some  wasting  or  atrophy  of  the  muscle  fibres.  This  state  is  most  commonly 
met  with  in  very  fat  persons  and  in  those  who  are  addicted  to  excessive 
beer-drinking.  Occasionally  forms  of  amyloid  and  hyaline  degeneration  of 
the  heart  fibres  occur. 

Brown  induration  or  atrophy  of  the  heart  is  often  seen  in  cases  of 
chronic  valvular  disease  and  in  old  persons.  The  muscle  is  more  dense 
than  normal  and  reddish-brown  in  hue,  and  about  its  nuclei  brown  pig- 
ment is  deposited.  Calcareous  degeneration,  in  which  the  muscle  fibres 
become  infiltrated  with  lime  salts,  is  rare. 

Under  the  name  of  fragmentation  and  segmentation  there  is  seen  a  state 
of  the  heart  muscle  in  which  its  fibres  are  broken  across  in  fragments,  or 
its  cells  are  separated  at  the  point  of  junction  (segmented).  These  changes 
may  occur  in  acute  infectious  diseases  or  in  cases  of  central  nervous  dis- 
ease. In  some  cases  they  are  probably  agonal,  and  it  may  be  that  similar 
appearances  are  of  postmortem  origin,  but  the  frequency  with  which 
granular  change  is  seen  at  autopsy  strongly  indicates  that  it  may  be 
present  and  unrecognized  in  life,  not  only  in  fatal  cases,  but  in  those 
who  recover. 

Symptoms  of  Myocardial  Degeneration. — The  symptoms  of  degeneration 
of  the  heart  of  the  albuminous  type  cannot  be  considered  as  pathognomonic. 
Indeed,  there  may  be  no  evidence  of  cardiac  failure  until  a  sudden  and 
perhaps  fatal  attack  of  syncope,  after  a  slight  exertion,  reveals  the  alarming 
state  of  the  heart  muscle.  In  other  instances  the  feeble  cardiac  sounds  on 
auscultation  indicate  the  real  condition  of  the  heart. 

When  fatty  degeneration  is  present  the  same  absence  of  symptoms  may 
exist  until  the  final  fatal  syncope,  or  the  patient  may  suffer  from  repeated 
attacks  of  syncope,  or  of  vertigo  with  anginoid  seizures.  (See  Stokes-Adams 
Disease,  page  475.)  The  frequency  and  severity  of  these  attacks  are, 
however,  by  no  means  in  direct  proportion  to  the  extent  of  the  lesion  in 
the  heart  muscle.  In  one  instance  a  fatal  syncope  occurs,  yet  the  heart 
scarcely  seems  altered  in  its  fibres.  In  another  case  the  life  of  the  patient 
persists  and  fairly  good  health  is  maintained  for  years,  yet  at  autopsy  the 
heart  muscle  is  so  fatty  and  soft  that  the  fingers  can  be  pushed  through  it 
as  if  it  were  wet  paper. 

In  some  instances  the  symptoms  complained  of  by  the  patient  seem  to 
be  epigastric  and  due  to  disordered  digestion.  How  often  do  we  hear  of  a 
man  of  advanced  years  dying  of  acute  indigestion,  which  is  really  cardiac 
failure  with  gastric  symptoms,  or  cardiac  failure  caused  by  an  overdistended 
stomach. 


DISEASE  OF  THE  MYOCARDIUM  475 

The  heart  sounds  when  the  patient  is  in  his  average  state  of  health  are 
distant  and  feeble,  and  his  slow  pidse  is  small  and  of  low  tension.  Not 
rarely  his  radial  and  temporal  arteries  are  very  calcareous,  but  in  other 
cases  they  are  soft  and  devoid  of  resistance  on  pressure. 

There  still  remains  to  be  considered  several  notable  facts  in  connection 
with  this  disease.  Notwithstanding  the  great  feebleness  of  the  heart  in 
some  cases  and  the  exceedingly  weak  circulation  of  blood,  dropsy  in  any 
form  is  a  very  rare  condition.  Indeed,  if  dropsy  occurs  it  is  certainly  due 
to  some  complicating  state.  A  second  fact  is  that  in  some  cases  in  place 
of  anginoid  attacks  an  epileptiform  or  apoplectiform  seizure  occurs.  The 
epileptiform  seizure  is  not  that  of  grand  mal,  but  petit  mat,  with  this  differ- 
ence, that  while,  as  in  petit  mal,  there  are  no  convulsions,  there  is  a  period 
of  profound  unconsciousness  which  is  rather  a  syncope  than  a  coma,  such  as 
is  seen  in  true  epilepsy. 

The  apoplectiform  seizures  may  very  closely  resemble  true  cerebral 
hemorrhage,  even  to  the  stertorous  breathing,  the  hemiplegia,  the  uncon- 
sciousness, and  Cheyne-Stokes  respirations.  That  the  case  is  not  one  of 
apoplexy  is  usually  proved  by  finding  that  the  high-tension  pulse  of  cerebral 
hemorrhage  is  absent  and  replaced  by  the  low  tension  and  slow  pulse  of 
fatty  degeneration. 

Prognosis  of  Myocardial  Degeneration.^ — The  prognosis  in  all  cases  of 
cardiac  degenerative  change  is,  of  course,  very  grave.  When  it  is  present 
in  children  after  acute  infectious  diseases  recovery  may  ensue  under  a 
course  of  arsenic,  phosphorus,  and  nux  vomica,  with  absolute  rest,  and 
fresh  air  and  sunshine,  but  even  in  this  class  of  cases  sudden  death  often 
intervenes.  In  the  fatty  heart  of  advanced  age,  whether  the  years  be  great 
or  the  patient  prematurely  old,  the  outlook  is  bad;  but  as  no  one  can  tell 
the  extent  of  the  lesions  in  the  heart,  a  statement  as  to  a  brief  duration 
of  life  is  very  prone  to  bring  the  physician's  opinion  into  discredit  if 
he  attempts  to  name  the  time  of  dissolution.  The  wise  physician  rarely 
expresses  a  positive  opinion  as  to  the  probable  time  of  death  in  any  case, 
much  less  in  fatty  heart. 

Stokes-Adams  Disease. — Cases  of  extreme  slow  pulse  with  vertigo,  or 
syncope,  or  apoplectiform  or  epileptiform  seizure,  have  been  given  the 
name  of  the  "Stokes-Adams  syndrome." 

Associated  with  the  slowness  of  the  pulse  there  is  marked  pulsation  in 
the  veins  of  the  neck,  and  to  use  Stokes'  own  words,  written  in  the  Dublin 
Quarterly  Journal  of  Medical  Science  in  1846,  the  number  of  reflex  pulsa- 
tions is  difficult  to  be  estabhshed,  but  they  are  more  than  double  the 
number  of  the  manifest  ventricular  contractions.  Experimental  and  clinical 
studies  by  Erlanger  {Journal  of  Experimental  Medicijie,  vol.  vii..  No.  6, 
November  25,  1905,  pp.  676-724,  and  vol.  viii.,  No.  1,  January  25,  1906, 
pp.  8-58),  with  clinical  and  autopsy  findings  by  Stengel  and  others,  indicate 
that  the  symptom-complex  in  most  if  not  all  cases  of  this  condition  is  due 
to  what  is  now  denominated  "heart -block."  In  this  state  the  auricles 
beat  two,  three,  or  four  times  as  rapidly  as  do  the  ventricles.  Erlanger 
has  repeatedly  produced  at  will  any  particular  rhythm  or  even  entire  in- 
dependence  of  the   auricular  and  ventricular  contractions   in   the  dog  by 


476  DISEASES  OF  THE  HEART 

varying  mechanical  compression  of  the  auriculo-ventricular  muscle  bundle 
of  His.  This  muscle  bundle,  wliich  is  17  to  20  mm.  long,  2.5  mm.  wide, 
and  1.5  mm.  thick,  extends  from  a  point  in  the  auricular  septum  below 
the  foramen  ovale  downward  through  the  auriculo-ventricular  junction  and 
terminates  in  the  ventricular  septum  a  short  distance  below  the  beginning 
of  the  aorta.  The  impulse  which  causes  ventricular  contraction  appears 
to  be  transmitted  from  the  auricles  to  the  ventricles  through  this  bundle 
and  consequently  lesions  affecting  it  lead  to  slowing  of  the  ventricle,  ^^^len 
the  latter  chambers  cease  beating  for  some  seconds  syncope  ensues.  Most 
cases  of  Stokes-Adams  disease  appear  to  be  primarily  arteriosclerotic  or 
syphilitic  in  natm'e  though  myocardial  lesions  of  other  origin  may  be  the 
cause.  Autopsy  in  some  reported  cases  has  shown  no  evident  lesion  and 
these  have  been  pronounced  neurotic  in  character,  Erlanger  states,  how- 
ever, that  as  yet  there  has  been  described  no  typical  case  of  Stokes-Adams 
disease  which  might  not  have  been  caused  by  heart-block.  A  point  to  be 
noted  in  autopsies  upon  cases  of  this  disease  is  whether  lesions  of  the 
mesial  leaflet  of  the  tricuspid  valve  can  interfere  with  the  integrity  of  the 
m.uscle  bundle  of  His. 

Myocarditis.  Definition, — This  term  is  an  unfortunate  one  in  that  it  is 
often  loosely  applied  to  the  degenerative  changes  just  described  as  well 
as  to  those  about  to  be  mentioned.  It  is  also  unfortunate  because  it  seems 
to  indicate  that  there  is  a  primary  inflammatory  state  of  the  cardiac  muscle 
fibres,  whereas  the  changes  in  the  fibres  are  secondary  to  inflammatory 
affections  of  the  interstitial  tissues  of  the  heart  and  of  its  bloodvessels,  which 
thereby  cause  atrophic  and  degenerative  changes  in  the  muscle. 

There  are  several  forms  of  so-called  myocarditis,  of  wliich  the  most  com- 
mon is  a  slow,  low-grade  inflammatory  change  called  chronic  interstitial 
myocarditis,  manifested  by  a  wasting  of  the  muscle  fibres  and  the  inter- 
calation of  fibrous  or  fibroelastic  tissues.  There  is  also  an  acute  process, 
acute  interstitial  myocarditis,  of  which  there  are  suppurative  and  non- 
suppurative varieties,  the  former  being  a  manifestation  of  pyogenic 
infection  of  the  heart  wall. 

In  the  great  majority  of  cases  the  chronic  form  is  the  result  of  patho- 
logical changes  in  the  coronary  arteries.  These  vessels  suffer  from  an 
obliterative  arteritis  in  their  finer  branches,  undergo  atheromatous  change, 
or  become  plugged  by  an  embolus  or  thrombus.  The  lesions  which  result 
from  these  changes  differ  widely  in  character,  but  all  greatly  impair  the 
usefulness  of  the  heart.  In  all  conditions  lessening  the  vascular  lumen  and 
so  decreasing  the  nutrition  of  the  heart,  there  develops  an  overgrowth  of 
interstitial  tissue  with  atrophy  of  the  muscle  fibres.  It  is  probable  that 
the  process  is  at  no  time  a  true  inflammation,  but  rather  one  in  which 
diminished  blood  supply  causes  atrophy  of  the  muscle,  followed  by  a  substi- 
tutive fibrosis. 

When  a  branch  of  a  coronary  artery  is  plugged  the  affected  area  may 
manifest  the  changes  seen  in  an  infarct,  or  when  enough  nourishment  is 
available  to  prevent  actual  necrosis  the  deficient  nutrition  gives  rise  to 
fatty  degeneration.  In  either  case  the  affected  area  may  become  softened, 
and  give  way,  causing  rupture,  or  fibrous  tissue  gradually  takes  the  place  of 


DISEASE  OF  THE  MYOCARDIUM  477 

the  degenerated  fibres.  Later  the  scar  tissue  yields  to  pressure  and  a  cardiac 
aneurysm  ensues. 

Hypertrophied  hearts  may  show  a  shght  increase  in  the  fibrous  tissue, 
and  in  faihng  compensation  and  progressing  dilatation  this  increase  in 
interstitial  tissue  may  be  conspicuous. 

In  some  instances  chronic  myocarditis  is  not  the  result  of  vascular 
change,  but  of  inflammatory  processes  in  the  pericardium  and  endocardium; 
and  in  syphilis  there  is  often  seen  a  marked  increase  in  the  interstitial 
tissues  of  the  heart,  which  is  not  surprising  in  view  of  the  serious  changes 
produced  by  this  disease  in  the  small  bloodvessels  everywhere.  Chronic 
myocarditis  is  more  common  in  males  than  in  females. 

Symptoms  of  Myocarditis. — The  iinmediate  efl^ects  upon  the  patient  produced 
by  the  lesions  just  named  vary  to  an  extraordinary  degree.  Plugging  of 
one  of  the  large  branches  of  a  coronary  artery  usually  results  in  sudden 
death. 

In  some  instances,  however,  the  patient  survives  a  severe  attack  of  cardiac 
disturbance,  but  under  these  circumstances  the  plugging  is  usually  in  a 
small  vessel,  and  a  gradual  substitution  circulation  is  established,  not  by 
anastomosis,  for  these  vessels  are  end  arteries,  but  by  the  so-called  ves- 
sels of  Thebesius,  which  in  some  cases  are  able  to  supply  the  heart  with  an 
adequate  quantity  of  blood. 

When  the  closure  of  the  vessel  is  gradual  it  not  rarely  happens  that 
necrosis  of  the  area  deprived  of  blood  is  prevented  by  a  blood  supply 
through  the  vessels  of  Thebesius,  so  that  the  death  of  the  patient  is  post- 
poned until  a  very  extraordinary  degree  of  atheroma  and  narrowing  in 
both  coronary  arteries  is  developed.  The  coronary  arteries  of  a  well- 
known  member  of  the  medical  profession  in  Philadelphia,  who  died  a  few 
years  since,  were  so  diseased  that  only  a  thread-like  passageway  existed  in 
these  vessels,  yet  he  led  an  active  life  to  the  end.  Such  patients  may  have 
no  marked  cardiac  symptoms,  but,  as  a  rule,  repeated  attacks  of  angina 
pectoris  of  increasing  intensity  give  warning  of  the  sudden  death  to  come. 
The  other  symptoms  are  the  same  as  those  described  under  fatty  degen- 
eration of  the  heart. 

The  physical  signs  of  myocardial  degeneration  are  feebleness  of  the 
apex  beat,  equalization  of  the  first  and  second  sounds  of  the  heart,  and 
evidences  of  feeble  circulation  in  the  lungs  and  in  the  peripheral  systemic 
vessels. 

The  prognosis  depends  entirely  upon  the  situation  and  the  degree  of  the 
cardiovascular  change.  So  far  as  recovery  is  concerned,  that  is  impossible. 
The  probable  duration  of  life  is  also  difficult  to  determine.  Many  cases 
with  all  the  symptoms  of  severe  myocarditis  live  a  long  period,  while  others 
die  with  unexpected  suddenness. 

Treatment. — We  cannot  expect  very  much  from  treatment  in  patients 
suffering  from  chronic  myocarditis.  It  must  be  evident  from  what  has 
been  said,  under  the  discussion  of  the  pathological  conditions  which 
cause  these  states,  that  the  harm  is  done  before  the  physician  has  an 
opportunity  to  place  the  patient  under  treatment.  The  only  hope  is 
that  by  regulating   the    manner  of    life,  by  increasing  the  action  of    the 


478 


DISEASES  OF  THE  HEART 


kidneys,  if  they  are  sluggish,  by  attending  to  tlie  digestive  apparatus, 
and  by  preventing  undue  cardiac  strain  through  excessive  muscular  or 
mental  exercise,  we  may  be  able  materially  to  prolong  the  patient's  life. 
In  instances  in  which  the  bloodvessels  are  distinctly  atheromatous  or 
fibroid,  the  use  of  the  iodide  of  strontium  or  sodium,  in  doses  varying  from 
10  to  40  grains  three  times  a  day,  is  usually  advantageous.  This  treat- 
ment may  be  continued  for  several  weeks,  and  then  the  patient  may 
receive  a  course  of  Fowler's  solution  as  a  general  tonic,  with  perhaps  a 
small  quantity  of  nux  vomica  or  strychnine  added  to  it. 

If  arterial  tension  is  high,  he  should  be  given  nitroglycerin  in  doses  vary- 
ino-  from  ywo  to  gV  o^  ^  grain  tlu'ee  or  four  times  a  day,  in  order  that  the 
resistance  which  is  offered  by  tense  vessels  to  the  action  of  the  heart  may  be 
lessened.  Under  these  circumstances,  too,  small  doses  of  digitalis  sometimes 
act  advantageously,  particularly  if  nitroglycerin  is  given  at  the  same  time. 
To  give  digitalis  to  a  failing  heart  and  yet  to  permit  the  arterial  tension 
to  remain  high  is  of  little  ultimate  advantage  to  the  patient,  since  it 
increases  the  labor  of  the  heart  without  material  advantage.  It  is  much 
more  important  to  diminish  the  labor  by  the  use  of  nitroglycerin  than  to 
stimulate  this  viscus  to  increased  endeavor  by  large  doses  of  foxglove. 
Five  minim  doses  of  tincture  of  cactus  grandiflora  often  do  much  good  under 
these  circumstances.  It  must  be  remembered  that  if  the  heart  has  under- 
gone distinct  degenerative  changes  there  is  little  muscular  fibre  upon  which 
the  digitalis  may  exert  its  stimulating  influence,  and  there  may  be  danger 
by  increasing  intracardiac  pressure  of  causing  rupture  of  some  area  of  white 
necrosis,  thereby  causing  cardiac  aneurysm. 

It  is  hardly  necessary  to  add  that  these  patients  should  be  warned  against 
excessive  muscular  exercise  or  any  severe  cardiac  strain,  and  they  should 
be  advised  to  he  down  and  rest  several  times  a  day,  in  order  that  the 
heart  may  at  each  period  of  rest  recover  as  much  strength  as  possible. 

Digestive  disturbances,  which  by  accumulation  of  gas  may  disturb  the 
action  of  the  heart,  must  be  prevented  by  the  institution  of  an  easily  digested 
and  simple  diet,  small  quantities  of  food  being  taken  often  so  as  to  avoid 
overloading  the  stomach.  If  there  is  a  tendency  to  an  accumulation  of 
o-as  in  the  bowel  salol  may  be  given  as  an  intestinal  antiseptic,  or  in  its 
place  the  capsule  of  taka-diastase,  pancreatin,  nux  vomica,  and  capsicum, 
which  is  recommended  in  the  article  on  Angina  Pectoris,  may  be  adminis- 
tered. Some  of  these  patients  seem  to  be  greatly  benefited  by  the  use  of 
gentle  massage  every  day  or  every  other  day,  with  the  object  of  aiding  in 
the  circulation  of  the  juices  of  the  body.  Great  care  should  be  taken  that 
the  massage  is  not  so  vigorous  that  the  patient  is  fatigued  by  it.  Strychnine 
in  the  dose  of  ^  of  a  grain  three  or  four  times  a  day  is  often  exceedingly 
beneficial  to  these  patients,  particularly  if  there  is  any  tendency  to  shortness 
of  breath  on  lying  down. 

In  many  instances  when  the  heart  is  feeble  as  the  result  of  fibroid  changes 
in  its  muscle,  or  when  the  patient  is  convalescing  from  some  disease  hke 
influenza,  which  seriously  impairs  the  functional^  activity  of  this  organ, 
excellent  results  are  sometimes  obtained  by  the  institution  of  what  is  known 
as  the  Nauheim  baths,  which  were  originally  brought  before  the  profession 


CARDIAC  ANEURYSM  479 

by  Schott,  of  Nauheim  in  Germany.  These  baths  are  composed  of  water 
which  is  charged  by  nature  with  large  quantities  of  carbonic  acid  gas. 
The  water  is  also  naturally  warm.  The  patient  is  immersed  in  a  bathtub, 
and  immediately  there  is  attached  to  the  surface  of  his  skin  myriads  of 
tiny  bubbles  of  carbonic  acid  gas,  which  as  they  break  produce  a  slight 
tingling  sensation  and  exercise  a  stimulant  influence  upon  the  peripheral 
capillaries,  as  the  result  of  which  these  capillaries  are  dilated  and  dermal 
hypersemia  is  induced.  In  this  manner  the  circulation  is  equalized,  internal 
congestions  are  overcome,  and  the  heart  finds  it  easier  to  pump  blood  through 
the  dilated  superficial  capillaries  than  under  ordinary  conditions.  Not 
infrequently  when  the  patient  first  enters  the  bath  a  primary  contraction 
of  the  peripheral  capillaries  ensues,  and  this  results  in  a  momentary  increase 
in  the  work  of  the  heart,  so  that  the  patient  for  a  time  feels  somewhat 
oppressed.  Usually  he  remains  in  the  tub  for  ten  or  fifteen  minutes,  but 
this  period  is  governed  by  the  physician  who  superintends  the  use  of  the 
baths.  On  his  removal  from  the  bath  the  patient  is  carefully  dried  by  an 
attendant  and  has  absolute  rest  for  one  or  two  hours.  After  the  baths  have 
been  used  for  some  time  additional  salt  is  added  to  the  bath,  and  water 
containing  larger  quantities  of  gas  is  employed.  In  addition  to  these  baths 
the  patients  are  subjected  to  gentle  resistance  movements  and  massage  so 
as  to  improve  the  circulation  of  blood  and  lymph  in  the  muscles.  Great 
care  must  be  taken  that  these  movements  are  not  sufficient  to  tire  the 
heart.  When  valvular  disease  is  very  marked,  these  baths  are  contra- 
indicated. 

The  Nauheim  baths  are  also  contraindicated  in  cases  of  advanced  arterio- 
sclerosis, and  in  chronic  Bright's  disease  if  it  is  well  developed,  although  if 
the  renal  difficulty  is  largely  due  to  congestion  this  plan  of  treatment  is 
advantageous.  Aneurysm  also  contraindicates  them,  and  bronchial  asthma 
and  chronic  bronchitis  contraindicate  them,  or  at  least  require  great  caution 
in  their  use.  Cases  of  pulmonary  tuberculosis  with  cardiac  disease  also 
should  not  be  subjected  to  this  method,  nor  should  patients  who  are  suffer- 
ing from  far-advanced  degeneration  of  the  heart  muscle  receive  it.  These 
baths  should  never  be  taken  except  under  the  care  of  a  local  physician. 

Attempts  have  been  made  to  introduce  artificial  Nauheim  baths  in  this 
country,  but  it  has  been  found  impossible  to  satisfactorily  charge  the  water 
with  carbonic  acid,  and  the  difficulties  connected  with  the  preparation 
of  the  bath  have  been  such  that  its  employment,  except  at  Nauheim,  has 
largely  passed  out  of  use. 

It  is  important  to  note  that  the  resistance  exercises,  which  are  carried  out 
in  connection  with  this  plan  of  treatment,  are  probably  equally  beneficial, 
if  not  more  beneficial,  than  the  baths  themselves.  They  consist  in  having 
the  patient  extend  and  flex  his  joints  against  the  resistance  offered  by  the 
attendant. 

CARDIAC  ANEURYSM. 

Aneurysm  of  the  heart  may  occur  in  one  of  three  forms,  \az.,  aneurysm  of 
the  heart  walls,  aneurysm  of  the  valves,  and  aneurysm  of  the  coronary  arte- 
ries.    Aneurysm  of  the  cardiac  walls  consists  in  a  localized  dilatation  or 


480 


DISEASES  OF   THE  HEART 


Fig.  67 


pouching  of  the  wall,  and  is  to  be  separated  from  dilatation  of  the  heart,  to 
which  the  term  aneurysm  is  sometimes  applied  by  French  writers.  The 
aneurysm  usually  affects  the  ventricular  wall.  Hall  has  recently  collected  112 
cases,  in  which  the  site  of  the  aneurysm  was  as  follows :  left  ventricle,  92 
cases;  right  ventricle,  1  case;  left  auricle,  2  cases;  ventricular  septum — 
(a)  muscular  part,  8  cases;  (b)  membranous  part,  7  cases;  auricular  septum, 
2  cases. 

The  left  ventricle  is  therefore  affected  more  commonly  than  all  of  the 
other  chambers  combined.  The  aneurysm  is  usually  near  the  apex  of  the 
ventricle  or  in  the  anterior  wall,  just  above  the  apex;  67  of  Hall's  cases  were 
so  situated. 

The  condition,  as  one  would  naturally  expect,  is  found  more  frequently  in 
males.  In  the  relative  frequency  in  the  two  sexes,  Thurnam's,  Legg's,  and 
Hall's  and  my  own  statistics  show  a  remarkable  resemblance.  Of  Thur- 
nam's 40  cases,  30  were  males,  10  females;  of  Legg's  88  cases,  64  were  males, 
24  females;  and  of  80  cases  collected  by  me,  59  males,  21  females.  In  a 
total  of  208  cases,  74  per  cent,  were  males,  and  26  per  cent,  females. 

Aneurysm  of  the  heart  is  a  sequel  of  the  secondary  myocardial  changes 
already  described.    Thus  the  fibrous  tissue  which  replaces  the  tissues  which 

have  undergone  necrotic  change  may  gradu- 
ally yield  before  the  blood  pressure  in  the 
ventricle  and  form  a  sac,  which  is  a  true 
aneurysmal  dilatation.  This  sac  may  com- 
municate with  the  ventricle  by  a  small  open- 
inff.  In  other  cases  the  ventricular  wall  at 
this  point  yields,  so  that  the  opennig  may 
be  the  full  width  of  the  sac.  As  in  aneu- 
rysm of  the  bloodvessels,  the  wall  of  the  sac 
is  composed  of  several  layers  made  up  of 
the  visceral  layer  of  the  pericardium,  and 
perhaps  of  the  parietal  layer  as  well,  if  it 
has  become  adherent.  Under  this  is  the 
fibrous  tissue,  and  beneath  this  again  form- 
ing the  inner  layer  is  the  endocardium. 
Rarely  several  sacs  are  present. 

Three  conditions  may  develop  in  such 
sacs.  They  may  give  way  under  pressure, 
causing  sudden  death,  they  may  become 
filled  with  a  clot,  or  their  walls  may  be 
calcified.  Sometimes  an  aneurysm  of  this 
sort  forms  in  the  septum  and  ruptures  into 
the  right  ventricle. 

In  some  cases  the  aneurysm  may  be  due 
to  fatty  degeneration,  without  primary  vas- 
cular disease.  A  softened  spot  in  the  heart 
muscle  may  bulge  under  strain,  and  rupture 
may  occur  before  any  real  sac  is  formed. 
This   is   commonly  called  rupture  of   the 


Front  view  of  heart,  showing  aneu- 
rysm of  left  apex  of  ventricle,  which  has 
perforated  into  the  pericardium.  The 
swelling  of  the  aneui-ysm  is  visible  ex- 
ternally, and  the  heart  wall  at  the  apex 
is  no  thicker  than  brown  paper.  No 
pericardial  adhesion.  The  interventric- 
ular branch  of  the  left  coronary  artery 
is  dissected  out,  and  is  very  atheroma- 
tous, and  at  the  upper  end  of  the  groove 
is  completely  blocked  by  a  thrombus, 
■which  extends  dotvnward  for  t-wo  and 
one-half  inches.  (From  a  specimen  in 
Dr.  Littlejohn's  Museum.) 


ENDOCARDITIS  481 

heart,  and  usually  involves  the  anterior  wall  of  the  left  ventricle  near  the 
septum;  but  it  may  affect  any  part  of  the  walls  of  the  cardiac  cavities. 

Death  by  rupture  of  the  sac  does  not  occur  as  frequently  as  would  be 
imagined,  and  in  this  respect  cardiac  aneurysm  resembles  aortic  aneurysm. 
Out  of  60  cases  collected  by  Legg,  only  6  died  by  rupture. 

Aneurysms  of  the  cardiac  septa  are  so  rare  as  to  be  curiosities.  Hall  states 
that  only  2  cases  have  been  reported  in  twenty  years. 

An  aneurysm  of  a  valve  is  sometimes  formed  as  a  result  of  endocarditis. 
This  condition  usually  affects  the  aortic  and  mitral  leaflets  with  about  equal 
frequency.  One  leaflet  is  contracted  or  destroyed  and  another  leaflet  then 
yields  or  sags,  partly  because  of  deficient  support,  forming  a  pocket  or  sac 
which  projects  into  the  left  ventricle.  Sometimes  this  sac  ruptures,  and  so 
the  valve  becomes  perforated.  In  other  instances  the  entire  valve  becomes 
sacculated. 

Although  atheroma  of  the  coronary  arteries  is  a  very  frequent  lesion,  aneu- 
rysm of  these  vessels  is  exceedingly  rare.  Hall  could  find  only  25  recorded 
cases,  of  which  17  were  in  males. 

Symptoms. — The  symptoms  of  cardiac  aneurysm  are  not  definite  at  any 
time,  and,  unless  the  sac  is  large,  there  may  be  none.  Hall  tells  us  that  out 
of  76  cases  an  antemortem  diagnosis  was  made  only  once.  When  the  sac  is 
large  it  may  cause  a  marked  increase  in  the  area  of  cardiac  dulness  near  the 
apex,  and  produce  distinct  pressure  symptoms.  A  skiagraph  may  give  valuable 
information  of  the  lesion. 

WOUNDS  OF  THE  HEART. 

Wounds  of  the  heart  are  by  no  means  uncommon,  as  the  result  of  shooting 
or  stabbing.  Cases  of  recovery  after  both  of  these  forms  of  trauma  are 
recorded  in  considerable  number.  The  stab  wounds  probably  recover  in 
greater  number  than  those  which  suffer  from  bullet  wounds.  Death  is 
usually  due  not  to  the  direct  injury  of  the  heart,  but  to  the  fact  that  the  peri- 
cardial sac  soon  becomes  filled  with  blood,  and  the  heart  is  unable  to  expand. 
In  other  words,  even  severe  injury  to  the  heart  is  not  fatal  unless  the  hemor- 
rhage be  free,  or  the  organ  is  damaged  in  some  vital  spot,  as  in  Kronecker's 
"co-ordinating  centre."  I  proved  these  facts  in  a  research  carried  out  on 
dogs  many  years  ago,  and  a  number  of  surgeons  have  now  reported  cases  in 
which  a  stab  wound  of  the  heart  has  been  exposed  and  sutured,  and  recovery 
has  ensued.  Further  than  this,  I  have  seen  the  heart  punctured  and  blood 
aspirated  from  its  cavities  without  injury  to  the  patient. 

Gibbon  and  Stewart,  of  the  Jefferson  College  Hospital  staff,  have  recently 
reported  interesting  cases  in  which  cardiac  wounds  were  stitched  with 
success. 

ENDOCARDITIS. 

Definition. — Endocarditis  in  an  inflammation  of  the  lining  membrane  of 
the  heart,  the  endocardium.     In  the  great  majority  of  instances  it  chiefly 
affects  the  endocardium  where  it  covers  the  valves  (valvular  endocarditis), 
31 


482  DISEASES  OF  THE  HEART 

and  rarely  it  involves,  that  part  which  covers  the  walls  of  the  cavities  (mural 
endocarditis).  A  distinction  should  also  be  drawn  between  the  acute  and 
chronic  form  of  the  disease  and  between  the  acute  simple,  or  benign, 
form,  and  the  so-called  acute  malignant,  or  ulcerative  type.  It  is  proper 
to  state,  however,  that  many  persons  deny  the  correctness  of  this  division, 
and  regard  the  two  conditions  as  different  stages  or  degrees  of  the  same  pro- 
cess. Finally,  it  is  to  be  recalled  that  there  are  two  types  of  chronic  endo- 
carditis, namely,  that  which  Js  the  result  of  the  acute  variety  and  that  which 
arises  in  association  with  chronic  arteriocapillary  fibrosis  and  atheroma, 
which  is  a  slow,  retractile  form  of  the  disease. 

Acute  Endocarditis. — Synonyms:  Verrucous  Endocarditis,  Simple  Endo- 
carditis, Benign  Endocarditis,  Papillary  Endocarditis. 

Etiology. — The  bacterial  origin  of  endocarditis  is  generally  admitted,  but 
all  efforts  to  identify  any  particular  organism  as  the  specific  cause  have 
proved  fruitless.  Many  organisms  have  been  identified  in  the  vegetations. 
Of  these  should  be  mentioned  those  found  in  acute  rheumatism,  pneumo- 
cocci,  streptococci,  and  staphylococci,  and,  less  frequently,  the  colon 
bacillus,  typhoid  bacillus,  influenza  bacillus,  tubercle  bacillus,  and  a  number 
of  other  bacteria. 

In  the  article  on  acute  Articular  Rheumatism  attention  has  already  been 
called  to  the  frequency  with  which  this  condition  complicates  that  malady.  So 
constant  is  this  lesion  during  the  course  of  acute  articular  rheumatism  that  it 
may  be  regarded  as  the  condition  next  in  constancy  to  the  inflammation  about 
the  joints.  It  is  probable  that  in  all  cases  of  acute  rheumatism  a  slight  endo- 
carditis is  present,  but  it  may  be  so  slight  that  no  physical  signs  of  its  exist- 
ence can  be  elicited. 

In  children  suffering  from  acute  rheumatism  the  involvement  of  the 
endocardium  is  far  more  frequent  than  it  is  in  adults.  Thus,  it  is  gener- 
ally considered  that  from  60  to  80  per  cent,  of  children  who  have  acute 
rheumatism  develop  endocarditis;  whereas,  the  percentage  usually  accepted 
for  adults  is  about  21  per  cent.  Eighty  per  cent,  is  probably  too  high, 
and  21  per  cent,  is  certainly  too  low  an  estimate.  It  is  especially  important 
to  bear  in  mind  that  mild  articular  symptoms  are  not  rarely  accom- 
panied by  severe  cardiac  lesions,  although,  as  a  rule,  the  severity  of  the 
articular  symptoms  and  the  severity  of  the  heart  lesions  go  hand  in  hand. 
The  first  attack  of  rheumatic  fever  is  more  frequently  the  cause  of  cardiac 
lesions  than  subsequent  attacks,  and  the  signs  of  endocardial  inflammation 
usually  develop  during  the  first  ten  days  of  the  illness,  although  in  rare  cases 
a  murmur  may  be  heard  before  any  arthritic  signs  develop. 

When  acute  rheumatism  causes  endocarditis,  it  commonly  affects  the 
mitral  valve.  The  aortic  leaflets  are  comparatively  rarely  affected,  and  the 
valves  on  the  right  side  of  the  heart  only  in  very  rare  instances. 

Next  to  acute  rheumatism  as  a  cause  of  acute  endocarditis  must  be  noted 
its  association  with  chorea,  in  which  disease,  in  its  well-developed  and  typical 
forms,  lesions  of  the  lining  membrane  of  the  heart  are  very  often  present. 
The  occurrence  of  endocardial  disease  in  chorea  is  in  direct  proportion  to  the 
severity  of  the  disease,  but  it  is  diflScult  to  decide  how  frequently  true  endo- 
carditis is  actually  present,  because  many  choreic  patients  present  on  auscul- 


ENDOCARDITIS 


483 


tation  functional  murmurs  in  the  heart  which  disappear  so  rapidly  that  it  is 
inconceivable  that  they  could  have  been  organic  in  origin.  Again,  so  few 
cases  of  chorea  come  to  autopsy  during  or  immediately  after  the  attack  that 
it  is  impossible  to  study  the  exact  state  of  the  endocardium.  If  the  various 
statistics  of  frequency  of  heart  murmurs  are  added  together,  we  find  that 
these  sounds  occur  in  about  31  per  cent,  of  cases  of  chorea. 

In  a  very  considerable  proportion  of  cases  endocardial  infection  takes 
place  during  acute  tonsillitis.  Another  cause  of  endocarditis  is  gonor- 
rhoea, which  causes  the  ulcerative  type  of  the  disease  more  commonly  than 


Fig.  68 


Heart,  acute  endocarditis.  The  lesion  on  the  aortic  leaflets  is  verrucose  and  at  points  ulcerating.  On 
the  lateral  ventricular  aspect  of  the  mitral  valves  are  a  number  of  vegetations,  although  the  contact 
line  and  auricular  surfaces  of  this  valve  were  not  involved.  The  vegetations  on  the  ventricular  surface 
probably  resulted  from  inoculation  by  projecting  vegetations  situated  on  the  aortic  leaflet.  It  is  to  be 
remembered  that  endocarditis  affects  the  mitral  valves  more  commonly  than  the  aortic  valves. 


the  benign  form.  Scarlet  fever  may  also  be  a  causative  factor,  but  whether 
this  is  due  to  direct  infection  of  the  endocardium  by  the  micro-organism 
which  causes  scarlet  fever  or  by  its  toxins,  or  results  from  the  mixed  infection 
so  frequent  in  this  disease,  is  not  known.  Rarely  endocarditis  is  apparently 
due  to  tuberculosis,  for  this  bacillus  has  been  found  in  the  valve  lesions. 
Traumatic  forms  and  endocarditis  due  to  syphilis  have  been  described. 
Occasionally  acute  endocarditis  develops  as  a  result  of  an  exacerbation  of 
the  chronic  form  of  the  disease, 


484  DISEASES  OF  THE  HEART 

Endocarditis  has  been  reported  as  present  in  the  foetus  as  a  result  of  the 
infection  of  the  blood  through  the  placenta.  In  this  period  of  existence  the 
pulmonary  valves  are  the  parts  affected. 

Pathology  and  Morbid  Anatomy. — ^The  degree  of  inflammation  in  the  endo- 
cardium covering  the  cardiac  valves  varies  greatly  in  different  cases.  Its 
frequency  on  the  left  side,  particularly  in  the  mitral  valves,  is  due  principally 
to  the  greater  stress  to  which  these  leaflets  are  subjected  and  also  to  the 
higher  oxygen  content  of  the  arterial  blood.  The  lesions  develop  in  the 
auricular  aspect  of  the  mitral  leaflets  and  the  ventricular  side  of  the  aortic 
valves ;  this  distribution  depends  upon  the  friction  and  impact  of  the  blood, 
and  the  same  factors  determine  the  distribution  of  the  vegetations  along  the 
lines  of  greatest  pressure,  where  the  leaflets  impinge  one  upon  another  when 
closed. 

The  earliest  lesions  are  rarely  seen,  because  death  seldom  occurs  at  this 
time.  The  affected  area  is  clouded  and  the  valves  slightly  swollen,  due  to 
cellular  infiltration  and  oedema.  In  this  softened  condition  the  impact  of 
one  valve  upon  another  roughens  the  surface  along  the  hne  of  contact,  and 
there  is  deposited  at  this  point  blood  platelets,  leukocytes,  and  fibrin,  the 
quantity  of  each  varying  at  different  stages  and  in  different  cases.  This 
deposit  on  the  leaflet,  tendon,  or  muscle  is  at  first  microscopic,  but  by  accre- 
tion may  attain  relatively  massive  proportions,  and  constitutes  what  is  called 
a  vegetation;  essentially  it  is  a  thrombus.  Often  a  row  of  these  wart-like 
bodies  is  festooned  along  the  line  of  contact  or  project  into  the  blood  stream. 
Their  disturbance  of  the  blood  current  by  obstruction  and  by  rendering 
accurate  coaptation  of  the  opposed  leaflets  impossible,  and  thereby  permit- 
ting regurgitation,  causes  a  murmur  an  appreciation  of  which  is  necessary 
for  accurate  diagnosis  during  life. 

Once  formed,  these  vegetations  are  subject  to  important  changes.  They 
may  be  detached  and  swept  off  into  the  circulation,  or  they  may  soften  and 
possibly  be  absorbed.  Adhesions  between  leaflets  may  occur,  but  commonly 
the  vegetations  organize  and  permanently  alter  the  contour,  flexibility,  and 
elasticity  of  the  valves,  thereby  interfering  with  their  proper  functions. 
Finally  calcifying  deposits  may  further  add  rigidity  to  the  already  damaged 
leaflets.  In  favorable  cases  the  valve  surface  becomes  smooth,  but  little 
thickening  results,  and  function  is  more  or  less  fully  restored. 

Acute  endocarditis  ends  in  one  of  three  ways:  1.  The  acute  inflammation 
may  subside  and  leave  Httle  or  no  alteration  behind  it.  2.  The  vegetations 
may  persist  and  form  large  masses  of  an  almost  nodular  character  upon  valves. 
3.  The  valves  become  eroded  or  adherent,  or  cicatricial  contractions  may 
lead  to  distortions  and  consequent  immediate  insuflficiency  or  obstruc- 
tion. 

Symptoms. — In  distinction  from  physical  signs,  there  are  no  symptoms  of 
ordinary  acute  endocarditis  of  the  benign  form.  It  is  true  that  the  pulse 
may  be  a  little  quicker  than  before  the  endocardium  was  affected  and  the 
fever  a  little  higher,  but  neither  of  these  symptoms  are  constant  or  character- 
istic. Some  'pal'pitation  may  be  present,  but  so  frequently  are  all  symptoms 
absent  that  all  too  frequently  the  physician  who  is  not  careful  fails  to  dis- 
cover endocardial  disease  until  the  patient  begins  to  move  about  and  com- 


ENDOCARDITIS  485 

plains  of  cardiac  weakness  or  dys'pnoea,  and  then  the  damage  is  done  and  is 
almost  irreparable.  Even  the  presence,  on  physical  examination,  of  a  mur- 
mur over  the  mitral  or  aortic  area  does  not  prove  the  presence  of  endocarditis, 
because  it  not  infrequently  happens  that  a  murmur  due  to  anaemia  or  to 
relaxation  of  the  orifice  is  present.  The  presence  of  the  murmur,  while  not 
pathognomonic  of  acute  endocarditis,  is,  however,  sufiicient  ground  for  the 
physician  to  treat  his  patient  as  a  case  with  this  lesion. 

Complications. — These  consist  most  commonly  of  pericarditis  and  embolism 
of  one  of  the  cerebral  or  pulmonary  arteries.  Rarely  acute  cardiac  dilatation 
ensues,  and  sometimes  in  infectious  cases  pneumonia  and  pleuritis  develop. 

Diagnosis. — Care  must  be  taken,  as  just  stated,  that  anaemic  murmurs, 
murmurs  due  to  relaxation  of  the  orifices,  and  pericardial  friction  sounds  are 
not  mistaken  for  those  due  to  endocardial  disease.     (See  Valvular  Disease.) 

Prognosis. — Death  is  very  rarely  due  to  acute  simple  endocarditis  in  the 
sense  that  death  comes  during  the  acute  stage  of  the  disease.  All  too  fre- 
quently it  follows  as  a  consequence  of  the  changes  produced  in  the  valves  and 
heart  muscle  months  or  years  after  the  acute  stage  has  passed.  A  bad 
prognosis  can  always  be  given  if  the  physician  does  not  strenuously  insist 
upon  the  patient  resting  in  bed  for  several  weeks  after  all  articular  and 
valvular  signs  have  ceased.  Ill-health  and  death  may  not  come  soon  in  these 
cases,  but  it  often  comes  years  afterward,  as  time  and  chronic  disease  weakens 
the  valves  and  heart  muscle.  Children  who  develop  acute  endocarditis  and 
are  permitted  to  move  about  too  soon  almost  always  succumb  before  or  at 
puberty  to  these  secondary  changes. 

Treatment. — To  prevent  endocarditis  in  the  course  of  all  infectious  dis- 
eases, and  particularly  in  acute  rheumatism,  the  physician  must  insist  on 
absolute  rest  in  bed  all  through  the  illness  and  for  some  time  after  the  attack 
has  passed.  The  diet  should  be  light  and  easily  digested,  and  at  no  time 
should  the  digestive  apparatus  be  overburdened,  for  active  and  prolonged 
digestion  tires  the  heart.  If  acute  rheumatism  is  present,  the  salicylates 
should  be  used  freely  at  once,  not  that  they  protect  the  valves  directly,  but  they 
shorten  the  illness  and  so  diminish  the  chance  of  involvement  of  the  endo- 
cardium. Over  the  prsecordium,  as  a  preventive  of  endocarditis  and  peri- 
carditis, should  be  placed  six  or  eight  flying  blisters,  and  alkaline  diuretics, 
like  citrate  of  potassium,  should  be  freely  used.  An  ice-bag  may  be  placed 
over  the  heart  if  it  is  very  irritable,  and  tincture  of  aconite  may  be  given  for 
the  same  purpose.  After  the  endocardial  symptoms  have  developed,  rest 
of  the  most  absolute  character  is  the  only  useful  plan  of  treatment.  During 
convalescence  rest  is  again  the  sine  qua  non.  For  the  anaemia  often  present 
iron  and.  arsenic  are  useful,  as  is  also  cod-liver  oil.  Subsequent  cardiac 
feebleness  is  to  be  treated  by  small  doses  of  digitalis,  as  3  to  5  drops  of  the 
tincture  with  10  drops  of  tincture  of  nux  vomica  three  times  a  day. 

Ulcerative  Endocarditis.  Definition. — Ulcerative  endocarditis,  of  which 
the  synonyms  have  already  been  given,  is  a  state  in  which  the  endo- 
•cardium  is  ulcerated,  vegetations  are  present,  and  there  is  an  actual  loss  of 
substance  in  the  valvular  tissues,  so  that  a  valve  or  even  a  septum  may  be 
perforated.  A  French  physician,  Bouillaud,  first  recognized  this  cardiac 
state  with  its  associated  signs  of  pyaemia,  but  Kirkes,  of    England,  first 


486  DISEASES  OF   THE  HEART 

emphasized  the  fact  that  the  heart  was  the  seat  of  the  difficulty,  and  that  the 
symptoms  arose  from  its  condition.  Since  his  time  a  host  of  pathologists, 
including  Virchow,  Wilks,  Murchison,  Charcot,  Vulpian,  and  Birch-Hirsch- 
feld  in  Europe,  and  Osier  in  this  country,  have  studied  this  malady.  It 
is  important  to  remember  that  ulcerative  endocarditis  occurs  in  an  acute 
and  chronic  form. 

Etiology. — The  disease  is  always  due  to  microbic  infection  of  the  endo- 
cardium. It  may  be  due  to  a  secondary  infection,  during  the  course  of  one 
of  the  acute  infectious  diseases  like  typhoid  fever,  scarlet  fever,  pneumonia, 
or  tonsillitis,  or  it  more  rarely  arises  as  a  primary  lesion.  The  organisms  are 
usually  the  Staphylococcus  pyogenes  aureus,  the  Streptococcus  pyogenes,  and 
the  Pneumococcus,  the  Bacillus  typhosus,  the  Gonococcus,  the  Bacillus  coli 
communis.  Acute  endocarditis  due  to  the  meningococcus  of  Weichselbaum 
is  very  rare.  A  number  of  cases  have  been  reported  in  which  the  meningo- 
coccus has  been  found  in  the  circulating  blood :  one  by  Gwyn  in  1889, 
another  by  Salomon  in  1902,  and  a  third  by  Warfield  and  Walker  in  1903. 
The  last  of  these  is  the  only  one  in  which  the  meningococcus  was  demon- 
strated to  be  the  cause  of  the  endocarditis.  Any  damage,  new  or  old,  to  the 
surface  of  a  valve  predisposes  that  part  to  infection. 

Pathology  and  Morbid  Anatomy. — Anatomically,  the  ulcerative  form  may 
be  but  a  later  stage  of  the  acute  simple  type,  and  many  cases  occur  in  which 
no  sharp  line  of  demarcation  can  be  drawn.  Not  infrequently  it  is  engrafted 
upon  an  old  or  chronic  valvular  lesion,  and  patients  having  such  lesions 
should  be  watched  closely  during  an  attack  of  any  infectious  disease 
associated  with  the  constant  or  frequent  occurrence  of  bactersemia.  The 
infective  process  in  the  ulcerative  type  leads  to  necrosis  of  the  already  formed 
or  forming  vegetations,  and  even  of  the  affected  leaflet  or  adjacent  myocar- 
dium. The  fragments  thrown  into  the  circulation  cause  infarction  and 
metastatic  lesions  in  many  tissues,  especially  in  the  spleen,  kidneys,  and 
brain.  Marrow  lesions,  joint  complications,  and  other  manifestations  of 
septicopyeemia  are  often  conspicuous.  Whether  the  secondary  processes  be 
suppurative  or  not  depends  upon  the  character  of  the  infecting  organism. 
When  involving  the  valves  of  the  right  heart  (as  it  does  more  commonly  than 
the  acute  simple  form),  pulmonary  complications  may  be  conspicuous, 
which,  taken  with  the  fact  that  it  may  be  a  sequence  or  complication  of 
pneumonia,  further  tends  to  obscure  the  seat  of  the  primary  lesion.  Occa- 
sionally the  almost  symptomless  progress  of  the  malady  is  due  to  the  low 
toxicity  of  the  infecting  organism,  while  intensely  toxicogenic  bacteria 
reverse  the  picture  and  cause  evidences  of  severe  infection  and  toxeemia 
to  be  manifest. 

Symptoms. — The  objective  symptoms  of  ulcerative  endocarditis  may  be 
no  more  marked  than  those  of  the  simple  form.  Fever  may  not  occur.  If 
the  disease  develops  during  the  course  of  one  of  the  acute  infectious  diseases 
or  as  a  result  of  septicaemia,  its  existence  may  not  be  suspected.  If  it  develops 
primarily  the  physician  who  does  not  carefully  study  the  heart  may  believe 
that  the  fever  in  its  acute  period  of  rise  and  fall  is  the  manifestation  of  one 
of  the  acute  infectious  diseases  or  he  may  suspect  sepsis,  typhoid  fever,  or 
malaria.    Because  of  these  symptoms,  the  disease  may  be  divided  into  the 


ENDOCARDITIS  487 

septic  form,  the  typhoid  form,  and  the  malarial  form.  A  cerebral  form  also 
exists. 

In  the  seytic  form  the  patient  presents  the  ordinary  signs  of  septi- 
cjiemia.  Chill  after  chill  develops,  and  between  the  chills  high  fever  and 
sweats  are  present.  The  patient  looks  profoundly  septic,  the  tongue  is  dry, 
the  eyes  sunken,  and  petechise  may  be  present  in  the  skin.  The  marked 
anfemia  is  very  noteworthy,  and  its  severity  is  diagnostic.  Leukocytosis  is 
present.  Multiple  metastatic  abscesses  may  be  found.  The  heart  may  or 
may  not  produce  a  murmur,  but  its  action  is  hurried  and  feeble. 

The  typhoid  type  is  closely  allied  to  that  just  described.  The  dry  tongue, 
the  subsultus,  the  tympanites,  the  diarrhoea,  the  mental  stupor,  the  swollen 
spleen,  and  the  remitting  fever  may  all  present  so  typical  a  picture  of  a  case 
of  typhoid  fever  that  only  the  constant  recollection  that  such  symptoms  may 
be  due  to  ulcerative  endocarditis  will  save  the  physician  from  an  error  in 
diagnosis.    Even  epistaxis  may  develop. 

In  the  malarial  type  the  constant  recurrence  of  moderate  chills,  moderate 
fever,  anaemia,  and  some  sweating  may  be  very  misleading. 

In  the  cerebral  form  there  is  severe  headache,  unconsciousness,  and 
convulsions  due  to  an  associated  meningitis.  In  some  instances  the 
simultaneous  development  of  septic  arthritis  makes  the  case  resemble  acute 
rheumatism.  Burrows  has  reported  a  case  in  which  vomiting  and  purging 
were  so  severe  that  he  believed  the  patient  to  be  suffering  from  homicidal 
poisoning. 

Cases  are  recorded  in  which  the  splenic  enlargement  was  so  great  that  the 
patient  was  thought  to  be  suffering  from  splenomedullary  leukaemia.  In 
other  cases  the  diagnosis  of  acute  tuberculosis  has  been  made. 

Albuminuria  and  hcematuria  are  common  symptoms,  but  renal  infarction 
may  take  place  without  either  albumin  or  blood  being  found  in  the 
urine. 

Endocardial  murmurs  are  not  always  present.  They  are  shifting  in  time 
and  in  character  and  may  be  found  one  day  and  be  lost  the  next.  Further, 
it  sometimes  happens  that  the  murmurs  change  in  character  from  day  to 
day,  owing  to  the  progressive  character  of  the  lesions.  When  murmurs  exist 
they  are  more  frequently  due  to  old  lesions  than  to  the  new  ones  produced 
by  the  acute  infection. 

Complications. — The  complications  of  ulcerative  endocarditis  are  many 
and  serious.  It  not  infrequently  happens  that  a  septic  embolus  not  only  plugs 
an  important  vessel,  and  so  causes  an  infarct  in  such  organs  as  the  kidney,  the 
lung,  and  the  spleen,  but  it  acts  as  a  focus  of  septic  development.  Such 
embolic  closure  frequently  occurs  in  the  branches  of  the  left  middle  cerebral 
artery,  and  causes  temporary  or  permanent  aphasia  or  hemiplegia.  Peripheral 
vessels,  such  as  the  popliteal  or  brachial  or  lingual  arteries,  may  also  be 
affected.  Occasionally  violent  abdominal  pain,  followed  by  bloody  stools 
and  signs  of  collapse,  indicates  that  embolism  of  the  mesenteric  vessels  has 
taken  place.  Sometimes  uraemia,  due  to  the  septic  nephritis  which  is  present, 
ends  the  patient's  life. 

Diagnosis. — The  points  of  value  in  diagnosis  are  the  suddenness  of  onset 
in  some  cases,  the  up-and-down  temperature  waves,  which  form  steep  curves 


488  DISEASES  OF   THE  HEART 

on  the  charts,  the  repeated  rigors,  the  presence  of  distinct  leukocytosis,  the 
presence  of  pyogenic  organisms  in  the  blood,  the  absence  of  the  malarial 
organism  and  of  the  Widal  reaction,  and,  finally,  the  presence  of  great  feeble- 
ness and  irregularity  of  the  heart's  action.  In  some  cases,  however,  the 
diagnosis  from  physical  signs  may  be  practically  impossible.  The  Widal 
test  may  throw  much  light  on  the  case  if  persistently  positive. 

Prognosis. — It  is  hardly  necessary  to  state  that  the  prognosis  is  most  grave. 
Recovery  rarely  occurs,  and  death  may  take  place  in  the  first  two  weeks  or 
earlier.  Sometimes  life  is  preserved  for  weeks.  The  duration  depends 
largely  upon  the  character  of  the  infection,  the  condition  of  the  heart  and  of 
its  valves,  and  the  occurrence  of  complications.  Some  cases  extend  over  a 
period  of  several  months,  and  most  of  them  last  for  several  weeks.  That 
healing  may  take  place  and  recovery  occur  in  cases  of  true  ulcerative  endo- 
carditis is  proved  by  a  large  number  of  cases  now  on  record,  in  which  the 
condition  has  been  proved  by  subsequent  autopsies  to  have  existed,  the 
patient  dying  of  another  malady. 

Treatment. — The  treatment  of  ulcerative  endocarditis  is  not  very  satisfac- 
tory. Antistreptococcic  serum  may  be  of  benefit  in  a  few  cases,  provided 
that  the  streptococcus  is  the  cause  of  the  disease,  and  provided  that  the  variety 
of  streptococcus  used  in  the  preparation  of  the  serum  is  the  same  as  that 
present  in  the  heart.  Aside  from  this  specific  treatment,  the  only  thing  to  do 
is  to  support  the  system  by  the  wise  use  of  tonics,  such  as  tincture  of  the 
chloride  of  iron  and  the  tonic  bitters.  Full  doses  of  quinine  may  be  used. 
The  most  important  function  of  the  physician  is  to  maintain  nutrition  by  the 
use  of  good  food  and  to  order  no  drugs  which,  by  disordering  digestion,  will 
interfere  with  the  digestive  and  assimilative  functions. 

Chronic  Endocarditis. — As  already  stated,  chronic  endocarditis  is  fre- 
quently a  sequence  of  one  of  the  acute  forms  just  described,  and,  therefore, 
as  a  rule,  it  affects  the  left  side  of  the  heart  and  the  mitral  leaflets  oftener 
than  the  aortic  valves.  In  some  instances,  however,  it  depends  upon 
alcoholism,  gout,  and  syphilis,  in  which  case  associated  changes  in  the  heart 
muscle  and  bloodvessels  are  also  found.  A  slowly  progressing  valvulitis 
or  sclerosis  of  the  valves,  which  comes  on  insidiously,  is  frequently  asso- 
ciated with  arteriosclerosis  (arteriosclerotic  endocarditis),  with  chronic 
renal  disease,  chronic  metallic  poisoning,  especially  that  due  to  lead, 
and  other  conditions  associated  with  high  arterial  tension,  with  or 
without  the  presence  in  the  blood  of  some  specific  irritant  to  which 
the  changes  may  be  ascribed.  As  the  acute  inflammatory  process 
merges  into  the  chronic  form,  one  of  two  changes  appear  in  the 
endocardium.  There  is  an  overproduction  of  connective  tissue  in  the 
endocardium,  with  thickening,  stiffening,  and  lessened  elasticity,  which 
chiefly  affects  the  valvular  leaflets.  Following  this  condition,  as  a  result 
of  further  degenerative  changes,  we  find  contractions  or  localized  yieldings 
of  the  valves  which  produce  an  unevenness  of  their  surfaces,  so  that  their 
edges  can  no  longer  be  accurately  approximated;  nor  do  they  permit  the 
free  flow  of  blood  through  the  orifice  which  they  guard,  since  they  are  unable 
to  yield  during  the  period  at  which  a  free  flow  of  blood  should  normally  take 
place.     Even  when  the  valves  are  thickened  and  distorted  they  may  still  be 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     489 

adequately  covered  by  endothelium,  but  in  some  instances  the  endothehum 
may  be  absent,  thereby  exposing  calcareous  and  roughened  surfaces  upon 
which  fibrin  is  sometimes  deposited.  The  chief  factors  in  producing  cardiac 
failure  in  chronic  endocarditis  are  irregular  contractions  which  distort  the 
valves,  causing  their  edges  to  become  everted,  inverted,  or  curled  up.  In 
addition  the  chordae  tendineae  which  control  the  valves  guarding  the  auriculo- 
ventricular  orifices  become  shortened  and  thickened  so  that  they  interfere 
with  the  free  movement  of  the  valves.  (See  Diseases  of  the  Myocardium.) 
In  that  form  of  the  disease  in  which  mural  endocarditis  is  present,  patches 
of  sclerosis  or  cicatrices  may  be  seen  over  the  walls  of  the  ventricles.  (See 
Chi'onic  Valvular  Disease.) 

CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  CHRONIC 
ENDOCARDITIS. 

Chronic  valvular  disease  of  the  heart  is  very  constantly  met  with  in 
medical  practice,  and  its  frequency  is,  as  a  rule,  in  direct  proportion  to  the 
age  of  the  patient  examined.  This  is  due  to  the  sclerotic  changes  which  are 
prone  to  take  place  in  the  valves  as  age  advances,  and  to  the  fact  that  in 
those  who  have  passed  the  period  of  middle  life  the  heart  in  all  its  parts  is 
unable  to  withstand  the  strains,  which  may  come  to  it,  as  well  as  in  earlier 
periods.  The  chief  causes  of  valvular  lesions  may  be  placed  in  three  divisions, 
namely:  (1)  those  due  to  infectious  diseases,  particularly  rheumatism,  which 
may  leave  behind  damage  which  only  becomes  apparent  when  age  or  some 
unusual  strain  weakens  the  heart  muscle;  (2)  fibroid  or  sclerotic  changes 
ensuing  as  a  result  of  age,  gout,  syphilis,  and  alcoholism;  (3)  definite 
myocardial  degeneration  and  dilatation  which  does  not  cause  direct  but 
indirect  valvular  failure  in  function,  as  described  elsewhere.  (See  Relative 
Insufiiciency.) 

Experience  in  the  larger  London  hospitals,  some  fifteen  years  ago,  led  me 
to  believe  that  cardiac  valvular  disease  was  much  more  common  in  England 
than  in  America.  It  is  interesting  to  note,  however,  that  this  view  is 
incorrect,  for  out  of  59,762  medical  cases  which  are  recorded  in  hospitals 
in  London,  there  were  3059  cases  of  valvular  heart  disease,  or  a  percentage 
of  5.1;  and  out  of  91,985  medical  cases  in  hospitals  in  different  cities  in  the 
United  States,  there  were  4108  cases  of  valvular  disease,  or  a  percentage 
of  4.4.  The  actual  difi'erence  in  frequency  in  England  and  America  is, 
therefore,  not  very  marked,  not  only  as  regards  endocarditis,  but  acute  rheu- 
matism as  well.      (See  Acute  Rheumatism.) 

Valves  Affected. — Series  of  statistics  differ  somewhat  as  to  the  relative 
frequency  with  which  different  valves  are  affected.  One  difficulty  is  that 
there  has  never  been  a  sufficiently  large  collection  of  statistics  to  give 
results  free  from  error.  Another  difficulty  lies  in  the  diiferentiation  of  true 
and  false  aortic  stenosis;  for  it  is  evident  that  certain  statistics  which 
give  a  large  percentage  of  this  lesion  include  cases  in  which  there  is  not 
true  simple  stenosis  (which  is  quite  rare  without  regurgitation)  and  cases  in 
which  atheroma  and  aortic  roughening  cause  a  systolic  aortic  murmur. 

All  clinicians  and  pathologists  are  in  accord  in  stating  that  mitral  re-- 


490  DISEASES  OF   THE  HEART 

gurgitation  is  the  most  common  lesion  by  long  odds.  Jiirgensen  has 
analyzed  2470  cases  of  valvular  cardiac  disease,  with  the  following  results 
as  to  the  relative  frequency  with  which  valvular  disease  occurs:  mitral 
disease,  1616;  aortic  disease,  457;  pulmonary  valvular  disease,  56;  tricuspid 
disease,  10;  associated  aortic  and  mitral  disease,  224;  associated  mitral  and 
tricuspid  disease,  45;  lesions  at  the  mitral,  aortic,  and  tricuspid  valves,  24; 
and  at  the  aortic  and  tricuspid  valves,  2.  Unfortunately  he  does  not  state 
what  the  lesions  are — i.  e.,  regurgitant  or  stenotic.  It  is  an  open  question, 
too,  how  many  of  the  cases  of  so-called  mitral  disease  and  tricuspid  disease 
were  secondary  murmurs  due  to  dilatation  of  those  orifices  and  not  to  true 
valvular  defects. 

Some  years  ago,  T.  G.  Ashton,  my  then  chief  of  clinic  at  the  Jefferson 
Hospital,  made  an  analysis  of  1024  cases  of  valvular  disease  met  with  in 
life  insurance  examinations.  His  results  showed  that  of  these  557  were  cases 
of  mitral  regurgitation,  136  were  aortic  stenosis,  47  were  aortic  regurgitation, 
32  were  mitral  stenosis,  and  11  tricuspid  regurgitation.  I  believe  that  these 
statistics,  while  accurate  in  themselves,  are  to  some  extent  misleading,  and 
that  the  proportion  of  cases  of  aortic  stenosis  is  too  high.  (See  article  on 
Aortic  Stenosis.)  The  following  figures  obtained  by  the  analysis  of  908 
cases  of  valvular  heart  disease  treated  in  Westminster  Hospital,  London, 
show  that  the  most  common  single  lesions  are  mitral  regurgitation,  mitral 
stenosis,  aortic  regurgitation,  and  aortic  stenosis,^  in  order  of  arrangement, 
and  that  of  double  lesions  at  one  orifice  the  relative  frequency  is  double 
aortic,  double  mitral,  double  pulmonary,  and  double  aortic  with  double 
mitral.  Mitral  regurgitation  quite  frequently  occurs  as  the  result  of  aortic 
regurgitation,  through  dilatation  of  the  mitral  orifice. 

Mitral  disease  affects  more  women  than  men;  aortic  disease  more  men 
than  women. 

Aortic  regurgitation  is  the  most  fatal  lesion.  Mitral  stenosis  ranks  second 
in  fatality,  aortic  stenosis  third,  and  mitral  regurgitation  fourth.  The  mor- 
tality of  double  aortic  lesions  is  greater  than  that  of  double  mitral. 

The  statistics  of  A.  Lockhart  Gillespie,  based  on  a  study  of  1914  cases 
treated  in  the  Edinburgh  Royal  Infirmary,  are  especially  interesting  in  that 
they  show  the  mortality  of  valvular  lesions  in  the  two  sexes  according  to 
age.  Gillespie  found  that  the  maximum  mortality  in  males  with  aortic 
incompetence  or  stenosis  occurs  between  the  age  of  fifty  and  sixty-nine, 
but  in  those  with  double  lesions  the  years  from  twenty  to  twenty-nine  are 
those  with  the  highest  mortality.  The  female  maximum  mortality  in  aortic 
incompetence  and  aortic  stenosis  falls  between  the  years  of  forty-nine  and 
fifty.  Mitral  stenosis  proves  most  fatal  at  from  thirty  to  thirty-nine  years 
in  males,  and  from  forty  to  forty-nine  in  females.  The  death  rate  in  females 
between  twenty  and  twenty-nine,  forty  and  forty-nine,  and  fifty  and  sixty- 
nine  is  higher  than  in  males  at  similar  periods.  The  death  rate  in  mitral 
incompetence  in  both  sexes  rises  progressively  with  the  age.  In  cases  of 
double  mitral  lesion,  the  male  maximum  mortality  falls  between  thirty  and 
forty-nine,  and  in  the  female  between  fifty  and  sixty-nine. 

1  This  probably  refers  to  true  stenosis  and  not  to  cases  in  which  only  the  aortic  systolic  murmur  was 
present.     (See  Aortic  Stenosis.) 


Fig. 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     491 

Before  proceeding  to  a  consideration  of  the  various  valvular  lesions  it  is 
essential  that  the  mechanism  of  the  valves  in  health  and  disease  be  clearly 
understood  (Fig.  69).  The  cardiac  valves  are  arranged  in  such  a  way  that 
they  prevent  a  reflux  of  blood  into  that  cavity  which  the  blood  has  just  left 
in  the  progress  of  the  normal  circulation.  As  a  rule,  these  valves  are  capable 
of  _  fitting  together  so  tightly  that  they  completely  and  effectively  close  the 
orifice  which  they  guard,  but  even  without  the  presence  of  any  condition 
of  disease  they  may  at  times  give 
way,  and  permit  some  reflux.  The 
moderate  reflux  occurring  during  great 
muscular  strain  may  be  regarded  as 
a  physiological  attempt  to  relieve  the 
blood  pressure  in  the  cardiac  cavities, 
and  if  it  is  not  maintained  for  too 
great  a  length  of  time  it  does  no  harm. 

It  must  also  be  recalled  that  there 
are  at  least  two  ways  in  which  the 
cardiac  valves  may  become  incompe- 
tent to  prevent  reflux  of  blood.  In 
the  first,  and  by  far  the  most  common 
type,  the  valves  are  diseased,  as  already 
described  in  the  article  on  endocar- 
ditis, so  that  they  cannot  become 
closely  approximated,  or  they  are 
glued  together  in  such  a  way  that  the 
same  result  is  achieved,  and  so  they 
also  obstruct  the  flow  of  blood.  In 
the  second  type  the  rings,  which  form 
the  bases  of  the  valves  and  the  mar- 
gins of  the  orifices,  yield,  and  as  they 
relax  the  orifice  becomes  too  large  to 
be  closed  by  the  valves,  which  may  still 
be  practically  normal  in  themselves. 
This  condition  exists  for  a  brief  space 
of  time  in  acute  cardiac  strain,  as  just 
stated.  It  persists  for  a  long  time  or 
becomes  permanent  in  instances  where 
the  heart  is  feeble  and  the  strain  is  very  severe  or  prolonged,  and  it  is  fre- 
quently found  in  cases  of  dilatation  and  feebleness  of  the  heart  muscle. 

Those  forms  of  valvular  incompetence  which  occur  in  athletes  or  others 
after  severe  exertion  can  therefore  be  put  aside  as  beyond  the  scope  of 
these  particular  pages,  although  they  will  again  be  discussed  under  the 
head  of  functional  disorders  of  the  heart. 

In  those  cases  in  which  the  valve  becomes  incompetent  to  close  an  orifice, 
and  so  permits  regurgitation  to  take  place,  the  failure  of  the  valve  is  so 
gradual,  as  a  rule,  that  there  develops  simultaneously  an  increase  in  the 
size  and  strength  of  the  heart  muscle,  so  that  it  may  by  increased  power 
and  activity  compensate  for  the  leakage  which  occurs.    As  a  result  it  very 


Diagram  modified  from  Page  to  show  the  relation 
of  the  various  valves.  A  study  of  this  diagram 
will  render  clear  the  time  of  the  various  cardiac 
murmurs.  Thus  in  mitral  regurgitation  the  blood 
passes  back  from  the  left  ventricle  to  the  left  auri- 
cle during  systole,  and  is  dammed  up  in  the  pul- 
monary veins,  the  openings  of  which  are  seen  in 
the  auricular  wall,  producing  pressure  on  the 
pulmonary  valves,  the  sounds  of  which  are  thereby 
accentuated. 


492 


DISEASES  OF   THE  HEART 


frequently  happens  that  this  compensatory  hypertrophy  is  fully  equal  to  the 
increased  demands  made  on  the  heart  muscle,  and  not  until  the  occurrence 
of  a  severe  illness,  or  until  advancing  years  impairs  the  power  of  its  fibres, 
are  any  manifestations  of  valvular  lesions  to  be  foimd  in  the  patient,  save 
the  physical  signs  of  hypertrophy  and  the  murmur  caused  by  the  regurgitating 
blood.     Sometimes  even  the  murmur  may  disappear  for  a  time. 

In  cases  in  which  a  valve  is  ruptured  or  severely  damaged  by  disease  so 
that  it  fails  in  its  function  before  the  heart  can  undergo  compensatory 
hypertrophy,  we  often  see  signs  of  great  circulatory  embarrassment  from 
the  very  first  part  of  the  illness. 

In  all  cases  of  valvular  disease  in  their  early  stages  much  depends 
upon  the  inherent  strength  of  the  heart  muscle  and  its  ability  to  increase  in 
power,  and  therefore  it  is  evident  that  it  is  of  vital  importance  for  the 
patient  to  rest  at  this  period  in  order  that  the  strength  of  the  heart  may  be 
conserved,  and  in  order  that  it  may  not  be  subjected  to  a  severe  strain  with 
associated  dilatation  at  the  most  critical  period  of  its  existence.  This  is 
the  more  important  because  diseases  which  secondarily  infect  the  valves 
usually  impair,  to  some  extent  at  least,  the  myocardium  as  well. 

In  health,  when  the  valves  are  intact,  the  heart  always  possesses  a  con- 
siderable degree  of  reserve  energy  and  power,  using  only  a  small  part  of 
its  store  of  energy  in  a  day's  work.  As  a  consequence  a  healthy  man  can 
run  a  considerable  distance,  or  leave  his  desk  and  go  hunting,  without 
engendering  anything  more  than  fatigue  of  his  voluntary  muscles  and  some 
healthy  cardiac  tire.  This  reserve  energy  is  kept  for  just  such  purposes. 
On  the  other  hand,  if  a  man  who  is  a  sufferer  from  valvular  or  myocardial 
disease,  even  if  he  is  seemingly  in  perfect  health,  attempts  to  follow  the 
first  one,  he  soon  begins  to  suffer  from  cardiac  embarrassment,  and  if  he 
persists  may  become  very  gravely  ill  from  acute  cardiac  failure,  and  rupture 
his  compensation  by  excessive  exercise  to  such  an  extent  that  he  may  be 
bedridden  for  the  rest  of  his  days.  In  the  latter  instance  nearly  all  his 
reserve  energy  is  being  used  daily  in  the  maintenance  of  a  normal  circula- 
tion and,  having  little  reserve,  he  cannot  undertake  feats  that  demand  great 
calls  upon  his  reserve.    This  is  illustrated  in  the  following  squares: 


All  Energy 

In 

Constant 

Use. 


In  health,  large  reserve.         In  disease,  small  reserve. 


Far  advanced  disease, 
no  reserve 


In  the  last  square  it  is  seen  that  all  the  reserve  is  in  constant  use,  and, 
therefore,  if  any  extra  exertion  is  made,  the  heart  promptly  fails  and  death 
may  occur.  Even  in  those  cases  in  which  sufficient  hypertrophy  develops 
to  adequately  compensate  for  the  leak  in  the  valve,  the  heart  is  never  as 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS      493 

capable  for  work  as  in  health  because  the  reserve  is  never  restored  com- 
pletely and  the  degree  of  leakage  may  increase  at  any  moment  of  strain. 

A  consideration  of  these  facts  makes  one  therapeutic  fact  stand  pre- 
eminent above  all  others,  namely,  that  rest  is  the  chief  measure  to  be  insti- 
tuted whenever  compensation  is  failing,  as  by  rest  alone  can  we  expect  to 
restore  reserve  energy. 

These  remarks  have  so  far  dealt  with  regurgitant  conditions.  In  stenosis 
of  the  cardiac  orifices  the  same  facts  hold  true,  for  in  such  cases  the  question 

Fig.  70 


A  large  vegetation  on  the  mitral  leaflet.     (Kast  and  Rumpler.)      It  can  be  readily  seen  that  this 
would  cause  both  a  mitral  obstructive  and  a  mitral  regurgitant  murmur. 

is  whether  the  heart  muscle  possesses  enough  strength  to  drive  the  blood 
through  the  obstructed  area. 

Given  a  case  of  valvular  disease  the  prospects  of  survival  depend  almost 
entirely  upon  the  ability  of  the  heart  to  undergo  compensatory  hypertrophy, 
and  therefore  the  prognosis  depends  largely  upon  the  state  of  the  muscle, 
the  absence  of  arterlocapillary  fibrosis,  which,  if  present,  strains  the  heart 
and  wearies  it,  the  ability  of  the  patient  to  pursue  an  easy  occupation  and 
his  willingness  to  avoid  habits  of  life  which  strain  the  heart. 

With  these  preliminary  remarks  we  may  pass  on  to  a  discussion  of  the 


494  DISEASES  OF  THE  HEART 

individual  valvular  lesions,  taking  up  jQrst  of  all  the  most  common  of  them, 
namely : 

Mitral  Regurgitation. — Mitral  regurgitation,  often  called  "mitral  incom- 
petency" or  "mitral  insufficiency,"  depends  in  the  great  majority  of  cases 
upon  thickening,  shortening,  or  distortion  of  the  mitral  leaflets,  those  bicuspid 
valves  which  in  health  guard  the  left  auriculoventricular  orifice,  in  such  a 
way  that  the  blood  when  pressed  upon  by  the  contracting  walls  of  the 
ventricle  cannot  regurgitate  into  the  left  auricle. 

Associated  with  this  valvular  defect  there  are  usually  vegetations  on  the 
edges  of  the  valves  which  prevent  proper  approximation  of  their  edges. 
The  chordae  tendinese,  which  extend  from  the  ventricular  wall  to  the  leaflets 
for  the  purpose  of  giving  them  support,  are  shortened  so  that  they  will  not 
permit  the  full  movement  of  the  valves.  In  some  instances  the  valves,  their 
fibrous  bases,  the  chordse  tendinese,  and  even  the  endocardium  are  so  com- 
pletely calcareous  that  the  ordinary  physiological  functions  of  the  part  are 
impossible.  It  is  evident  that  it  is  almost  impossible  for  such  advanced 
changes  to  be  present  without  at  the  same  time  causing  some  obstruction 
to  the  flow  of  blood  from  the  auricle  to  the  ventricle,  and  therefore  we  find 
that  in  nearly  all  cases  of  well-developed  mitral  regurgitation  some  mitral 
stenosis  also  exists. 

Pathology. — -The  morbid  anatomy  has  already  been  discussed  under  the 
heading  of  Endocarditis.  The  morbid  physiology  or  pathology  of  mitral 
regurgitation  is  as  follows: 

During  systole  the  blood  from  the  left  ventricle  in  cases  of  mitral  regurgi- 
tation flows  in  two  directions.  A  larger  part  escapes  into  the  aorta,  as  in 
health,  and  a  smaller  part  of  it  regurgitates  through  the  imperfectly  guarded 
mitral,  or  left  auriculoventricular  orifice,  into  the  left  auricle.  The  results 
of  this  regurgitation  are  multiple.  In  the  first  place  the  auricle  receives 
more  blood  during  diastole  than  is  normal,  for  it  receives  not  only  the  blood 
which  comes  to  it  from  the  pulmonary  veins,  but  it  also  receives  the  blood 
which  regurgitates  from  the  left  ventricle.  This  excess  of  blood  requires 
the  auricle  to  dilate  beyond  its  ordinary  capacity,  and  if  the  excess  of 
blood  is  great  this  dilatation  of  necessity  means  distention.  If  the  regurgitation 
progresses  gradually  there  is  developed  a  certain  amount  of  hypertrophy 
in  the  auricular  walls  which  enables  the  auricle  when  it  contracts  to  empty 
itself  completely  and  to  prevent  continuous  overdistention,  but  the  muscular 
fibres  in  the  auricle  are  never  well  developed  as  compared  to  those  of 
the  ventricle,  and  therefore  compensatory  hypertrophy  can  never  be  so 
complete. 

The  second  result  of  this  lesion  is  dilatation  and  h^q^ertrophy  of  the  left 
ventricle,  which  is  due  to  several  causes,  namely,  the  fact  that  when  the 
left  auricle  empties  itself  it  delivers  to  the  ventricle  an  excess  of  blood  over  the 
normal  quantity,  for  the  reasons  just  given-  To  hold  this  excess  of  blood 
the  ventricle  must  dilate,  and,  to  expel  it  on  contraction,  the  ventricle  must 
undergo  hypertrophy.  The  general  system  still  requires  as  much  blood 
as  before,  and  in  order  to  provide  it  with  that  quantity  the  ventricle  must 
increase  its  activity  in  order  that  the  amount  lost  by  regurgitation  may  be 
compensated  for  by  increased  cardiac  action, 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     495 

The  third  result  is  found  in  dilatation  and  hypertrophy  of  the  right 
ventricle,  the  labors  of  which  are  increased  by  the  fact  that  the  engorgement 
of  the  left  auricle  renders  it  difficult  for  the  pulmonary  veins  to  empty 
themselves  into  it.  As  a  consequence  they,  and  their  tributary  branches, 
become  engorged,  raising  the  resistance  in  the  pulmonary  vessels,  and  so 
the  right  ventricle  finds  it  less  easy  to  pump  blood  through  the  lungs. 
If  the  pulmonary  engorgement  is  very  marked,  and  dilatation  develops 
in  the  right  ventricle  more  rapidly  than  does  compensatory  hypertrophy, 
there  is  produced  an  insufficiency  of  the  tricuspid  valves  guarding  the  right 
auriculoventricular  orifice. 

Fourth,  the  right  auricle  now  feels  the  same  stress  as  was  felt  primarily 
by  the  left  auricle,  and  it  undergoes  dilatation  and  hypertrophy,  but  this 
hypertrophy  is  rarely,  if  ever,  adequate  to  the  task  set  before  it,  and  as  it 
fails  to  properly  empty  itself,  evidences  of  engorgement  of  the  systemic 
veins  becomes  manifest  in  that  they  become  swollen,  the  liver  and  kidneys 
are  congested,  and  oedema  develops  in  the  lower  extremities. 

Fifth,  certain  definite  changes  take  place  in  the  hmgs.  As  a  result  of 
their  being  constantly  engorged  with  blood,  they  suffer  from  brown  induration 
and  atheromatous  changes  appear  in  the  pulmonary  arteries  and  veins  as 
years  go  by.  Finally,  when  the  systemic  veins  are  engorged  we  find  in 
addition  serious  congestion  at  the  bases  of  the  lungs  as  a  result  of  impotence 
of  the  right  ventricle  and  obstruction  to  the  flow  of  blood  from  the  pulmonary 
veins. 

Lastly,  we  find,  at  autopsy,  in  these  cases  red  atrophy  of  the  liver  and 
engorged,  cyanotic  kidneys. 

In  those  cases  in  which  there  is  no  primary  disease  of  the  mitral  leaflets, 
but  in  which  they  fail  because  of  acute  dilatation  of  the  ventricle  so  that 
the  auriculoventricular  orifice  is  widened  and  the  valves  cannot  close  it, 
there  is  developed  the  same  train  of  symptoms  save  that  they  are  more 
rapid  in  onset  and  more  severe.  This  condition  develops  after  great  cardiac 
strain,  in  which  the  aortic  valves  are  ruptured  or  the  left  ventricle  and  its 
auriculoventricular  orifice  greatly  dilated.  The  resulting  engorgement  of 
the  lungs  may  be  so  severe  that  their  bloodvessels  may  rupture  and  profuse 
haemoptysis  ensue.  These  patients  nearly  always  succumb  shortly,  or  remain 
chronic  invalids,  because  the  stress  develops  so  suddenly  that  compensatory 
hypertrophy  cannot  take  place.  We  have,  therefore,  an  apparent  paradox, 
namely,  that  actual  disease  of  the  mitral  valves  is  rarely  so  serious  in  its 
consequences  as  is  incompetency  of  these  valves  due  to  other  causes. 

Still  another  cause  of  mitral  incompetence,  aside  from  actual  primary 
valvular  disease,  is  Bright's  disease,  which  increases  arterial  tension  and 
thereby  throws  an  increased  strain  on  the  left  ventricle  and  the  mitral  valves 
when  the  blood  is  to  be  thrown  out  into  the  aorta.  Usually  in  these  cases 
the  renal  condition  indirectly  impairs  the  power  of  the  ventricle,  rendering 
its  nutrition  faulty  through  impoverishment  of  the  blood  and  toxaemia, 
and  valvular  failure  then  arises  as  a  result  of  gradual  widening  of  the 
auriculoventricular  orifice. 

Symptoms. — It  must  be  evident  from  what  has  just  been  said  that  many 
cases  of  mitral  regurgitation  may  present  no  symptoms  for  years  after  the 


496 


DISEASES  OF  THE  HEART 


lesion  is  established,  for  as  it  develops  so  does  a  compensatory  hypertrophy 
develop.  It  is  only  upon  extra  exertion,  which  the  heart  is  not  prepared  to 
meet,  that  symptoms  of  cardiac  embarrassment  ensue,  and  if  the  exertion 
is  not  very  severe  and  not  repeated,  the  dyspncea  and  palpitation  from 
which  the  patient  suffers  may  be  considered  by  him  as  due  to  indigestion. 
If  no  illness  impairs  the  heart  muscle  and  no  laborious  pursuit  causes  it  too 
great  stress,  the  patient  advances  in  comfort  to  old  age,  when  symptoms 
develop  as  a  result  of  the  fact  that  his  arterial  tension  gradually  increases, 
thereby  giving  his  heart  more  work  to  do  at  each  beat,  and  at  the  same  time 


Showing  at  x  the  apex  beat,  where  the  murmurs  of  mitral  regurgitation  and  obstruction  can  be  best 
heard.  The  arrow  pointing  to  the  axilla  indicates  the  direction  in  which  the  regurgitant  murmur 
is  transmitted,  and  the  arrow  pointing  to  the  sternum  the  direction  of  transmission  of  the  obstructive 
murmur. 

his  heart  muscle  undergoes  the  changes  incident  to  advancing  years.  Under 
these  conditions  compensation  "ruptures,"  to  use  the  ordinary  term  applied 
to  this  unfortunate  state,  and  subjective  and  objective  signs  appear. 

The  subjective  symptoms  (that  is,  those  felt  by  the  patient)  vary  consider- 
ably in  the  early  and  mild  degrees  of  failing  compensation.  In  some  instances 
shortness  of  hreath  on  exertion  brings  the  patient  to  the  physician,  in  other 
instances  digestive  disturbances  due  to  hepatic  congestion  and  secondary 
gastric  catarrh  are  complained  of,  and  in  others  the  patient  may  com- 
plain of  a  cough,  which  is  due  to  a  mild  pulmonary  congestion  and  bron- 
chitis having  its  origin  in  the  cardiac  failure.  In  still  another  class  they 
may  suffer  excessively  from  cold  in  moderately  cold  weather,  and  perhaps 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     497 

become  easily  fatigued  while  walking  in  cold  air  because  the  cold  contracts 
the  peripheral  capillaries  and  so  increases  the  labor  of  the  heart.  When 
the  failure  of  the  heart  is  well  marked,  then  dyspnoea,  inability  to  lie  down 
because  of  oppression,  and  pain  in  the  epigastrium  are  perhaps  the  symptoms 
of  which  the  patient  will  most  complain. 

The  objective  symptoms  (that  is,  those  seen  by  the  physician)  are  even 
more  characteristic.  The  capillary  circulation  is  sufficiently  impaired  to 
produce  some  stasis  and  consequent  cyanosis  of  the  lips  and  finger-tips  or 
even  of  the  face.  The  fingers,  particularly  in  young  persons  in  whom  the 
disease  has  lasted  for  some  time,  are  club-shaped — that  is,  they  do  not  taper, 
but  have  thickened  tips;  there  is  more  or  less  oedema  of  the  feet  and  ankles, 
and  perhaps  blood-spitting  as  a  result  of  intense  pulmonary  engorgement 
or  infarction. 

Physical  Signs. — The  physical  signs  in  such  a  case  are  usually  well 
developed.  Inspection  of  the  prgecordium  reveals  a  diffuse  and  perhaps 
forcible  apex  beat.  Palpation  shows  a  distinct  thrill  in  children,  and  in 
this  class  of  patients  this  thrill  can  frequently  be  seen  as  well.  The  apex 
beat  may  be  distinctly  felt  well  outside  and  below  the  nipple  line.  If  the 
compensating  hypertrophy  is  well  developed  the  apex  beat  may  be  forcible, 
but  if  compensatory  hypertrophy  is  lacking  it  is  feeble  and  diffuse.  On 
percussing  the  prsecordium  the  normal  area  of  cardiac  dulness  will  be 
found  to  be  enlarged.  This  enlargement  is  usually  transverse  or  lateral, 
so  that  it  may  extend  to  the  right  edge  of  the  sternum  owing  to  enlarge- 
ment of  the  right  ventricle,  and  as  far  as  the  left  of  the  nipple  from 
dilatation  and  hypertrophy  of  the  left  ventricle. 

Auscultation  provides  us  with  the  signs  that  determine  the  exact  nature 
of  the  lesions,  for  the  signs  so  far  described  are  not  distinctive  of  mitral 
regurgitation.  When  the  ear  of  the  physician  is  applied  over  the  apex  of 
the  heart  there  is  heard  a  soft,  and  often  quite  loud,  murmur,  which  occurs 
synchronously  with  the  apex  beat,  or  with  systole,  or  contraction  of  the 
ventricle.  This  murmur  is  transmitted  to  the  left  axilla,  and  it  may  be 
to  the  angle  of  the  left  scapula.  If  it  is  very  loud  it  may  be  heard  in  any 
part  of  the  chest.  If  the  regurgitation  is  great  enough  to  cause  engorge- 
ment of  the  lung  the  pulmonary  second  sound,  due  to  a  quick  shutting 
of  the  pulmonary  valves  guarding  the  orifice  of  the  pulmonary  artery,  may 
be  louder  than  normal.  This  is  best  heard  at  the  third  left  costal  cartilage. 
When  the  regurgitation  is  severe  enough  to  have  resulted  in  tricuspid 
regurgitation  from  engorgement  of  the  right  side  of  the  heart,  there  may  be 
heard  at  the  fifth  costal  cartilage  on  the  right  side  a  comparatively  soft 
systolic  murmur  due  to  this  secondary  leak,  but  in  some  instances  the 
mitral  murmur  completely  obscures  the  tricuspid  murmur.  In  others  the 
tricuspid  murmur  can  be  heard  only  at  the  ensiform  cartilage. 

It  is  of  vital  importance  for  the  physician  to  recall  the  fact  that  a  murmur 
so  slight  as  to  be  almost  inaudible  is  not  an  indication  of  the  presence  of 
a  small  and  unimportant  lesion  of  the  mitral  valve.  On  the  contrary,  the 
presence  of  a  faint  murmur  often,  but  not  always,  indicates  that  the  heart 
is  too  feeble  to  drive  the  blood  with  sufficient  force  to  make  the  murmur 
clearly  audible. 
32 


498  DISEASES  OF   THE  HEART 

The  pulse  of  mitral  regurgitation  varies,  of  course,  with  the  extent  of 
the  lesion  and  the  degree  of  compensation.  It  is  usually  nearly  normal, 
though  lacking  somewhat  in  volume  even  when  compensation  is  complete. 
It  is  irregular  and  small  when  compensation  is  insufficient.  When  com- 
pensation is  ruptured,  it  is  very  small  and  hobbling. 

Diagnosis. — It  is  desirable  to  separate  mitral  regurgitation  due  to  dila- 
tation of  the  mitral  orifice  from  mitral  regurgitation  due  to  true  valvular 
disease.  This  is  in  many  cases  impossible  if  the  action  of  the  heart  is 
already  seriously  impaired,  the  more  so  because  in  many  instances  the 
secondary  dilatation  produces  some  widening  of  the  orifice.  While  the 
physical  signs  may  not  be  distinctive  the  absence  of  any  history  of  rheu- 
matism or  other  infection  which  affects  the  valves,  and  the  presence,  or 
history  of  the  presence,  of  any  exhausting  illness  which  weakens  the  heart 
muscle,  or  of  any  strain  which  has  dilated  the  orifice,  would  indicate  that 
dilatation  rather  than  true  valvular  disease  is  present.  This  is  particularly 
true  if  the  strain,  though  moderate,  has  occurred  during  convalescence, 
while  the  heart  is  weak.  This  differentiation  is  important  because  in  some 
cases  with  returning  health  and  strength  the  leak  may  cease  and  perfect 
recovery  ensue,  whereas  if  the  valve  is  actually  diseased  good  health  can  only 
come  from  compensatory  hypertrophy  and  the  murmur  will  probably 
always  persist. 

The  possibility  of  a  murmur  being  due  to  ansemia  is  also  to  be  recalled, 
but  hsemic  murmurs  are  usually  very  soft  and  are  best  heard  near  the 
base  rather  than  at  the  apex. 

The  diagnosis  of  mitral  regurgitation  is  therefore  chiefly  based  upon  the 
presence  of  a  murmur  heard  most  clearly  with  systole  at  the  apex  and  trans- 
mitted to  the  axilla. 

Prognosis. — ^The  prognosis  in  a  case  of  mitral  regurgitation  depends  upon 
the  age  of  the  patient,  his  occupation,  the  general  condition  of  his  vitality, 
and  the  severity  of  the  lesion.  When  a  child  develops  mitral  disease  it  often 
does  not  survive  puberty,  chiefly  because  dilatation  in  such  a  case  is 
usually  excessive  and  because  the  constantly  increasing  demands  of  its 
growth  require  of  its  heart  more  than  it  can  provide.  In  young  adults  who 
will  rest  after  damage  to  the  valves  during  an  attack  of  rheumatism  until 
compensation  is  really  established,  the  prognosis  is  good,  provided  that  the 
subsequent  occupation  is  not  too  strenuous,  although  with  the  onset  of 
old  age  vascular  changes  will  probably  cause  breakdown.  In  feeble 
persons,  however,  the  prognosis  may  be  unfavorable  from  the  onset, 
particularly  if  hypertrophy  is  lacking  and  dilatation  is  marked.  In  old 
persons  the  prognosis  is  bad  for  obvious  reasons,  since  the  heart 
cannot,  at  this  time  of  life,  readily  gather  new  strength  to  meet  new 
demands. 

If  syphilis  or  alcoholism  are  factors  in  the  case  the  prognosis  is  grave,  and 
if  the  kidneys  are  diseased  the  prognosis  is,  of  course,  very  bad.  So,  too, 
the  presence  of  arteriocapillary  fibrosis  with  high  arterial  tension  is  a 
serious  or  grave  factor,  in  that  it  gives  the  heart  so  much  work  to  do.  (For 
the  relationship  of  this  lesion  to  age  and  mortality,  see  page  490  in  article 
on  Chronic  Valvular  Disease.) 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS      499 

Treatment. — (This  is  discussed  at  the  end  of  the  articles  on  Valvular 
Disease.) 

Mitral  Stenosis.  Definition.  —  By  mitral  stenosis  we  mean  a  condi- 
tion of  the  tissues  composing  the  mitral  valves  or  surrounding  the  left 
auriculoventricular  orifice  whereby  the  blood  is  prevented  from  passing 
with  normal  ease  from  the  left  auricle  to  the  left  ventricle.  It  is  some- 
times  called  "mitral  obstruction." 

Etiology  and  Pathology. — Mitral  stenosis  is  far  more  common  in  females 
than  in  males,  although  the  reason  for  this  is  not  clear.  Sir  Dyce  Duckworth 
found  that  out  of  264  cases  of  this  disease  177  were  females,  and  other 
statistics  are  practically  in  accord  with  Duckworth's.  It  is  due  in  the  great 
majority  of  instances  to  gluing  together  of  the  mitral  valves  as  the  result 
of  acute  endocarditis  arising  from  acute  rheumatism. 

With  this  adhesion  of  the  valves  there  is  often  associated  a  growth  of 
vegetations  on  their  edges  and  not  uncommonly  thickening  and  sclerosis  of 
the  chordae  tendinese,  the  papillary  muscles  and  the  leaflets  themselves,  so 
that  the  parts  lose  their  elasticity  and  are  so  stiffened  that  they  are  unable 
to  move  out  of  the  way  of  the  blood  stream  when  it  seeks  to  pass  into  the 
ventricle.  This  sclerotic  process  is  so  marked  in  some  cases  that  the 
tissues  may  seem  almost  cartilaginous  in  character,  and  in  advanced  life 
lime  salts  may  be  deposited  to  such  an  extent  that  the  fibrous  tissue  is 
calcareous  and  even  the  walls  of  the  ventricle  are  infiltrated  by  calcareous 
masses.  In  some  instances  the  adhesions  are  so  complete  that  the  valves 
form  a  funnel-shaped  tube  through  which  the  blood  must  find  its  way.  In 
other  instances  the  edges  of  the  valves  are  adherent  and  their  margins 
thickened,  leaving  only  a  small  orifice  between  them,  forming  the  so-called 
"button-hole"  mitral  orifice,  and  in  still  other  cases  the  conjoined  edges  of 
the  valves  are  so  drawn  or  puckered  that  the  orifice  when  the  auricle  is 
opened  looks  like  the  normal  anus. 

The  funnel-shaped  opening  is  most  commonly  seen  in  children,  but  it 
is  not  always,  as  some  have  thought,  a  congenital  lesion;  the  button-hole 
orifice  is  much  more  common  in  adults.  Sansom  states  that  the  proportion 
is  one  button-hole  to  eight  funnels  in  children,  and  that  as  adult  life  is 
reached  the  proportion  changes  to  twenty-five  button-holes  to  one  funnel. 

There  can  also  be  no  doubt  that  chronic  contracted  kidney  with  associated 
arteriocapillary  fibrosis  not  only  causes  mitral  stenosis,  but  that  even  the 
funnel-shaped  opening  just  described  may  be  developed  in  this  type  of 
cases.  The  studies  of  Duroziez  and  Huchard  in  France,  and  of  Goodhart, 
Sansom,  and  Pitt  in  England  prove  this  fact.  In  542  autopsies  in  cases  of 
interstitial  nephritis,  Pitt  found  mitral  stenosis  33  times. 

The  results  of  mitral  obstruction  are  overdistention  of  the  left  auricle 
and  scanty  blood  supply  to  the  left  ventricle.  The  engorgement  of  the  left 
auricle  results  from  its  inability  to  empty  itself,  and  leads  to  dilatation  and 
to  some  degree  of  hypertrophy.  In  some  instances  the  growth  of  muscle 
fibres  is  so  scanty  that  no  true  hypertrophy  ensues,  in  others  they  seem  to 
become  actually  atrophied,  but  in  other  instances  very  complete  compen- 
satory hypertrophy  develops,  so  that  the  auricular  wall  is  distinctly  thicker 
than  normal.    Indeed,  it  may  appear  as  a  firm,  muscular  mass  which  does 


500  DISEASES  OF  THE  HEART 

not  collapse  at  autopsy  as  the  ordinary  auricle  is  wont  to  do.  "\Miether 
hypertrophy  exists  or  not,  dilatation  is  always  present.  ^Mien  such  an 
auricle  is  opened  the  endocardium  is  often  found  to  be  thickened  and  a 
laminated  clot  may  hue  its  cavity.  In  other  instances  polypoid  or  globular 
coagula  are  attached  to  the  auricular  walls,  and  these  globular  thrombi  may 
almost  fill  the  auricle.  At  times  the  thrombus  is  free,  acting  as  a  ball 
valve  in  the  auriculoventricular  orifice. 

The  wall  of  the  left  ventricle  in  these  cases  is  often  thinner  than  usual, 
but  dilatation  and  hypertrophy  may  be  present. 

The  accumulation  of  blood  in  the  auricle  leads  to  the  engorgement  of 
the  lung,  and  the  same  changes  occur  in  its  vessels  and  tissues  that  have 
been  described  under  "Pulmonary  Congestion"  and  "Mitral  Regurgitation." 
So,  too,  the  right  ventricle  undergoes  hypertrophy  and  dilatation  from  similar 
causes,  and  the  tricuspid  valves,  even  more  frequently  than  in  mitral  regurgi- 
tation, give  way,  so  that  pulsation  of  the  jugular  veins,  pulsation  of  the 
liver,  and  oedema  of  the  lower  extremities  finally  develops.  Embolism 
often  occurs  in  mitral  stenosis,  and,  as  in  all  cases  of  embohsm  arising  in 
the  heart,  the  embolus  usually  lodges  in  the  left  hemisphere  of  the  brain. 

If  the  narrowing  of  the  auriculoventricular  orifice  is  not  progressive,  and 
if  the  auricle  undergoes  compensatory  hypertrophy,  the  signs  of  advanced 
disease  may  not  ensue.  It  is  only  when  auricular  hypertrophy  fails  that 
the  malady  becomes  manifest  and  causes  the  symptoms  of  cardiac  failure 
which  in  aU  respects  resemble  those  described  under  mitral  regurgitation, 
save  that  the  venous  and  hepatic  pulsation  just  described  are  more  fre- 
quently present. 

Physical  Signs. — The  physical  signs  of  mitral  obstruction  are  as 
follows:  Inspection  of  the  chest  may  reveal  pulsation  at  the  apex  of  the 
heart  near  the  nipple,  and  also  near  the  base  of  the  heart  close  to  the 
sternum,  in  the  second  or  third  left  intercostal  spaces.  Not  rarely  there 
may  be,  in  addition,  epigastric  pulsation.  If  a  straw,  or  piece  of  card- 
board, be  placed  over  the  pulsating  spots  at  the  apex  and  base,  it  will  be 
found  that  they  do  not  move  synchronously,  but  the  lower  one  moves  with 
the  ventricle  and  the  upper  one  with  the  auricle.  It  has  been  claimed 
that  the  auricle  does  not  produce  this  upper  pulsation,  and  that  it  is  due 
to  the  movement  of  the  conus  arteriosus  of  the  right  ventricle,  but  this  is 
seemingly  disproved  by  the  fact  that  the  two  movements  are  not  syn- 
chronous"^ with  systole.  If  the  patient  be  a  child  these  pulsations  are  much 
more  noticeable'than  if  he  be  an  adult,  at  which  time  of  life  pulsation  may 
be  absent.  In  children  bulging  of  the  chest  wall  close  to  the  sternum  and 
near  the  epigastrium  may  be  quite  marked,  and  if  pulsation  be  well  defined 
in  this  area  and  absent  from  the  region  of  the  nipple,  indicating  hyper- 
trophy of  the  right  ventricle,  the  diagnosis  of  mitral  stenosis  is  strength- 
ened, provided  that  adherent  pericardium  can  be  excluded. 

Palpation  does  not  always  give  us  much  information,  but  sometimes  it 
practically  decides  the  diagnosis,  for  there  are  three  signs  on  palpation 
which  are  noteworthy  in  this  lesion.  There  is  a  thrill  which  is  pre- 
systolic  in  point  of  time  and  is  felt  in  the  fourth  or  fifth  interspace  inside 
the   nipple  line.     It  is  characterized  by  sudden  arrest  at  the   moment  of 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     501 

systole.  This  sign  may  be  considered  diagnostic  of  mitral  stenosis  provided 
we  have  excluded  the  possibility  of  aortic  regurgitation,  which  sometimes 
causes  a  similar  sign.  This  thrill  may  be  present  at  one  time  and 
entirely  absent  at  another,  and  it  may  be  absent  when  the  patient  is 
in  the  dorsal  decubitus  and  present  when  he  is  erect,  or,  again,  it  is  pres- 
ent after  exercise  and  absent  after  rest.  The  second  sign  of  some  im- 
portance in  the  diagnosis  of  this  disease  by  palpation  is  the  heaving 
impulse,  felt  just  below  the  margin  of  the  last  costal  cartilage  on  the  left 
side  without  such  impulse  near  the  nipple.  This  has  already  been  spoken 
of  under  inspection  as  indicative  of  hypertrophy  of   the   right    ventricle. 


MO  shows  area  of  greatest  intensity  of  a  mitral  obstructive  murmur;  TK  slio'ws  area  of  greatest 
intensity  of  a  tricuspid  regurgitant  murmur.  The  fine  lines  indicate  the  area  in  which  is  felt  the 
characteristic  thrill  of  mitral  stenosis. 

Care  must  be  taken,  however,  that  signs  of  hypertrophy  of  the  left  ven- 
tricle are  really  absent,  for  it  sometimes  happens  that  an  overlapping  of 
the  lung  covers  the  left  side  of  the  heart  so  that  it  does  not  transmit  its 
impulse  to  the  chest  wall.  The  third  sign  on  palpation  is  the  discovery 
of  the  edge  of  the  enlarged  liver,  which  pulsates,  below  the  level  of  the 
floating  ribs  on  the  right  side.  Here,  again,  care  is  necessary,  for  it  often 
happens  that  the  liver  is  moved  by  a  transmitted  impulse  from  the  heart 
muscle  through  the  diaphragm. 

Percussion  of  the  prsecordium  may  reveal,  in  cases  of  mitral  stenosis,  a 
distinct  increase  in  the  area  of  cardiac  dulness  to  the  right,  with  comparatively 
little  extension  of  dulness  to  the  left.    This  is  due  to  the  enlargement  of  the 


502  DISEASES   OF   THE  HEART 

right  ventricle.  Allien,  however,  the  disease  is  far  advanced  and  the  heart 
is  greatly  dilated  or  hypertrophied  the  left  margin  of  dulness  is  distinctly 
extended,  and  in  such  cases  the  area  of  cardiac  dulness  to  the  left  of 
the  nipple  line  may  be  very  great. 

Auscultation  is,  of  course,  the  most  important  aid  in  the  diagnosis  of 
mitral  stenosis,  since  it  presents  no  less  than  six  points  of  interest.  The 
first  of  these  is  the  presence  of  a  murmur  which  occurs  just  before  sys- 
tole, a  'presystolic  murmur,  and  is  best  heard  between  the  nipple  and  the 
sternum,  on  the  nipple  level  (Figs.  71  and  72) .  In  most  cases  the  murmur  can 
only  be  heard  in  this  area,  but  in  some  instances  it  is  so  loud  as  to  extend 
all  over  the  chest.  The  murmur  is  usually  harsher  than  that  of  mitral 
regurgitation,  and  is  vibratory  in  character.  It  is  due  to  the  passage  of 
the  blood  through  the  obstructed  auriculoventricular  orifice,  and  it  ceases 
with  the  close  of  auricular  systole.  In  some  cases  the  murmur  may  ex- 
tend all  through  ventricular  diastole.  At  times  it  is  so  metallic  as  to  be 
musical  rather  than  purring. 

Another  sign  of  importance  is  the  accentuation  of  the  pulmonary  second 
sound,  which  is  best  heard  at  the  third  left  interspace,  and  is  due  to  the  high 
pressure  in  the  pulmonary  artery,  produced  by  back  pressure  on  the  column 
of  blood  in  the  lungs.  This  accentuation  is,  however,  not  so  constant  in 
stenosis  as  in  regurgitation  because  of  the  greater  irregularity  of  the  heart 
in  stenosis. 

A  third  sign  is  the  reduplication  of  the  second  sound  of  the  heart  so 
that  it  appears  as  a  "tap-tap,"  or  resembles  the  "postman's  knock."  It 
is  very  characteristic  of  mitral  stenosis  and  is  heard  at  two  places:  at 
the  apex  and  at  the  base  of  the  heart.  It  is,  however,  supposed  to  be  due 
to  different  causes  at  each  spot.  At  the  apex  Sansom  believes  it  is  due  to 
the  sudden  rush  of  the  blood  into  the  ventricle  through  the  narrow  orifice 
under  the  pressure  of  the  hypertrophied  auricle.  In  other  words,  this  sound 
is  associated  with  the  normal  pulmonary  and  aortic  second  sounds.  \Vhen 
this  reduplicated  second  sound  is  heard  at  the  base,  and  this  is  where  it  is 
usually  heard,  it  is  most  diagnostic,  and  is  supposed  to  be  due  to  an  asyn- 
chronous closure  of  the  aortic  and  pulmonary  valves,  but  in  all  probability 
the  cause  is  similar  to  the  sound  at  the  apex.  This  is  sometimes  called  the 
"gallop  rhythm." 

The  fourth  sign  of  importance  is  the  loud  and  sudden  snapping  sound 
which  is  heard  at  the  close  of  systole  of  the  ventricle.  It  is  supposed  to 
be  due  to  forcible  snapping  to  of  the  bicuspid  or  mitral  valves. 

The  fifth  sign  is  not  only  somewhat  indicative  of  stenosis,  but  much  more 
of  cardiac  breakdown,  namely,  absence  of  the  first  sound  of  the  heart  at 
the  apex. 

Still  a  sixth  sign  of  mitral  stenosis  is  sometimes  of  value,  namely,  great 
irregularity  as  to  rhythm  and  force.  In  no  form  of  valvular  lesion  with 
rupture  of  compensation  is  the  heart  so  tumultuous  as  in  this  disease. 
As  already  stated,  the  absence  of  a  murmur  may  be  more  indicative  of 
grave  valvular  disease  than  its  presence. 

When  cardiac  breakdown  ensues  it  not  infrequently  happens  that  the 
presystolic  murmur  itself  disappears  because  the  auricle  is  too  feeble  to  drive 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     503 

the  blood  through  the  auriculoventricular  orifice  with  enough  force  to  make 
a  murmur. 

Diagnosis. — Mitral  stenosis  is  at  times  the  most  difficult  of  all  the  cardiac 
lesions  to  diagnosticate,  chiefly  because  when  compensation  is  ruptured  no 
murmur  may  be  present,  and  the  action  of  the  heart  being  exceedingly 
irregular  its  sounds  are  confused.  Again,  stenosis  is  so  frequently  associated 
with  mitral  regurgitation  that  the  double  murmur  may  cause  confusion,  the 
more  so  as  only  one  murmur  may  be  present  at  one  time  and  both  at  another 
time,  and  also  because  the  regurgitant  murmur  is  often  so  loud  that  it 
covers  the  stenotic  murmur,  with  the  result  that  unless  the  physician  is  on 
the  qui  vive  to  discover  the  less  noticeable  sound  it  is  overlooked.  In  cases 
which  are  manifestly  ones  of  mitral  stenosis  the  physician  need  not  hesitate 
to  express  an  opinion,  but  in  the  obscure  forms  of  the  disease  he  should 
always  reserve  his  statement  until  he  has  had  an  opportunity  of  examining 
the  heart  several  times  under  conditions  of  rest  and  exercise,  and,  perhaps, 
after  the  use  of  digitalis  or  some  other  drug  to  strengthen  the  muscle. 

As  the  physical  signs  have  already  been  thoroughly  described,  it  is  only 
necessary,  at  this  point,  to  differentiate  mitral  stenosis  from  those  con- 
ditions which  resemble  it. 

The  most  important  of  these  is  the  so-called  "Flint's  murmur"  first 
described  in  1862  by  Dr.  Austin  Flint,  of  New  York.  It  occurs  in  some 
cases  of  aortic  regurgitation,  and  is  supposed  to  be  due  to  the  regurgitating 
blood  striking  upon  the  mitral  valves  and  chordae  tendinese  in  such  a  way 
that  they  vibrate  and  so  cause  a  sound.  This  sound  is  diastolic  in  point 
of  time  because  it  occurs  after  the  blood  has  been  sent  out  into  the  aorta  and 
while  the  ventricle  is  receiving  more  blood  from  the  auricle.  Its  time  of 
occurrence  is,  therefore,  practically  identical  with  the  murmur  of  mitral 
stenosis. 

The  following  points  make  the  differentiation  between  mitral  stenosis 
and  "Flint's  murmur"  in  most  cases,  although  in  some  cases  the  sepa- 
ration may  be  impossible.  In  cases  with  aortic  regurgitation  auscultation 
at  the  second  right  costal  cartilage  and  along  the  sternum  will  reveal  a 
diastolic  murmur  which  will  not  be  well  defined  in  these  areas  in  mitral 
stenosis  unless  the  mitral  murmur  is  so  loud  as  to  be  heard  pretty  much 
everywhere  in  the  chest.  The  pulse  in  aortic  regurgitation  is  characterized 
by  a  full  wave  followed  by  a  sudden  fall — the  "Corrigan  pulse" — whereas 
the  pulse  of  mitral  obstruction  is  a  fine  thread,  irregular  and  feeble. 
Again,  in  cases  of  aortic  regurgitation  with  "Flint's  murmur"  there  are 
rarely,  if  ever,  those  well-developed  signs  of  pulmonary,  hepatic,  and  splenic 
engorgement  which  have  been  described  as  occurring  in  mitral  stenosis, 
nor  does  the  patient  so  frequently  suffer  from  haemoptysis  due  to  pul- 
monary congestion  or  infarction.  Further  than  this,  the  sharp,  snapping 
first  sound  of  the  heart  characteristic  of  mitral  obstruction  is  not  present 
with  "Flint's  murmur." 

A  second  condition  resembling  mitral  stenosis  is  tricuspid  stenosis.  On 
general  principles,  this  latter  lesion  can  be  excluded  on  the  rule  of  probabili- 
ties, for  tricuspid  stenosis  is  an  exceedingly  rare  lesion.  If  it  exists  it  is 
usually  heard  best  in  the  tricuspid  area  (the  area  of  the  fourth  right  inter- 


504  DISEASES  OF   THE  HEART 

costal  space),  but  it  may  be  clearly  heard  in  the  mitral  area,  and  as  tricuspid 
stenosis  and  mitral  stenosis  exist  together  in  some  cases  and  occur  simul- 
taneously, they  may  not  be  separable  and  nothing  be  known  of  the  lesion  on 
the  right  side  of  the  heart  until  autopsy. 

At  times  children  suffering  from  adhesive  pericarditis  present  a  presystolic 
sound  like  that  of  stenosis.  It  is  to  be  discovered  by  the  signs  of  adhesive 
pericarditis  (which  see).  In  every  case  of  valvulitis  due  to  rheumatism  we 
should  bear  in  mind  the  possible  if  not  the  probable,  presence  of  adherent 
pericardium.  The  presence  of  this  condition  is  rendered  likely  if  the  liver 
is  not  only  enlarged,  but  very  firm,  and  if  ascites  develops  in  excess  of 
that  seen  in  cardiac  dropsy.  This  point  is  of  importance,  because  if  the 
pericardium  is  adherent  we  cannot  expect  veiy  good  results  from  digitalis 
nor  from  any  other  method  of  treatment. 

When  a  patient  presents  himself  with  a  disordered  circulation  and  con- 
fused or  irregular  heart  sounds,  and  no  murmur,  it  must  be  recalled  that  while 
such  a  state  may  be  due  to  tobacco  heart,  it  may  also  be  caused  by  mitral 
stenosis  with  no  murmur. 

Prognosis. — The  prognosis  of  mitral  stenosis  is  not  as  favorable  as  is  that 
of  mitral  regurgitation  or  aortic  stenosis,  and  children  nearly  always  suc- 
cumb to  it  before  they  reach  adult  years.  Adults  who  have  a  severe  lesion 
also  rarely  survive  for  many  years  after  it  begins,  but  there  are  very  marked 
exceptions  to  this  rule.  Thus,  I  have  under  observation  at  present  a  case 
of  mitral  stenosis  which  I  examined  twenty-two  years  ago,  and  who  was  told 
thirty  years  ago  that  the  lesion  existed.  During  all  these  years  (he  is  now 
sixty-nine  years  of  age)  he  has  led  a  very  active  life,  both  physical  and 
mental,  with  no  cardiac  embarrassment,  although  he  had  an  attack  of 
hsematuria  when  I  first  saw  him,  which  was  due  to  an  infarction  of  the 
kidney.  During  this  time  he  has  taken  no  treatment,  except  at  rare 
intervals,  his  compensation  being  complete. 

In  young  women  with  mitral  stenosis,  marriage  and  consequent  child- 
bearing  often  cause  rupture  of  compensation  and  death. 

The  average  age  at  death  in  cases  of  this  disease  is  stated  by  Sansom  to 
be  about  thirty-two  and  seven-tenth  years.  (See  General  Discussion  of 
Valvular  Lesions  and  Their  Effect  on  Mortality,  page  490.)  (For  treat- 
ment see  close  of  these  articles.) 

Aortic  Stenosis.  Definition. — Aortic  stenosis,  often  called  "  aortic  obstruc- 
tion," is  a  condition  in  which  the  left  ventricle  finds  it  more  difficult  than 
normal  to  expel  the  blood  through  the  aortic  orifice,  because  this  orifice  is 
narrowed  by  disease.  The  murmur  which  is  produced  by  the  blood  under 
these  circumstances  is  systolic  in  point  of  time,  for  it  occurs  as  the  left  ven- 
tricle expels  its  contents.  It  is  best  heard  at  the  second  right  costal  cartilage 
or  under  the  sternum,  at  its  upper  portion.  It  is  of  vital  importance,  how- 
ever, to  recall  the  fact  that  the  presence  of  a  systolic  murmur  at  this  point 
is  not  necessarily  indicative  of  actual  obstruction  of  the  aortic  orifice.  An 
aortic  systolic  murmur  does  not  necessarily  mean  an  aortic  valvular  lesion. 
The  murmur  is  usually  due  to  roughening  of  the  lining  of  the  aorta  by 
atheromatous  plaques.  Aneurysm  may  also  be  provocative  of  such  a  sound. 
So  rare  is  true  simple  aortic  obstruction  that  it  may  be  said  that  the  presence 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     505 

of  a  systolic  aortic  murmur  is  in  most  cases  probably  not  clue  to  this  lesion, 
unless  it  is  found  associated  with  aortic  regurgitation.  Some  clinicians  of 
repute  assert  that  they  have  never  seen  pure  aortic  stenosis  without  regurgi- 
tation. Cabot  states  that  in  252  autopsies  made  at  the  Massachusetts 
General  Hospital  on  persons  with  valvular  disease,  there  was  not  a  single 
instance  of  uncomplicated  aortic  stenosis. 

Etiology. — The  causes  of  aortic  obstruction  are  multiple.  In  the  first 
place,  it  may  be  the  result  of  rheumatic  endocarditis  of  so  severe  a  type  that 
not  only  the  mitral  but  the  aortic  valves  are  involved,  for  it  is  only  in  rare 
cases  that  rheumatism  attacks  the  aortic  valves  and  leaves  the  mitral  valves 
untouched.  In  such  a  case  the  endocardium  covering  the  valves  is  roughened 
in  patches,  and  upon  these  patches  is  deposited  fibrin  from  the  blood  stream, 
which,  with  proliferated  cells,  forms  granulations  and  vegetations,  fibrous 
thickening,  and,  finally,  the  deposition  of  lime  salts.  If  the  inflammation  is 
severe  the  edge  of  the  valves  may  become  glued  together,  and  so  a  funnel- 
shaped  opening  is  formed,  which  is  much  narrower  than  the  normal  aortic 
orifice.  In  rare  instances,  instead  of  the  valves  being  adherent  and  thickened, 
they  are  adherent  and  thinned,  so  that  they  appear  atrophied.  Such  a  condi- 
tion is  found  at  times  in  children  and  is  thought  to  be  congenital,  but  even 
in  young  children  the  cause  may  be  rheumatism,  and  Sansom  asserts  that 
the  condition  may  be  due  to  rheumatic  endocarditis  in  intrauterine  life. 
Rheumatism  may  be  considered  the  usual  cause  of  aortic  obstruction  in 
children  or  in  those  who  have  not  as  yet  reached  advanced  years. 

The  cause  of  aortic  obstruction  is  often  not  acute  in  character,  as  in  the 
types  just  described,  but  chronic,  being  due  to  a  gradual  atheromatous 
change,  which,  having  involved  the  aorta  itself,  spreads  to  the  aortic  valves, 
and  causes  a  slowly  progressive  thickening  and  calcification  of  their  tissues. 
This  is  the  form  of  stenosis  which  is  often  of  a  very  advanced  type,  so  that 
the  orifice  may  be  but  a  small  slit  or  chink  through  which  the  blood  escapes. 

From  what  has  just  been  said,  it  is  easy  to  understand  how  it  is  that 
obstruction  to  the  flow  of  blood  in  the  area  of  the  aortic  valve  is  exceedingly 
rare  as  a  single  lesion.  The  very  nature  of  the  morbid  changes  which  take 
place  in  the  tissues  at  this  point  renders  the  simultaneous  existence  of  aortic 
obstruction  and  regurgitation  probable,  for  the  valves  at  the  aortic  orifice 
are  either  glued  together  as  a  result  of  rheumatic  endocarditis,  or,  more 
commonly,  are  thickened  by  chronic  endocarditis  and  calcareous  deposits. 
In  either  instance  they  are  not  only  in  the  way  of  the  blood  as  it  passes  out 
of  the  ventricle,  but  they  are  incapable  of  preventing  its  regurgitation,  since 
they  are  too  thick  and  too  stiff  to  approximate  their  edges.  In  other  instances 
the  presence  of  vegetations  on  the  valves,  in  addition  to  these  changes,  adds 
to  the  impairment  of  their  functional  activity. 

The  secondary  changes  produced  by  aortic  obstruction  are  chiefly  con- 
nected with  the  left  ventricle.  Under  favorable  conditions  this  portion  of 
the  heart  usually  develops  a  satisfactory  compensatory  hypertrophy,  the 
muscle  fibres  gaining  in  strength  and  size  as  the  process  of  narrowing  in  the 
aortic  area  gradually  progresses.  As  a  consequence,  it  not  rarely  occurs  that 
even  an  extreme  degree  of  aortic  obstruction  is  accompanied  by  such  a  com- 
plete compensatory  hypertrophy  that  the  presence  of  the  lesion  is  only  dis^ 


506 


DISEASES  OF   THE  HEART 


covered  at  autopsy.  It  is  interesting  to  note  that  the  hypertrophy  of  aortic 
obstruction  differs  somewhat  from  that  of  aortic  regurgitation  in  the  fact 
that  the  ventricular  walls  increase  in  thickness  without  undergoing  any 
great  dilatation,  whereas,  in  aortic  regurgitation  they  both  dilate  and 
hypertrophy,  causing  eccentric  hypertrophy. 

So  long  as  the  compensatory  hypertrophy  of  the  left  ventricle  in  aortic 
obstruction  is  adequate,  practically  no  changes  occur  in  the  other  parts  of 
the  heart.  It  is  only  when  compensation  ruptures  that  symptoms  of  impaired 
circulation  ensue,  or  the  mitral  valves  give  way  under  the  strain,  and  con- 


FiG.  73 


Showing  area  of  greatest  intensity  and  the  direction  of  transmission  into  subclavian  and  carotid 
arteries  of  the  aortic  obstructive  murmur. 


gestion  of  the  left  auricle  and  of  the  lungs  develops.  This  may  in  time 
increase  the  labor  of  the  right  ventricle  and  lead  to  its  hypertrophy. 

Symptoms  and  Physical  Signs. — Patients  suffering  from  aortic  obstruction 
rarely  present  or  complain  of  any  symptoms  which  are  in  any  way  charac- 
teristic of  the  lesion.  At  times  a  sense  of  constriction  or  oppression  is  felt 
over  the  aortic  area,  as  it  is  in  cases  of  aortitis  or  atheroma  of  the  aorta, 
and  as  it  is  felt  in  some  cases  of  true  angina  pectoris.  When  there  is  an 
associated  aortic  regurgitation,  the  symptoms  are  of  that  lesion.  (See 
Aortic  Regurgitation.) 

The  'physical  signs  vary  considerably  with  the  type  of  patient  exam- 
ined and  with  the  stage  of  the  disease.  In  old  men  whose  chest  walls  are 
thickened  and  rigid  and  whose  lungs  are  often  emphysematous,  so  that  the 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     507 

edge  of  the  left  lung  projects  between  the  heart  and  the  chest  wall,  it  may 
not  be  possible  to  either  see  or  feel  an  apex  beat,  even  though  the  heart 
be  considerably  hypertrophied.  On  the  other  hand,  if  the  patient  be 
young,  or  the  chest  wall  pliable,  the  apex  beat  may  be  seen  and  felt  dis- 
tinctly and  forcibly,  and  it  is  usually  a  little  below  and  a  little  outside  the 
nipple  because  of  the  hypertrophy.  If  the  action  of  the  heart  is  forcible 
and  the  fingers  are  placed  over  the  second  right  intercostal  space,  a  dis- 
tinct thrill  can  be  felt.  This  thrill  is  in  the  nature  of  a  vibration  and  is 
often  transmitted  down  the  sternum  and  even  up  into  the  carotids.  This 
thrill  felt  in  the  area  described  is  very  characteristic  of  aortic  obstruction, 
but  it  is  also  felt  in  aortic  aneurysm. 

The  area  of  cardiac  dulness  on  percussion  is  not  materially  enlarged,  unless 
associated  regurgitation  has  caused  its  well-known  secondary  cardiac  changes. 

Auscultation  reveals  a  murmur  which  is  loudest  at  the  second  right 
costal  cartilage  near  the  sternum. 

This  sound  is  transmitted  in  most  cases  into  the  vessels  of  the  neck,  and 
not  infrequently  it  is  heard  over  the  sternum  as  low  as  the  ensiform  cartilage. 
It  occurs  with  systole  of  the  heart,  and  it  is  usually  loud  if  compensation  is 
preserved.  Not  only  is  it  loud,  but  it  is  apt  to  be  harsh  and  even  musical, 
and  it  is  long  and  blowing  in  character.  The  aortic  second  sound  is 
usually  absent. 

When  rupture  of  an  aortic  valve  takes  place  the  murmur  is  usually  widely 
diffused,  very  loud  and  musical.  I  showed  a  patient  to  the  College  of  Physi- 
cians of  Philadelphia  in  1902  that  possessed  a  murmur  capable  of  being 
heard  when  the  ear  was  eighteen  inches  from  the  chest.  It  could  be  heard 
on  top  of  his  head,  in  his  radial  arteries,  and  if  the  stethoscope  was  placed  so 
that  his  lips  encircled  it  the  murmur  could  be  heard  in  his  mouth.  There 
was  also  a  loud  aortic  regurgitant  murmur  in  his  case.  The  patient  was  a 
brakeman  who  suffered  from  sudden  and  severe  dyspnoea  and  syncope  on 
lifting  a  heavy  weight,  and  who  had  a  history  of  syphilis. 

The  pulse  in  aortic  obstruction  is  small  (pulsus  parvus)  because  the 
heart  cannot  expel  a  large  wave  of  blood  through  the  narrow  aortic  opening. 
The  wave  rises  gradually  and  then  falls  gradually,  unlike  the  sharp  upward 
jerk  felt  in  aortic  regurgitation. 

Diagnosis. — Sufficient  emphasis  has  already  been  placed  on  the  fact  that 
a  systolic  murmur  at  the  second  right  costal  cartilage  does  not  mean,  neces- 
sarily, aortic  obstruction,  but  if  the  time  of  the  murmur,  the  thrill,  the 
peculiar  pulse  and  atheromatous  vessels  are  present  in  an  old  person 
the  diagnosis  is  fairly  certain.  When  the  murmur  is  due  to  atheroma 
of  the  aorta  alone  the  aortic  second  sound  is  usually  sharp  and  clear 
instead  of  being  impaired  as  it  is  in  true  obstruction.  Aneurysm  is 
excluded  by  the  absence  of  the  characteristic  signs  of  that  state.  (See 
Aortic  Aneurysm.) 

Sewall  asserts  that  an  aortic  stenotic  murmur  heard  at  the  apex  disappears 
on  pressure  of  the  stethoscope,  and  so  separates  itself  from  the  systolic 
murmur  of  mitral  regurgitation. 

Prognosis. — ^The  prognosis  in  a  case  of  aortic  stenosis  is  generally  con- 
sidered as  more  favorable  than  in  any  other  valvular  lesion,  but  in  each 


508  DISEASES  OF   THE  HEART 

individual  case  the  physician  must  base  his  prophecy  as  to  life  upon  the 
age  of  the  patient,  the  state  of  his  arteries,  and  the  condition  of  the 
kidneys.  The  mere  presence  of  far-advanced  atheroma  in  aged  per- 
sons who  have  an  aortic  stenotic  lesion  is  not  necessarily  of  evil  import. 
As_  Clifford  Allbutt  weh  says,  "We  see  well-to-do  old  ladies  leading  tran- 
quil lives  up  to  four-score  years  or  more  with  systolic  aortic  murmurs  of  a 
quarter  of  a  century's  standing."  On  the  other  hand,  in  somewhat  younger 
persons,  who  have  more  fibrous  and  less  calcareous  arterial  changes,  the 
prognosis  is  not  so  good,  either  because  they  are  at  a  period  of  life  when 
they  are  prone  to  resort  to  exercise  and  so  strain  the  heart,  or  because  there 
is  a  tendency  to  fibroid  heart  as  well.  Allbutt's  view  that  "a  person  who  in 
young  or  middle  life  begins  to  suffer  overtly  from  the  sjTnptoms  of  aortic 
stenosis  has  but  a  few  years  to  live"  is  certainly  correct.  (For  treatment 
see  end  of  article  on  Valvular  Disease.) 

Aortic  Regurgitation.  Definition.— Aortic  regurgitation  is  often  called 
''  aortic  insufficiency"  or  "  aortic  incompetency,"  and  consists,  as  its  names 
indicate,  in  a  condition  of  the  aortic  leaflets,  or  of  the  aortic  orifice,  whereby 
the  blood  after  being  expelled  by  the  contraction  of  the  left  ventricle  into 
the  aorta  is  permitted  to  return. 

Etiology  and  Pathology. — By  far  the  most  common  cause  of  this  lesion  is 
acute  rheumatism,  which  causes  the  same  changes  in  the  valves  at  the 
aortic  orifice  as  have  already  been  described  as  taking  place  in  the  mitral 
leaflets,  namely,  distortion,  retraction,  stift'ening,  and  the  development  of 
vegetations.  As  a  rule,  when  rheumatism  is  the  cause  the  mitral  valves  also 
suffer  seriously,  so  that  the  aortic  and  mitral  lesions  coexist.  A  second 
common  cause  is  aortitis,  or  atheroma  of  the  aorta,  which  extends  to  the 
valves  and  causes  sclerotic  and  degenerative  changes  which  alter  the  position 
and  functional  ability  of  the  aortic  cusps.  This  atheroma  may  be  due  to 
mere  senility,  or  to  syphilis,  gout,  or  even  malarial  infection.  It  is  remark- 
able how  many  of  these  cases  have  a  history  of  excessive  toil,  excessive 
venery,  and  excessive  drinking,  with  the  result  that  the  bloodvessels  and 
heart  have  had  to  stand  strain,  toxemia,  and  infection.  The  cases  of  aortic 
regurgitation  which  are  due  to  these  causes  suffer  the  greatest  destruction 
of  the  valves,  for  their  surfaces  may  ulcerate  or  the  deposition  of  an  excess 
of  hme  salts  causes  necrosis  to  such  an  extent  that  only  stumps  of  the  valves 
exist. 

A  third  cause,  which  is  much  more  rare,  does  not  primarily  involve  the 
valves,  but  the  aortic  orifice.  The  aortic  ring  undergoes  dilatation  and  as 
a  result  the  valves  cannot  become  approximated.  In  other  words,  the  open- 
ing is  too  large  for  them  to  close  it.  This  condition  is  met  with  in  cases  of 
aneurysm  of  the  aorta.  It  is  not  by  any  means  as  frequent  as  dilatation  of 
the  mitral  orifice,  because  the  ring  around  the  opening  of  the  aorta  is  largely 
made  up  of  fibrous  and  fibroelastic  tissues,  whereas  that  which  supports 
the  mitral  orifice  is  largely  muscular. 

A  fourth  cause  is  rupture  of  an  aortic  leaflet  as  the  result  of  violent  strain. 
This  accident  rarely,  if  ever,  occurs  unless  the  valve  has  already  been 
weakened  by  disease. 

A  fifth  cause  is  the  presence  of  vegetations  on  the  aortic  valves,  developing 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS      509 

in  the  course  of  the  acute  infections  or  chorea.  Some  of  these  lesions  differ 
from  those  due  to  ordinary  endocarditis  in  that  they  are  not  always  per- 
manent, but  may  entirely  disappear. 

A  sixth  cause  is  ulcerative  endocarditis,  in  which  great  destruction  of  the 
valves  may  take  place  or  abundant  vegetations  develop.  This  is  usually 
due  to  the  pneumococcus.     (See  Croupous  Pneumonia.) 

A  seventh  cause  is  congenital  malformation,  which  is  exceedingly  rare. 
Indeed,  aortic  regurgitation  due  to  this  cause  is  more  rare  than  are  con- 
genital defects  themselves,  for  congenital  defects  in  the  valves  may  not  be 
severe  enough  to  permit  leakage. 

Finally  (eighth)  a  functional  relaxation  of  the  aortic  orifice  occasionally 
is  met  with  in  which  temporary  regurgitation  takes  place  for  the  same 
reasons  as  have  been  described  elsewhere.  I  saw  a  case  of  this  character 
while  on  duty  at  St.  Clement's  Hospital  some  fifteen  years  ago,  in  a  young 
girl  who  had  a  loud,  aortic  regurgitant  murmur  and  apparently  a  fusiform 
aneurysm  of  the  innominate  artery.  At  the  autopsy  the  vessels  seemed 
perfectly  normal  in  size,  but  on  testing  them  they  were  found  to  be  unusually 
yielding  and  elastic. 

The  secondary  effects  of  aortic  regurgitation  upon  the  left  ventricle  are 
most  important  and  interesting.  The  left  ventricle  no  sooner  expels  its 
contents  into  the  aorta  and  begins  to  dilate  in  order  to  receive  the  blood  from 
the  auricle,  than  it  also  receives  part  of  the  blood  it  has  just  sent  into  the 
aorta  by  reason  of  the  fact  that  the  aortic  valves  permit  regurgitation.  The 
ventricle,  therefore,  contains  not  only  the  normal  amount  of  blood  from 
the  auricle,  but  an  additional  quantity  from  the  aorta,  and  so  it  becomes 
dilated  to  contain  this  excess  and  also  undergoes  hypertrophy  in  order  to 
expel  this  excess  into  the  aorta  and  empty  itself.  Any  strain  upon  the  heart 
increases  the  dilatation,  and  as  a  result  we  often  see,  particularly  in  those 
who  live  by  manual  labor,  an  extraordinary  increase  in  the  size  of  the 
heart,  which  is  both  greatly  dilated  and  greatly  hypertrophied,  the  so-called 
eccentric  hypertrophy  of  aortic  regurgitation  resulting  in  the  "ox  heart" 
or  cor  bovinuvi. 

The  rapidity  and  degree  of  the  hypertrophy  is  extraordinary  in  some  cases. 
Sansom  speaks  of  a  case  in  which  the  heart  was  thought  to  have  gained  an 
ounce  each  week  for  four  or  five  weeks,  and  Dulles  has  recorded  a  case  in 
which  the  heart  weighed  forty-eight  ounces.  ^Mien  the  ventricle  is  much 
dilated  the  ring  guarding  the  mitral  orifice  may  yield  and  insufficiency  of 
the  mitral  valves  ensue  and  thus  cause  dilatation  of  the  left  auricle,  con- 
gestion of  the  lungs,  and  hypertrophy  of  the  right  side  of  the  heart.  In 
some  cases  of  aortic  insufficiency,  when  the  cause  is  atheroma,  the  patho- 
logical process  of  fibrosis  and  calcification  gradually  extends  to  the  tissues 
around  the  opening  of  the  coronary  arteries,  which  are  then  unable  to 
properly  supply  the  heart  with  blood,  or  the  coronary  arteries  themselves 
become  atheromatous.  Under  such  conditions  compensatory  hypertrophy 
may  never  be  established,  or  if  established  rapidly  fails,  is  ruptured,  and 
death  ensues. 

S3miptoms  and  Physical  Signs. — The  symptoms  of  aortic  regurgitation  are 
more  characteristic  than  are  those  of  any  other  form  of  valvular  disease, 


510  DISEASES  OF  THE  HEART 

and  are  more  constantly  met  with  in  such  cases,  ahhough  compensation 
may  be  adequate  in  many  cases  for  a  time  at  least.  Dizziness  and  partial 
synco'pe  often  appear  on  suddenly  sitting  up  or  on  standing  up,  and  at 
times  are  present  even  when  the  patient  lies  down.  Palpitation  and  dyspnoea 
on  exertion  are  pressing  symptoms  if  the  heart  is  feeble,  and  even  when 
compensation  is  adequate  pain  in  the  region  of  the  heart  is  often  a  severe 
symptom,  being  radiated  into  the  arms  or  into  the  neck.  At  this  time  the 
attacks  may  be  identical  with  those  of  true  angina  pectoris.  Sudden  death 
occurs  more  frequently  in  this  form  of  valvular  disease  than  in  any 
other. 

When  compensatory  hypertrophy  is  lost  the  patient  is  forced  to  sleep 
sitting  erect  or  nearly  erect  in  an  easy  chair;  he  is  usually  very  pallid,  but 
at  times  cyanotic.  Cough  and  pulmonary  comphcations  do  not  ensue  until 
the  mitral  valves  give  way. 

When  the  cardiac  failure  is  well  marked,  and  it  is  evident  that  death 
cannot  be  many  days  away,  distressing  mental  symptoms  often  appear. 
Hallucinations  are  pressing  and  even  an  active  maniacal  delirium  may 
develop.  At  times  the  patient  becomes  suicidal  in  his  insanity.  In  some 
cases  these  mental  disturbances  are  due  to  disordered  and  inadequate  cere- 
bral blood  supply,  and  at  times  they  are  due  to  a  compUcating  nephritis 
arising  as  a  late  lesion  of  the  general  breakdown. 

Physical  Signs. — ^The  physical  signs  are  characteristic  when  well  devel- 
oped. On  inspection  the  carotid  arteries  are  seen  to  pulsate  markedly,  and 
even  the  head  may  be  moved  by  the  impulse  transmitted  to  it  by  the  heart. 
The  thorax,  in  the  prsecordium  and  neighboring  parts,  heaves  with  each  pul- 
sation of  the  heart  and  is  often  bulging,  owing  to  the  cardiac  hypertrophy  and 
dilatation.  An  ocular  examination  of  all  the  superficial  arteries  will  show  a 
characteristic  throbbing  or  jerking,  and  if  a  glass  slide  be  lightly  pressed 
against  the  lower  Hp  capillary  pulsation  is  readily  seen,  in  that  the  color  of 
the  mucous  membrane  rises  and  falls  with  the  movements  of  the  heart. 
Such  capillary  pulsation,  often  called  "Quincke's  pulse,"  can  be  seen  under 
the  thumb-nail  when  it  is  gently  pressed  upon,  and  in  the  red  line  produced 
on  the  skin  of  the  forehead  by  drawing  the  end  of  a  pencil  over  this  part. 
As  the  arteries  are  often  elongated,  and  therefore  more  tortuous  than  in 
health,  the  impulse  of  the  wave  of  blood  which  tends  to  straighten  the 
curves  makes  the  vessels  move  laterally  as  they  beat,  and  this  increases  the 
pumping  effect  which  is  produced  by  the  so-called  "Corrigan  pulse." 

The  apex  beat  is  always  far  below  and  far  outside  the  nipple  because 
of  the  dilatation  and  hypertrophy  of  the  left  ventricle,  and  also  because  of 
the  elongation  of  the  aortic  arch.  On  palpating  the  heart  the  impulse  on 
systole  is  powerful  and  diffuse  except  when  compensation  is  ruptured,  when 
it  is  feeble. 

The  pulse  when  felt  by  the  finger-tips  or  when  recorded  by  the  sphygmo- 
graph  feels  as  it  looks  on  inspecting  the  arteries.  With  each  systole  of  the 
heart  the  almost  empty  artery  suddenly  gives  to  the  finger  a  short,  sharp 
impulse,  which  equally  suddenly  disappears,  the  vessel  being  in  an  instant 
apparently  as  empty  as  before.  The  hypertrophied  and  dilated  heart  expels 
a  large  wave  of  blood  into  the  aorta,  of  which  a  part  at  once  falls  back  into 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     511 

the  ventricle,  so  that  what  might  be  called  the  tail  of  the  pulse  is  lost. 
This  is  the  so-called  "Corrigan  pulse,"  sometimes  called  the  "water-hammer 
pulse,"  or  "trip-hammer  pulse."  It  can  be  emphasized  in  the  radial 
arteries  by  raising  the  hand  above  the  head.  This  pulse  is  usually  regular 
as  tQ  rhythm  and  force.  If  it  becomes  constantly  irregular,  it  is  a  sign  of 
grave  cardiac  failure. 

On  'percussion  the  area  of  cardiac  dulness  is  found  to  be  greatly  enlarged, 
so  that  it  extends  far  over  to  the  anterior  axillary  line  in  some  instances, 
and  three  inches  below  the  nipple.  Dulness  due  to  the  enlarged  heart  is 
also  found  even  as  far  as  the  right  edge  of  the  sternum. 


Vu'..  74 


Showing  the  area  in  which  the  muriiiur  of  aortic   regurgitation  can  be  most  clearly  heard. 


Auscultation. — Auscultation  reveals  a  diastolic  murmur,  due  to  the  return 
of  the  blood  from  the  aorta  after  the  systole  has  expelled  it  into  the  vessel, 
and  while  the  ventricle  is  once  more  opening  for  a  new  supply  from  the 
auricle.  This  murmur  is  heard  in  its  greatest  intensity  at  the  fourth  left 
intercostal  space,  or  at  the  second  right  costal  cartilage  in  the  so-called 
aortic  area.  It  is  heard  at  the  fourth  left  intercostal  space  because  the 
reflux  of  blood  carries  the  murmur  back  into  the  ventricle,  and  because 
the  aortic  opening  as  a  matter  of  fact  is  nearer  this  area  than  the  second 
right  intercostal  space  (Fig.  74).  In  still  other  cases  the  diastolic  mur- 
mur may  be  very  clearly  heard  at  the  cardiac  apex  as  well  as  at  the  second 
right  intercostal  area,  although  between  the  two  no  murmur  at  all,  or  only 
a  very  faint  sound,  can    be   discovered.     The  explanation  of    this  is  that 


512  DISEASES  OF  THE  HEART 

the  right  ventricle  occupies  the  anterior  surface  of  the  heart,  except  at  the 
extreme  left  edge,  where  the  left  ventricle  protrudes  and  where  the  apex 
comes  closely  in  contact  with  the  chest  wall. 

The  murmur  of  aortic  regurgitation  is  not  widely  transmitted,  but 
is  limited,  as  a  rule,  to  the  area  described,  although  when  it  is  very  loud 
it  may  be  heard  everywhere  in  the  chest.  The  quality  of  this  murmur 
is  blowino-  or  purring.  There  is  no  accentuation  of  the  pulmonary  second 
sound  at  the  third  left  costal  cartilage,  unless  there  is  an  associated  mitral 
regurgitation  or  stenosis.  The  first  sound  of  the  heart  is  loud  or  pro- 
lono-ed  owing  to  the  large  amount  of  blood  which  has  to  be  expelled  at 
systole.  In  some  cases  a  diastolic  sound  near  the  apex  may  mislead  the 
physician  into  a  diagnosis  of  mitral  obstruction,  but  it  is  in  reality  the 
so-called  "Flint's  murmur."     (See  Mitral  Stenosis.) 

If  the  stethoscope  is  placed  over  any  one  of  the  large  superficial  arteries 
there  is  sometimes  heard,  in  cases  of  aortic  regurgitation,  a  sharp  systoHc, 
"pistol-shot"  sound,  which  is  said  to  be  due  to  sudden  filhng  of  the  vessel. 
This  sound  is  not  transmitted  from  the  heart,  but  is  local  in  origin.  It  is  a 
modification  of  the  arterial  sound  which  can  be  elicited  in  most  persons 
with  a  strong  pulse,  if  the  artery  is  occluded  by  pressure  v/ith  a  stetho- 
scope. Very  rarely  a  diastolic  arterial  sound  can  be  heard,  the  so-called 
"Duroziez  sign,"  which  is  thought  to  be  due  to  a  transmitted  cardiac 
sound. 

The  question  as  to  whether  a  diastolic  aortic  murmur  can  be  present 
without  disease  of  the  aortic  valves  has  been  much  discussed,  particularly 
of  late,  by  Cabot  and  Locke,  of  Boston,  and  Gibson,  of  Edinburgh.  As  is 
well  known,  the  aortic  ring  is  so  firm  that  it  seems  impossible  that  it  can 
yield  as  do  the  rings  of  the  pulmonary  and  mitral  orifices.  Cabot  and  Locke 
believe  that  diastolic  aortic  murmurs  are  not  uncommon  in  connection  with 
diffuse  or  localized  dilatation  of  the  aorta,  but  in  view  of  the  evidence  pre- 
sented by  Gibson,  we  must,  I  think,  agree  with  him  that  diastolic  murmurs, 
without  valvular  lesions,  are  rare  at  the  aortic  orifices,  and  that  when  they 
occur  they  are  due  to  defective  approximation  of  the  different  aortic  cusps 
rather  than  to  yielding  of  the  aortic  ring. 

Diagnosis. — ^The  sjnnptoms  and  physical  signs  of  aortic  regurgitation 
having  been  described,  it  remains  to  separate  them  from  those  conditions 
which  possess  a  resemblance.  Occasionally  in  some  persons  a  diastolic 
cardiopulmonary  murmur  is  heard,  but  it  disappears  with  change  in  posture 
and  is  dissipated  or  is  accentuated  by  forced  expiration  and  inspiration.  At 
the  level  of  the  second  and  third  rib  there  is  heard  at  times  a  hsemic  murmur 
or  hum  due  to  anaemia,  but  this  is  systolic  in  time.  Cabot  has,  however, 
reported  cases  in  which  diastoUc  murmurs  were  hsemic  and  due  to  anaemia. 

Finally,  it  is  to  be  recalled  that  the  aortic  regurgitation  murmur  is  often 
inconstant,  and  if  not  heard  at  one  examination  may  be  at  another,  or  when 
the  patient  exercises  or  changes  his  posture. 

Prognosis. — Facts  in  regard  to  the  relative  fatality  of  aortic  regurgitation 
have  already  been  given.  Allbutt  says  ten  years  constitute  a  long  time  of  life 
in  any  case  of  aortic  regurgitation.  It  is  not  only  a  serious  lesion,  but  it  is 
the  valvular  lesion  above  all  others  which  produces  sudden  death;  but  death 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     513 

in  aortic  regurgitation  is  not  always  sudden.  A  majority  of  cases  gradually 
"  play  out  "  with  dyspnoea,  dropsy,  and  cardiac  distress.  Much  depends  on 
the  age  of  the  patient,  his  previous  habits,  and  the  cause  of  the  disease. 
In  a  young  adult  with  a  good  history,  and  in  whom  the  lesion  has  followed 
rheumatism  without  great  injury  to  other  parts,  compensatory  hypertrophy 
may  carry  him  along  for  many  years  unless  he  ruptures  it  by  severe  strain, 
or  it  is  dissipated  by  illness.  When  the  lesion  comes  on  as  the  result  of 
atheroma  it  is  more  serious  because  it  is  evidence  of  general  cardiovascular 
degeneration,  and  the  coronary  arteries,  through  which  the  heart  is  chiefly 
nourished,  no  sooner  share  in  the  degenerative  change  than  feebleness  of 
the  heart  ensues.  If  perchance  the  kidneys  share  in  the  cardiocapillary 
fibrosis,  the  outlook  is  all  the  more  grave.  When  fast  living  and  debauchery 
are  factors  in  the  case,  and  an  old  syphilitic  infection  is  impairing  the  myo- 
cardium, the  outlook  is  worse  still.  (For  treatment  see  end  of  article  on 
Valvular  Disease.) 

Tricuspid  Regurgitation.  Definition. — Tricuspid  regurgitation,  or  insuf- 
ficiency, is  a  condition  in  which  the  blood  flows  backward  into  the  right 
auricle  from  the  right  ventricle,  upon  the  contraction  of  the  latter. 

Etiology  and  Pathology. — This  is  a  rare  lesion  and  is  due  to  two  chief 
causes.  It  occurs  most  commonly  as  a  result  of  disease  on  the  left  side  of 
the  heart,  whereby  the  blood  is  dammed  back  into  the  lung  and  so,  by 
preventing  free  pulmonary  circulation,  an  undue  strain  is  thrown  on  the 
tricuspid  leaflets.  In  other  instances  the  primary  obstruction  exists 
in  the  lungs,  as  in  pulmonary  emphysema,  fibroid  phthisis,  and  bronchiec- 
tasis. 

As  indicating  the  relative  frequency  of  these  causes,  Newton  Pitt  reports 
from  Guy's  Hospital  that  out  of  405  cases  of  tricuspid  regurgitation  examined 
at  autopsy,  in  a  period  of  twenty-five  years,  200  cases  were  due  to  left-sided 
failure  with  valvular  disease.  Of  this  number  64  were  cases  of  mitral 
regurgitation  with  mitral  endocarditis  or  adherent  pericardium,  66  were  due 
to  mitral  stenosis,  61  to  mitral  with  associated  aortic  disease,  and  9  had 
valvular  lesions  not  named.  In  71  cases  the  tricuspid  condition  was  due 
to  left-sided  failure  without  valvukr  disease,  in  56  cases  the  cause  lay 
in  muscular  failure  of  the  whole  heart,  and  in  55  the  lesion  was  not 
left-sided,  but  was  right-sided  alone.  Seven  cases  were  due  to  disease  of 
the  pulmonary  valves,  of  which  5  were  stenosis  and  2  pulmonary  regurgita- 
tion. In  4  cases  no  cause  could  be  found,  and  in  12  the  reports  as  to  the 
exact  state  of  the  heart  were  too  imperfect  for  analysis. 

The  valves  in  these  cases  are  usually  healthy  and  fail  to  close  the  right 
auriculoventricular  opening  because  the  orifice  is  enlarged  as  a  result  of 
dilatation  of  the  ventricle. 

The  second  cause  of  this  lesion  lies  in  the  heart  itself,  that  is,  an  endo- 
carditis invohang  the  right  side  of  the  heart.  This  is  generally  stated  to 
be  very  rare,  although  in  fetal  life  endocarditis  is  more  commonly  on  the 
right  side  of  the  heart  than  the  left.  Bramwell,  however,  combats  the 
statement  that  acute  endocarditis  rarely  affects  the  tricuspid  valves,  and 
believes  that  endocarditis  of  the  right  heart  often  exists  and  is  overlooked. 
Out  of  28  cases  of  recent  simple  endocarditis  he  found  disease  of  the  tricuspid 
33 


514  DISEASES  OF  THE  HEART 

valves  in  14,  or  50  per  cent.  Nevertheless,  the  lesions  are  not  so  pronounced 
as  those  due  to  this  cause  on  the  left  side  of  the  heart.  In  ulcerative 
endocarditis  Osier  found  the  tricuspid  valves  affected  in  19  cases  out  of 
238  instances  of  that  disease. 

A  case  in  which  tricuspid  disease  was  discovered  during  intrauterine  life 
is  reported  by  Peter,  of  Paris! 

Symptoms  and  Physical  Signs. — When  the  cause  exists  in  the  left  side  of 
the  heart  the  symptoms  are  those  naturally  arising  in  cases  of  pulmonary 
congestion  and  engorgement.  A  low-grade  bronchitis,  with  some  dulness 
at  the  bases  of  the  lungs  posteriorly  from  hypostatic  congestion,  with  cough 
and  occasionally  blood-stained  sputum,  is  discoverable.  The  jugular  veins 
become  distended  and  pulsate,  the  liver  becomes  enlarged  and  may  pulsate, 
and  there  is  marked  cyanosis.  It  is  a  noteworthy  fact  that  the  presence  of 
jugular  pulsation,  while  a  sign  of  well-developed  regurgitation,  is  not  by 
any  means  as  grave  a  sign  as  is  its  absence  in  the  presence  of  other  evidences 
of  cardiac  embarrassment,  because  if  the  right  ventricle  is  strong  it  may 
drive  the  regurgitating  blood  with  sufficient  force  to  cause  jugular  pulsation, 
whereas  if  it  be  weak  no  jugular  pulsation  can  ensue.  On  the  other  hand, 
the  presence  of  jugular  pulsation  shows  that  the  regurgitation  is  a  grave 
one,  because  it  does  not  occur  until  a  considerable  quantity  of  blood  flows 
into  the  auricle  and  distends  the  veins  sufficiently  to  interfere  with  the 
valves,  so  that  they  cannot  prevent  auricular  regurgitation  as  they  do  in 
health. 

A  distinct  impulse  in  the  upper  epigastrium  is  often  present. 

The  pidsation  of  the  liver  is  best  discovered,  if  not  seen,  by  placing  the 
finger-tips  or  hand  against  the  floating  ribs  at  the  side,  and  the  other  hand 
near  the  ensiform  cartilage,  and  then  exerting  gentle  pressure  upon  the 
liver  from  both  directions.  Care  must  be  taken  that  a  directly  transmitted 
impulse  from  a  hypertrophied  heart  is  not  taken  for  true  expansile  pulsation 
of  the  liver. 

On  percussion,  increase  in  the  area  of  cardiac  dulness  to  the  right  of  the 
sternum  is  demonstrable. 

On  auscultation  at  the  apex  a  soft  systolic  murmur,  or  purr,  can  be 
heard,  which  is  found  to  be  loudest  at  about  the  fifth  interspace,  to  the  right 
of  the  sternum  or  at  the  base  of  the  ensiform  cartilage,  and  which  may  be 
in  a  few  cases  transmitted  to  the  right  axillary  area.  The  murmur  of 
tricuspid  regurgitation  has  been  said  to  resemble  the  sounds  made  by  a 
small  jet  of  escaping  steam,  and  it  may  be  singing  or  musical.  Duroziez 
says  that  venous  blood  "sings"  more  than  arterial  blood. 

Diagnosis. — ^True  tricuspid  regurgitation  must  be  differentiated  from 
regurgitation  at  this  orifice,  which  is  temporary  and  not  constant.  These 
valves  not  rarely  give  way  from  severe  strain,  as  in  athletes  during  exer- 
tion. They  act  in  this  way  as  a  "safety-valve"  to  relieve  undue  pressure, 
and  as  soon  as  the  strain  ceases  the  heart  gradually  returns  to  its  normal 
size  and  the  murmur  disappe9,rs.  So,  too,  a  similar  murmur  may  develop 
in  cases  of  profound  asthenia  resulting  from  prolonged  fevers,  particularly 
if  the  heart  is  strained  by  the  patient  attempting  to  do  too  much.  Such  a 
murmur  may  or  may  not  pass  away  with  rest. 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     515 

Prognosis. — The  prognosis  depends  entirely  upon  the  exciting  cause,  the 
age  of  the  patient,  and  his  general  state  and  manner  of  life.  In  those  who 
have  to  do  manual  labor  the  prognosis  is  usually  bad. 

Tricuspid  Stenosis. — ^This  condition  sometimes  arises  as  the  result  of  an 
attack  of  endocarditis  involving  both  sides  of  the  heart,  and  is  usually  asso- 
ciated with  mitral  stenosis.  In  other  instances  it  is  congenital.  In  the  vast 
majority  of  cases  it  is  found  as  an  associated  lesion,  and  it  is  exceedingly 
rare. 

In  1899  Newton  Pitt  collected  87  cases  of  tricuspid  stenosis  from  the 
post-mortem  records  of  Guy's  Hospital  extending  over  a  period  of  twenty- 
six  years,  and  comprising  a  total  of  12,000  autopsies.  Leudet,  in  his  Paris 
thesis  on  tricuspid  stenosis,  gives  the  following  figures,  based  on  114  post- 
mortem examinations  which  were  collected  from  various  sources,  and  which 
include  the  cases  collected  by  Fenwick: 

Stenosis  of  the  tricuspid  valve  alone     .  .  .  .  .  .11 

Stenosis  of  the  tricuspid  and  of  the  orifice  of  the  pulmonary  artery       3 
Stenosis  of  the  tricuspid,  mitral,  and  pulmonary    ....       1 

Stenosis  of  the  tricuspid,  mitral,  and  aortic  .  .  .  .  .21 

Stenosis  of  the  tricuspid  and  mitral       .  .....     78 

F.  W.  Griffith,  of  Leeds,  has  examined  Leudet's  tabulation  of  cases  and  has 
shown  that  probably  only  two  of  them  were  unassociated  with  lesions  of  the 
other  valves.  These  figures  show  the  rarity  of  uncomplicated  tricuspid  stenosis. 

Diagnosis. — ^The  diagnosis  of  the  lesion  during  life  is  usually  very  difficult, 
but  it  can  be  made.  The  murmur,  if  present,  is  presystolic  in  time  and  has 
its  greatest  intensity  at  the  fifth  right  interspace  near  the  sternum.  As 
already  stated,  this  murmur  is  usually  associated  with  that  of  mitral  stenosis, 
and  its  existence  may  be  completely  masked  by  the  presystolic  murmur  at 
the  mitral  orifice.  Additional  physical  signs  of  tricuspid  stenosis  are  dis- 
tention of  the  jugular  veins  without  pulsation,  or  with  very  slight  pulsation 
due  to  the  feeble  auricular  regurgitant  impulse. 

As  dropsy  is  a  late  symptom  of  severe  mitral  stenosis,  the  early  develop- 
ment of  dropsy  in  a  case  with  a  presystolic  murmur  which  is  not  aortic 
strongly  indicates  tricuspid  obstruction. 

Disease  of  the  Pulmonary  Valves. — Lesions  of  the  pulmonary  valves  are 
so  rarely  met  with  that  many  practitioners  of  large  experience  have  never 
seen  a  case  presenting  them.  When  actual  lesions  occur  they  are  nearly 
always  congenital,  and  the  usual  lesion  is  that  of  pulmonary  stenosis  or 
obstruction,  for  pulmonary  regurgitation  is  the  rarest  of  cardiac  lesions. 
On  the  other  hand,  there  is  no  area  at  which  we  listen,  for  the  purpose  of 
determining  the  state  of  the  heart  valves,  in  which  murmurs  are  so  con- 
stantly found  as  the  so-called  pulmonary  area,  at  the  second  and  third  left 
intercostal  space.  These  murmurs  are  not  due  to  actual  disease  of  the 
pulmonary  valves  or  of  the  pulmonary  artery,  but  they  arise  from  causes  of 
a  non-organic  character  and  are  usually  systolic  in  point  of  time.  These 
functional  murmurs  may  be  due  to  one  of  several  causes,  as,  for  example, 
anaemia  and  chlorosis,  producing  the  so-called  hsemic  murmur.  They  also 
occur  in  pregnant  women  and  in  women  after  childbirth.    In  other  instances 


516  DISEASES  OF  THE  HEART 

they  are  present  as  a  sign  of  Graves'  disease  or  of  nervous  tachycardia,  and 
in  still  others  they  arise  from  some  abnormal  position  of  the  heart,  caused 
by  conditions  which  alter  the  relationship  of  the  heart  muscle  to  its  great 
vessels.  These  conditions  all  produce  a  pulmonary  murmur  which  may  be 
considered  as  within  the  area  of  the  pulmonary  artery  or  near  its  valves. 
In  addition  we  sometimes  hear  at  this  point  a  so-called,  cardiopulmonary 
murmur,  which  is  supposed  to  be  due  to  the  effect  of  the  bloodvessel  upon 
the  lung,  or  vice  versa,  in  that  the  murmur  occurs  during  forced  inspiration, 
or  expiration.  This  murmur  is  not  rarely  seen  at  this  point  in  early  tuber- 
culosis of  the  apex  of  the  left  lung. 

Pulmonary  Stenosis. — The  systolic  murmur  which  is  due  to  actual 
organic  disease  at  the  pulmonary  valve  is  due  to  stenosis,  as  already 
stated,  and  is  commonly  due  to  gluing  together  of  the  cusps  of  the  pul- 
monary valves  in  antenatal  life.  This  murmur  is  more  harsh  than  the  soft 
purring  murmurs  of  the  functional  type  just  described.  The  patient  usually 
has  a  history  of  having  been  cyanotic  all  his  life,  with  dyspnoea  on  the 
slightest  exertion.  Percussion  and  palpation  will  usually  reveal  a  distinct 
increase  of  cardiac  dulness  to  the  right  from  hypertrophy  of  the  right  ven- 
tricle. Palpation  also  will  reveal  a  distinct  systolic  thrill  over  the  area  of 
the  pulmonary  valves. 

The  points  by  which  the  true  systolic  murmur  is  to  be  separated  from 
the  functional  murmurs  already  described  are  the  absence  of  systolic  thrill 
in  the  case  of  the  functional  murmurs,  the  harshness  of  the  true  murmur, 
and  the  hypertrophy  of  the  right  ventricle  in  cases  of  actual  pulmonary 
disease.  From  aneurysm  of  the  descending  portion  of  the  aortic  arch  the 
true  pulmonary  murmur  is  separated  by  the  fact  that  in  such  a  case  the 
hvpertrophy  chiefly  involves  the  left  side  of  the  heart,  by  the  additional 
fact  that  there  is  a  bruit,  not  a  murmur,  and  by  the  presence  of  a  bruit 
posteriorly  on  the  left  side  between  the  vertebrae  and  scapula.  There  are 
also  pressure  symptoms  in  aneurysm  in  many  cases.  Finally,  if  it  be 
aneurysm,  percussion  of  the  third  left  costal  cartilage  will  reveal  dulness, 
which  is  absent  in  pulmonary  stenosis.  The  murmur  of  aortic  stenosis  is 
heard  louder  at  the  second  right  costal  cartilage  than  at  the  second  or  third 
left  cartilage,  and  is  transmitted  into  the  carotids,  but  the  pulmonary"  mur- 
mur is  not. 

Pulmonary  regurgitation,  the  rarest  of  all  valvular  lesions,  is  usually 
fetal  in  origin,  but  cases  have  been  recorded  in  which  it  has  arisen  as  a 
result  of  ulcerative  endocarditis.  The  murmur  due  to  this  cause  is,  of  course, 
diastolic,  and  is  produced  by  the  blood  faUing  back  from  the  pulmonary 
artery  into  the  right  ventricle.  It  is  to  be  separated  from  aortic  regurgitation 
by  the  fact  that  it  is  heard  best  to  the  left  of  the  sternum  instead  of  to  the 
right,  and  by  the  absence  of  the  Corrigan  pulse  of  aortic  disease.  There 
are  signs  of  dilatation  and  hypertrophy  of  the  right  ventricle,  and  the  pul- 
monary second  sound  may  be  accentuated.  It  is  by  no  means  uncommon 
for  the  existence  of  pulmonary  regurgitation  to  be  unsuspected  until  autopsy. 

Treatment  of  Chronic  Valvular  Disease. — It  is  of  vital  importance  that  the 
physician  remember  the  fact  that  the  mere  presence  of  a  valvular  lesion 


CHRONIC  VALVULAR  DISEASE  AS  A  RESULT  OF  ENDOCARDITIS     517 

in  the  heart  does  not  indicate  drug  treatment.  On  the  contrary,  much  harm 
is  frequently  done  by  the  administration  of  cardiac  stimulants  to  patients 
who  are  found  to  possess  a  valvular  lesion,  with  the  result  that  natural 
compensation  is  disturbed  and  cardiac  symptoms  may  be  noted  by  the 
patient  for  the  first  time  in  his  history.  It  is  only  when  the  patient  presents 
symptoms  which  indicate  failure  of  cardiac  function  that  the  physician 
should  think  of  administering  remedies  which  have  a  direct  influence  upon 
the  heart.  In  other  words,  when  compensation  is  complete,  no  cardiac 
treatment  is  indicated,  but  when  it  is  ruptured  therapeutic  measures  should 
be  instituted.  I  have  again  and  again  seen  patients  who  have  presented 
some  ailment  involving  other  organs  in  the  body  than  the  heart,  in  whom 
the  physician,  on  examination,  found  a  mitral  regurgitant  murmur,  and  im- 
mediately proceeded  to  administer  digitalis,  forgetting  that  the  presence  of  a 
murmur  in  the  absence  of  evidences  of  circulatory  failure  is  not  an  indica- 
tion for  the  use  of  the  drug. 

Another  important  point  to  be  borne  in  mind  when  the  physician  is 
called  upon  to  treat  a  case  in  which  compensation  is  failing  is  that,  far  and 
above  all  drugs  in  value,  is  rest  for  the  patient;  not  only  rest  of  the  body, 
but  rest  of  the  mind.  The  heart  is  an  organ  which,  of  course,  cannot  have 
complete  rest  at  any  time;  but  its  work  can  be  diminished  one-half  if  the 
patient  can  be  made  to  take  no  exercise,  and  if  he  will  carefully  abstain  from 
business  worries  and  cares.  It  is  a  remarkable  fact  that  disease  of  the 
coronary  arteries  and  of  the  heart  muscle  is  more  common  in  brain-workers 
than  in  those  who  gain  their  living  by  manual  toil,  and  this  is  an  indication 
of  the  fact  that  mental  labor  throws  a  severe  strain  upon  the  heart.  Care- 
ful observation  will  promptly  prove  that  patients  who  are  not  benefited 
by  digitalis  and  other  cardiac  stimulants,  when  suffering  from  ruptured 
compensation,  will  at  once  improve  if  rest  is  insisted  upon;  for,  manifestlv, 
the  rupture  of  compensation  is  largely  the  result  of  cardiac  fatigue,  and  this 
fatigue  cannot  be  put  aside  by  the  mere  administration  of  stimulants.  In 
order  that  the  juices  of  the  body  may  be  kept  moving,  it  is  useful  in  these 
cases,  when  they  are  made  to  rest  in  bed,  to  use  more  or  less  vigorous  massage 
daily,  its  vigor  depending  upon  the  strength  of  the  individual.  If  the  massage 
is  too  vigorous,  it  may  produce  very  considerable  fatigue,  and  it  should  not 
be  employed  to  this  extent. 

In  all  cases  of  ruptured  compensation  the  patient  should  be  warned  of 
the  danger  of  sudden,  severe  effort,  since,  even  if  death  does  not  ensue  under 
these  circumstances,  the  heart  may  be  so  dilated  or  fatigued  that  irreparable 
damage  is  done  to  it. 

Digitalis  is  without  doubt  facile  'princeps  the  best  of  cardiac  stimulants. 
I  have  proved  that  it  actually  increases  the  muscular  development  of  the 
heart,  and  the  manner  in  which  it  acts  results  in  an  increased  nerve  and 
blood  supply  to  this  viscus  which  is  not  equalled  by  the  results  obtained 
from  the  administration  of  any  other  remedy.  Digitalis  is,  in  a  large  number 
of  cases,  given  in  too  large  doses.  Not  infrequently  as  much  as  10,  or  even 
20  minims  of  the  tincture  are  given  three  times  a  day,  with  the  result  that  in 
the  course  of  a  few  days  the  heart  is  overstimulated  by  the  drug;  its  cumu- 
lative effect  is  produced,  and  instead  of  doing  good  it  may  do  serious  harm. 


518  DISEASES  OF  THE  HEART 

I  have  known  of  cases  in  which  the  use  of  full  doses  of  digitalis,  persisted 
in  for  a  considerable  period  of  time,  have  resulted  in  the  sudden  death  of 
the  individual. 

When  digitalis  is  given  in  overdoses  it  produces  a  curious  irregularity  of 
force  and  rhythm  in  the  heart,  with  imperfect  systole,  followed  by  wide 
diastole,  and  this  causes  a  hobbling  pulse.  The  urine  may  also  be  reduced 
in  amount  instead  of  increased,  as  it  should  be,  under  the  influence  of  the 
remedy. 

It  has  been  my  experience  that  if  the  patient  is  made  to  rest,  small  doses 
of  digitalis  produce  satisfactory  results,  not  more  than  5  drops  of  the  tincture 
being  given  three  times  a  day.  The  only  conditions  in  which  I  think  that 
the  use  of  large  doses  is  justified  are  when  the  condition  of  the  heart  is 
found  to  be  exceedingly  feeble,  and  the  patient's  condition  so  critical  that 
immediate  stimulation  is  necessary;  and  again,  when  because  of  idiosyncrasy 
or  other  cause  the  heart  is  found  not  to  respond  to  smaller  doses.  In  the 
first  class  of  cases  it  has  been  my  experience  that  it  is  better  to  overcome 
pressing  cardiac  weakness  by  more  rapidly  acting  and  diffusible  stimulants 
such  as  Hoffmann's  anodyne,  strychnine,  and  caffeine  for  the  first  twenty- 
four  of  forty-eight  hours  until  the  digitalis  has  a  chance  to  act;  for  it  must 
always  be  remembered  that  digitalis  is  a  drug  which  produces  its  effects 
very  slowly,  and  maintains  these  effects  for  some  time  after  its  use  has  been 
stopped.  When  large  doses  are  given,  it  has  been  my  experience  that  they 
may  be  decreased  to  about  one-half  or  one-quarter  the  original  quantity  at 
the  end  of  a  few  days,  and  their  effects  maintained  by  the  use  of  smaller 
quantities.  I  do  not  think  that  I  am  exaggerating  the  case  when  I  state 
that  digitalis,  through  its  abuse,  does  almost  as  much  harm  as  it  does  good. 
(See  my  Text-book  of  Therapeutics,  article  "Digitahs.") 

The  fluid  extract  of  digitalis  may  be  given  in  the  dose  of  from  ^  to  5 
minims,  according  to  the  needs  of  the  case.  One-half  to  1  minim  every 
eight  hours  is  usually  sufficient.  A  physiologically  tested  preparation  should 
always  be  employed. 

When  dropsy  is  present  it  has  been  held  that  the  infusion  of  digitalis  is 
the  best  preparation  on  the  ground  that  it  is  more  diuretic.  But  any  slight 
increase  in  diuretic  power  is,  I  think,  counterbalanced  by  the  fact  that  it  is 
much  more  apt  to  disorder  the  stomach,  which  is  in  a  disturbed  condition 
in  any  case  of  grave  disease,  and  particularly  so  in  heart  disease. 

When  digitalis  has  been  given  in  full  doses  to  a  patient  suffering  from 
ruptured  compensation,  he  should  be  warned  against  getting  up  suddenly, 
and  particularly  against  evacuating  the  bladder  when  in  a  standing  posi- 
tion, as  dangerous  syncope  may  occur  under  these  circumstances. 

Before  deciding  upon  the  administration  of  any  cardiac  stimulant  in 
a  case  with  ruptured  compensation,  the  physician  should  make  a  careful 
study  of  the  state  of  the  bloodvessels,  and  if  the  arterial  tension  is  higher 
than  normal  he  should  remember  that  the  use  of  nitroglycerin  to  reduce 
this  tension,  and  thereby  diminish  the  work  of  the  heart,  is  a  more  important 
therapeutic  procedure  than  the  administration  of  a  stimulant  which  simply 
urges  the  heart  to  do  more  work  in  the  face  of  vascular  obstruction. 
In  such  a  case  the  fact  that  digitalis  stimulates  the  vasomotor  system  and 


CHRONIC  VALVULAR  DISEASE   AS  A    RESULT  OF  ENDOCARDITIS     519 

raises  arterial  tension  should  also  be  remembered.  Nitroglycerin  can  often  be 
given  to  advantage  to  prevent  this  arterial  effect  of  the  drug.  Strophanthus, 
which  is  a  much  less  powerful  stimulant  than  digitalis,  possesses  the  advan- 
tage that  it  does  not  raise  arterial  pressure  by  stimulating  the  vasomotor 
system,  and  can  often  be  given  in  the  dose  of  5  to  10  minims  of  the  tincture 
every  eight  hours  with  advantage.  Large  doses  of  strophanthus  are  prone 
to  produce  an  irritative  diarrhoea. 

There  is  a  host  of  drugs  which  have  been  recommended  for  ruptured 
compensation,  but  none  of  them  approach  these  three  in  value,  and  often 
when  these  fail  the  failure  is  due  to  a  mistake  in  the  dose  rather  than  to 
a  fault  of  the  drug.  Should  there  be  any  tendency  to  hypostatic  congestion 
of  the  lungs  or 'pulmonary  oedema,  digitalis  may  be  freely  given,  and  strych- 
nine and  atropine  administered  as  vasomotor  stimulants.  Two  or  three 
dry  cups  over  the  base  of  each  lung  are  also  useful  under  these  circum- 
stances, and  sometimes  a  sharp  purgative  may  do  good  if  dropsy  is  present; 
but  the  possibility  of  the  purge  weakening  the  patient  must  always  be  borne 
in  mind. 

Attacks  of  acute  cardiac  failure  are  to  be  combated  by  Hoffmann's  anodyne 
in  the  dose  of  1  or  2  drachms  every  hour  or  two,  or  aromatic  spirit  of  ammonia 
in  the  dose  of  ^  to  1  drachm.  If,  associated  with  the  cardiac  failure,  there 
is  high  arterial  tension,  the  nitroglycerin  should  be  used  hypodermically 
in  the  dose  of  j^-^  to  yw  ^f  a  grain,  and  repeated  every  half-hour  until  the 
tension  is  lowered. 

When  marked  dropsy  is  present,  the  use  of  magnesium  sulphate  in  con- 
centrated solution,  a  heaping  teaspoonful  to  one-half  glass  of  water  taken 
before  breakfast,  will  often  do  good  by  removing  large  quantities  of  fluid 
from  the  patient's  body.  A  very  useful  remedy  in  cardiac  dropsy,  both 
by  reason  of  its  action  on  the  heart  and  because  of  its  diuretic  effect,  is 
apocynum  cannabinum  given  in  the  dose  of  from  5  to  30  minims  of  the 
tincture  twice  or  thrice  a  day  until  it  produces  slight  purgation.  Care 
should  be  taken  that  a  fluid  extract  of  real  apocynum  cannabinum  is  obtained. 
Much  of  that  on  the  market  is  apocynum  androsimsefolium,  which  has  no 
such  therapeutic  properties,  but  which  so  closely  resembles  apocynum  canna- 
binum that  its  leaves  are  often  unintentionally  substituted  for  the  true  drug. 

Another  very  useful  prescription  in  cardiac  dropsy  is  a  tablet  composed  of 

Extract  of  sourwood  leaves        .         .         .         .  .         .2  grains. 

Extract  of  elder  flowers    .......     2  grains . 

Extract  of  squill        ........     ^  grain. 

Take  one  or  two  tablets  three  times  a  day. 

For  generations  physicians  have  been  in  the  habit  of  employing  a  pill 
composed  of — 

Powdered  squill         ........      1  grain; 

Powdered  digitalis  leaves  ......      1  grain; 

Calomel    ..........      1  grain;  ♦ 

three  times  a  day  in  the  treatment  of  cardiac  dropsy,  for  its  stimulant  and 
diuretic  effect.     If  free  diuresis  is  not  produced  by  this  pill  at  the  end  of 


520  DISEASES  OF   THE  HEART 

the  third  day  it  should  be  stopped,  and  a  sahne  purgative  administered 
to  sweep  out  the  calomel  from  the  alimentary  canal. 

In  many  cases  of  cardiac  disease,  particularly  if  the  presence  of  anaemia 
is  marked,  iron  and  arsenic  are  indicated,  both  on  general  principles  and 
because  we  cannot  expect  to  improve  the  nutrition  of  the  heart  when  it  is 
supplied  by  impoverished  blood. 

It  is  important  to  remember  that  in  nearly  every  case  of  failing  compensa- 
tion there  is  a  certain  amount  of  hepatic  congestion.  This  is  best  relieved 
by  the  use  of  5  or  10  grains  of  blue  mass  given  every  week  or  ten  days. 
Frequently  digitalis  and  other  stimulants  will  act  much  better  after  the 
liver  has  been  unloaded  by  the  mercury  than  they  will  when  this  gland  is 
congested. 

When  the  rupture  of  compensation  has  resulted  in  dyspnoea  and  anxiety, 
morphine  proves  itself  a  most  valuable  remedy.  It  should  not  be  given  except 
in  cases  in  which  there  is  dire  need  of  rest,  since  if  used  too  frequently  it 
loses  its  good  effects,  and  frequently  causes  constipation  and  disorder  of 
digestion.  On  the  other  hand,  the  quiet  and  rest  produced  by  |-  to  I  of  a 
grain  of  morphine  will  often  cause  marvellous  improvement.  It  has  seemed 
to  me  that  it  is  most  satisfactory  in  mitral  lesions.  If  dropsy  is  present,  it 
cannot  be  given  hypodermically  because  it  will  not  be  absorbed. 

When  there  is  great  engorgement  of  the  jugular  veins,  and  manifest  dis- 
tention of  the  right  side  of  the  heart  with  pulmonary  congestion,  vene- 
section to  the  extent  of  about  8  ounces  to  a  pint,  according  to  the  size 
of  the  individual,  is  often  very  valuable  as  a  means  of  relief.  It  also 
is  a  remedy  which  is  to  be  reserved  for  somewhat  desperate  conditions,  as 
manifestly  it  is  not  proper  to  bleed  frequently. 

It  is  generally  considered  that  digitalis  does  less  good  in  cases  of  aortic 
regurgitation  than  in  other  valvular  lesions,  and  I  believe  this  opinion  is 
correct.  Some  have  taught  that  it  is  contraindicated  in  aortic  regurgitation. 
While  this  may  be  the  general  rule,  every  now  and  then  we  meet  with  cases 
in  which  cautious  use  of  the  drug  in  this  state  produces  excellent  results, 
provided  compensation  is  ruptured. 

In  some  instances  when  the  heart's  action  is  very  irregular  and  excitable 
an  ice-bag  applied  over  the  prsecordium  is  advantageous. 

When  the  patient  has  had  syphilis,  chronic  rheumatism,  or  gout,  or 
manifests  evidences  of  arterial  capillary  fibrosis,  iodide  of  sodium  or  iodide 
of  potassium  in  the  dose  of  10  or  15  grains  a  day  is  advantageous. 

The  diet  in  cases  of  valvular  disease  should  be  simple,  but  nutritious. 
The  patient  had  better  eat  four  or  five  small  meals  a  day  than  two  or  three 
hearty  ones,  and  the  greatest  possible  care  should  be  taken  that  foods 
which  are  prone  to  produce  gaseous  distention  of  the  stomach  and  bowels 
are  avoided.  Fatty  substances  are  very  apt  to  produce  such  symptoms,  as 
are  also  the  starches,  when  they  remain  in  the  stomach  undigested  for  a 
considerable  period  of  time.  This,  however,  can  be  put  aside  in  the  case 
of  the  starches  by  the  use  of  taka-diastase  or  pancreatin  and  by  the  use 
of  powdered  capsicum,  either  in  pill  or  upon  the  food,  for  the  purpose  of 
stimulating  the  gastric  mucous  membrane,  which  is  often  atonic  or  catarrhal 
as  a  result  of  the  impaired  hepatic  circulation. 


NEUROSES  OF   THE  HEART  521 


NEUROSES  OF  THE  HEART. 


Definition. — By  neuroses  of  the  heart  it  is  meant  to  include  a  number 
of  conditions  widely  separated  in  their  actual  causes,  but  depending  upon 
a  disorder  of  the  nerve  supply  of  this  organ,  so  that,  without  there  being 
necessarily  present  any  grave  organic  lesions,  its  functional  activity  is 
impaired  or  perverted. 

Palpitation. — Palpitation  of  the  heart  may  be  due  to  any  of  the  valvular 
or  other  lesions  that  cause  the  heart  to  beat  rapidly  or  irregularly  -when 
the  individual  takes  exercise.  In  other  cases  it  arises  from  the  accumulation 
of  gas  in  the  stomach  or  colon,  which  by  its  pressure  causes  cardiac  dis- 
turbance. In  other  instances  it  is  due  to  intense  nervous  erethism,  and  in 
still  others  it  arises  from  the  excessive  use  of  tobacco  or  of  coffee  or  tea. 
So,  too,  sudden  nervous  shock  may  cause  repeated  attacks  of  this  character. 
Probably  the  most  frequent  cause  of  cardiac  palpitation  is  not  connected 
with  the  nerves  supplying  the  heart,  but  is  due  to  irregularities  in  the  nervous 
control  of  the  vasomotor  system,  whereby  the  tension  of  the  vessels  is 
relaxed  and  as  a  result  the  heart  beats  rapidly  because  the  ordinary  pressure 
in  the  arteries  is  suddenly  removed.  It  is  remarkable  how  cases  of  palpi- 
tation get  well  if  attention  is  paid  to  the  state  of  the  bloodvessels  rather  than 
the  heart.  The  so-called  "irritable  heart  of  soldiers,"  first  described  by 
J.  M.  Da  Costa,  is  due  in  all  probability  to  this  cause  as  well  as  to  the 
imperfect  action  of  the  vagus.  Associated  with  the  disordered  cardiac  action 
it  w^ill  often  be  found  that  the  peripheral  capillaries  suddenly  become 
dilated,  so  that  the  blood  can  flov/  more  rapidly  than  normal  into  them. 
Profuse  diuresis,  in  which  the  urine  is  found  to  be  pale  and  clear,  shows 
that  a  similar  relaxation  of  the  renal  vessels  has  ensued.  These  symptoms 
often  cause  the  patient  great  alarm  and  bring  him  at  once  to  the  physi- 
cian with  the  statement  that  heart  disease  is  feared.  It  is  usually  the 
case  that  a  patient  who  says  he  has  heart  disease  has  only  a  neurosis, 
unless  some  physician  has  found  a  real  lesion  and  told  him  of  its  existence. 

Tachycardia. — Many  cases  of  neurosis  are  closely  allied,  if  not  identical, 
with  that  condition  of  rapid  heart  called  tachycardia.  This  may  be  due 
to  vasomotor  palsy,  to  a  deficient  action  of  the  vagus  nerves,  or  to  some 
central  nervous  lesion.  (The  tachycardia  of  exophthalmic  goitre  is  not 
considered  here.) 

Such  attacks  occur  in  young  hysterical  women  and  are  called  "pseudo- 
angina,"  because  a  sense  of  cardiac  expansion  is  often  present  with  the 
rapid  beating  of  the  heart.  They  also  appear  in  women  near  the  menopause, 
and  in  men  who  have  been  guilty  of  excessive  sexual  abuse.  A  few^  cases 
in  men  are  apparently  due  to  some  organic  nervous  lesion.  The  pulse  may 
rise  as  high  as  220.  The  tachycardia  may  be  paroxysmal  or  continuous. 
In  a  case  under  my  care  in  1890,  a  woman  who  had  seen  her  husband  and 
sons  drowned  in  the  great  Johnstown  flood,  and  had  been  swept  from  the  roof 
of  her  floating  cottage,  presented  a  pulse  rate  which  was  uncountable,  it 
was  so  fast.  This  persisted  for  months  and  was  present  two  years  after 
the  catastrophe. 


522  DISEASES  OF  THE  HEART 

Rapid,  feeble  heart  sounds,  in  which  the  first  and  second  sounds  appear 
aUke,  are  met  with  in  prolonged  exhausting  fevers  such  as  severe  typhoid 
fever,  and  to  this  state  is  given  the  name  "fetal  heart  sounds"  or  "  em- 
bryocardia." 

Bradycardia. — Great  slowness  of  the  heart's  action  (bradycardia)  is  caused, 
to  some  extent  at  least,  by  conditions  which  are  the  antithesis  of  those  that 
cause  tachycardia.  A  sudden  or  persistent  rise  of  arterial  pressure  may  cause 
a  very  slow  pulse,  as  the  heart  endeavors  to  force  blood  through  tightly 
contracted  vessels.  This  may  be  called  vascular  bradycardia.  Again,  it 
occurs  as  the  result  of  irritation  of  the  vagus  nerves  by  poisons  such  as 
digitalis  and  opium,  or  in  chronic  lead  poisoning,  or  again  in  cases  of  jaun- 
dice when  the  slowing  is  due  to  the  biliary  salts  in  the  blood.  It  is  also 
met  with  in  cases  of  apoplexy,  cerebral  tumor,  and  in  the  coma  following 
epilepsy. 

A  pulse  below  60,  or  even  as  low  as  40,  is  sometimes  felt  after  a  woman 
has  given  birth  to  a  child. 

Occasionally  cases  are  met  with  in  which  the  bradycardia  becomes 
extraordinary.  The  late  D.  W.  Prentiss  reported  to  the  Association  of 
American  Physicians  in  1889,  1890,  and  1891  the  case  of  a  man  whose 
pulse  at  times  fell  to  11  per  minute  and  rarely  rose  over  40  per  minute 
for  two  years.  In  this  case  no  very  distinct  morbid  lesions  were  found  at 
autopsy,  although  the  patient  died  suddenly  in  an  attack.  (See  Stokes- 
Adams  Disease. 

Arhythmia. — There  are  other  cases  met  with  in  which  cardiac 
arhythmia — that  is,  irregularity  as  to  the  speed  and  the  force  of  the 
heart  beats — occurs.  In  many  cases  this  is  due  to  a  neurosis  of  the 
vagus.  It  is  very  commonly  met  with  in  persons  who  have  taken 
excessive  doses  of  digitalis,  and  it  is  also  a  common  symptom  in  mitral 
stenosis  with  ruptured  compensation.  The  so-called  gallop  rhythm  may 
appear  in  these  cases.  (See  Mitral  Stenosis.)  Occasionally  arhythmia  is 
a  notable  s}miptom  in  cases  of  myocardial  degeneration,  but  cases  are 
recorded  in  which  arhythmia  has  lasted  for  several  decades  in  seemingly 
healthy  men. 

Treatment  of  Caxdiac  Neuroses. — In  the  treatment  of  the  various  cardiac 
neuroses  it  is  essential  that  the  physician  shall  first  determine  what  portion 
of  the  circulatory  system  is  chiefly  affected  by  disordered  innervation.  Not 
infrequently,  however,  it  will  be  found  that  both  the  heart  and  vasomotor 
system  are  out  of  order,  and  therefore  the  treatment  will  have  to  be  devoted 
to  regulating  the  nerve  supply  of  the  functions  of  both  of  these  important 
vascular  areas. 

When  it  is  believed  that  attacks  of  tachycardia  have  their  origin  in  a 
condition  in  which  the  pneumogastric  nerve  fails  to  control  the  action  of 
the  heart,  digitalis  is,  of  course,  a  valuable  remedy  in  that  it  exercises  a 
powerful  stimulating  influence  upon  the  pneumogastric  nerves.  In  some 
instances,  however,  the  action  of  the  heart  is  already  sufficiently  vigorous 
and  the  administration  of  digitalis,  while  stimulating  the  pneumogastric 
nerve,  also  stimulates  the  heart  to  such  an  excessive  degree  that  its  action 
becomes  too  violent.    Under  these  circumstances  it  is  well  to  combine  with 


ANGINA  PECTORIS  523 

the  digitalis  a  little  aconite,  which  drug  also  stimulates  the  pneumogastric 
nerve,  and  thereby  aids  the  digitalis  in  controlling  the  heart,  and  at  the 
same  time  combats  the  influence  of  the  digitalis  upon  the  heart  muscle 
itself,  thereby  preventing  overstimulation,  A  prescription  made  up  as  follows 
will  often  be  of  advantage,  the  quantities  of  the  ingredients  being  varied 
to  suit  the  needs  of  the  individual  case: 

R. — Tinct.  digitalis  (physiologically  tested)      .  .  •     ^5]    (4.0). 

Tinct.  aconiti f  gss  (2.0), 

Tinct.  belladonnse .     f  3  ij  (8.0). 

Tinct.  cardamom,  comp.  .  .         .         .       q.  s.  ad    f^iij. 

A  teaspoonful  to  a  dessertspoonful  three  or  four  times  a  day. 

The  efficiency  of  this  prescription  may  be  increased  by  the  application  of 
a  belladonna  plaster  over  the  heart. 

In  those  cases  in  which  the  cardiac  irregularity  depends  chiefly  upon 
alternate  spasm  and  relaxation  of  the  bloodvessels,  so  that  they  are  at  one 
moment  offering  too  much  resistance  and  at  another  too  little  resistance 
to  the  flow  of  blood,  much  benefit  can  be  produced  by  hydrotherapeutic 
measures,  such  as  directing  that  the  patient  shall  take  an  alternate  hot  and 
cold  sponging  in  the  morning  on  getting  up;  first,  drenching  himself  with  a 
sponge  dipped  in  as  hot  water  as  he  can  bear,  and  next  drenching  himself 
with  a  sponge  dipped  in  cold  water.  In  this  way  he  does  not  become  chilled, 
but  the  elasticity  and  tone  of  the  bloodvessels  is  much  improved.  The 
prescription  just  recommended  is  also  beneficial  in  many  of  these  cases,  and 
not  infrequently  moderate  doses  of  tincture  of  nux  vomica  are  advantageous. 
When  the  disorder  depends  upon  the  excessive  use  of  tobacco,  this  drug 
must,  of  course,  be  prohibited;  and  if  the  patient  is  overworked,  and  suffer- 
ing from  nervous  strain,  he  must  be  sent  away  on  a  vacation;  or,  if  his  con- 
dition is  grave,  be  given  a  "  rest  cure."  When  a  disordered  circulation  is 
associated  with  pain  in  the  neighborhood  of  the  heart,  small  doses  of 
antipyrin,  2  to  3  grains,  are  often  useful;  and  if  the  tension  is  high, 
nitroglycerin  should  be  given. 


ANGINA  PECTORIS. 

Definition. — By  angina  pectoris  is  meant  a  condition  in  which  a  patient, 
usually  in  or  past  middle  life,  is  seized  by  a  severe,  agonizing  pain  in  the 
cardiac  area,  which  extends  in  most  cases  down  the  left  arm  even  to 
the  wrist,  and  suffers  from  intense  mental  anxiety  and  a  sense  of  im- 
pending dissolution.  It  is  important  that  pseudoangina  be  not  confused 
with  it. 

Etiology  and  Pathology. — The  cause  of  true  angina  pectoris  is  usually 
atheromatous  change  in  the  coronary  arteries,  although  this  is  by  no  means 
always  the  case.  Thus,  Potain  found  stenosis  of  both  coronary  arteries  in 
20  out  of  45  cases  at  autopsy,  and  Huchard  in  38  out  of  70  cases.  It  is 
distinctly  a  disease  of  the  brain-worker  rather  than  of  him  who  gains  his 
bread  by  manual  labor.     The  laborer  and  artisan  present  to  us  very  com- 


524  DISEASES  OF  THE  HEART 

monly  the  most  surprising  degenerative  changes  in  their  arteries  in  the 
way  of  calcification  of  their  radials  and  temporals,  but  they  rarely  have 
true  angina.  On  the  other  hand,  the  man  who  is  subjected  to  nervous 
strain  rarely  shows  extraordinary  calcareous  changes,  but  he  is  the  unfortu- 
nate victim  of  this  terrible  malady.  Physicians  are  peculiarly  prone  to  it. 
The  number  of  deaths  among  the  leaders  of  the  profession  in  Philadelphia 
during  the  last  decade  from  this  cause  is  extraordinary.  Mental  strain 
with  a  sedentary  life  are,  therefore,  causes.  Gout,  syphilis,  and  renal  disease 
are  also  causes.  The  disease  affects  men  much  oftener  than  women.  Out 
of  65  cases  collected  by  me  only  4  occurred  in  women,  and  out  of  290  cases 
collected  by  Forbes,  Huchard,  and  Lartigue  only  47  occurred  in  women. 
Aside  from  the  narrowed  and  thickened  coronary  arteries  and  the  fibroid 
changes  in  the  heart  which  result  from  their  state,  there  are  no  characteristic 
lesions  of  true  angina  pectoris.  Among  the  exciting  causes  of  an  attack 
are  to  be  named  nervous  wear  and  tear,  anger,  or  muscular  exertion,  par- 
ticularly if  it  be  made  in  the  face  of  a  cold  wind,  which  contracts 
the  capillaries  and  so  increases  still  more  the  labor  of  the  heart.  So,  too, 
errors  in  diet,  by  causing  gastric  disorder,  may  reflexly  cause  an  attack. 

Sir  Douglas  Powell  and  Merklen  give  the  age  incidence  for  true  angina 
at  twenty  to  forty  years.  This  is  probably  too  young.  The  actual  age  is 
forty  to  sixty  years. 

Symptoms. — A'NHien  angina  pectoris  is  well  developed  there  is  no  symptom- 
complex  so  characteristic  and  dramatic.  Seized  on  a  sudden  or  with 
but  a  few  moments'  warning,  the  patient  stands  or  sits  transfixed  with 
pain  and  fear.  It  is  difficult  to  tell  whether  his  arrested  respiration  is 
controlled  by  the  disease  or  his  own  will-power.  The  sense  of  dissolution 
or  of  impending  death  is  so  real  that  the  patient  expresses  the  belief  that 
death  is  at  hand,  if  he  can  find  breath  to  speak.  The  expression  of  the  face 
is  one  of  intense  anxiety  or  horror,  the  skin  is  pallid  to  the  degree  of  cadaveric 
hue,  and  the  brow  is  marble  white  and  perhaps  bedewed  with  sweat  as 
the  attack  advances-  The  pulse  during  an  attack  is  usually  slow,  small,  and 
very  tense,  becoming  feebler  and  more  relaxed  as  the  paroxysm  passes 
away.  The  pain  is  often  beyond  the  patient's  power  of  description  after 
his  recovery,  both  as  to  severity  and  character.  Some  patients  say  that  the 
heart  feels  as  if  it  were  being  crushed  in  a  vice;  others  that  a  huge  stone 
is  crushing  the  chest  wah;  others  that  a  heavy  bar  of  steel  is  laid  across  the 
thorax.  At  times  the  pain  not  only  extends  down  the  left  arm  to  the  fingers, 
but  to  the  right  arm  as  well.  As  the  attack  passes  off  the  patient's  expression 
of  keen  suffering  is  modified.  A  flush  may  supplant  the  pallor  and  a  sigh 
reveals  that  the  seizure  has  passed.  At  this  time  the  patient  not  rarely 
belches  up  large  volumes  of  gas,  and  this  seems  to  give  much  relief.  It  is 
this  which  gives  rise  to  the  euphemistic  diagnosis  of  "acute  indigestion"  in 
some  of  these  cases.  Sometimes  more  than  one  attack  may  occur  in  an 
hour,  but  this  is  rare. 

Modified  forms  of  severe  angina  are  constantly  met  with  in  which  the 
pain  is  not  so  severe  as  in  the  cases  just  described.  The  degree  of  modifica- 
tion may  be  so  great  that  little  or  no  pain  is  felt,  this  form  being  called 
angina  pectoris  sine  dolore. 


ANGINA  PECTORIS  525 

Diagnosis. — When  angina  pectoris  presents  itself  in  its  well -developed 
form,  there  cannot  be  much  doubt  as  to  its  true  character.  The  question 
of  the  character  of  an  attack  is,  however,  often  in  doubt  when  the  symptoms 
are  not  all  present.  While  it  is  a  rule  that  valvular  disease  of  the  heart 
rarely  causes  pain,  it  is  a  fact  that  attacks  of  anginoid  pain  are  occasionally 
met  with  in  cases  of  aortic  regurgitation,  particularly  if  dilatation  of  the 
heart  is  marked.  This  state  can  be  determined  by  the  diastolic  murmur 
and  the  "Corrigan  pulse."  Again,  aortitis  may  cause  symptoms  practically 
identical  with  those  of  true  angina,  and  it  may  be  impossible  to  separate 
the  disease  of  the  aorta  from  that  of  the  coronary  arteries  because  the  lesion 
spreads  from  the  aorta  to  the  openings  of  these  vessels. 

It  is  of  some  importance  to  differentiate  the  angina  pectoris  due  to 
ordinary  coronary  sclerosis  and  secondary  myocardial  change  from  that  due 
to  syphilis.  This  is  probably  impossible  by  the  physical  signs  in  the 
circulation,  but  can  be  made  if  a  history  of  late  syphilis  can  be  obtained, 
or  if  the  patient  is  prematurely  aged.  While  these  changes,  when  due  to 
syphilis,  cannot  be  treated  as  successfully  as  can  secondary  syphilis,  for 
they  are  of  the  nature  of  parasyphilitic  affections,  more  aid  can  be  given 
by  the  use  of  the  iodides  than  in  those  cases  which  present  changes  in  the 
coronary  arteries  from  other  causes. 

A  form  of  pseudoangina  is  occasionally  seen  in  nervous  women  and  in 
men  who  resort  to  wine,  tobacco,  and  women  to  excess.  It  differs  from  true 
angina  pectoris  in  the  facts  that  the  man  is  usually  under  thirty  years 
rather  than  over  forty  years  of  age;  his  vessels  are  usually  in  fair  con- 
dition; there  is  a  history  of  neurosis  or  excessive  venery  and  of  the 
excessive  use  of  tobacco,  and  the  sensation  about  the  heart  is  that  of 
distention  instead  of  constriction. 

Prognosis. — From  what  has  been  said  as  to  the  state  of  the  vessels  and 
the  heart  muscle  in  true  angina  pectoris  it  must  be  evident  that  the  prog- 
nosis is  most  grave,  for  death  may  ensue  in  any  attack  and  an  attack  may 
come  on  at  any  time.  On  the  other  hand,  patients  sometimes  go  long 
periods  without  an  attack,  particularly  if  the  mode  of  life  can  be  quiet  and 
the  pulse  tension  can  be  reduced  by  the  iodides  and  nitroglycerin.  Much 
depends  in  prognosis  upon  the  degree  of  vascular  and  myocardial  change 
which  can  be  found.  In  many  of  these  cases  the  feeble  first  sound  shows 
how  weak  and  dilated  the  ventricles  have  become. 

Treatment. — The  treatment  of  angina  pectoris  may  be  divided  into  that 
which  is  devoted  to  the  improvement  of  the  circulatory  condition  with  the 
object  of  preventing  paroxysms  of  the  disease,  and  to  that  which  is  devoted 
to  the  relief  of  the  patient  during  the  paroxysm.  As  the  treatment  of  a 
paroxysm  requires  very  active  procedures,  it  will  be  considered  first.  If 
seen  as  a  paroxysm  is  commencing,  the  patient  should  inhale  from  3  to 
5  minims  of  nitrite  of  amyl,  or  if  this  drug  is  not  at  hand  a  few  whiff's 
of  chloroform  should  be  used.  Nitroglycerin  should  also  be  given  hypo- 
dermically  in  the  dose  of  y^Q-  or  even  Jq  of  a  grain.  If  the  patient  has 
become  accustomed  to  this  remedy,  larger  doses  are  indicated.  Sometimes 
it  is  advantageous  to  give  simultaneously  with  the  nitroglycerin  |  of  a  grain 
of  morphine ;  but  in  those  cases  in  which  the  paroxysm  is  not  of  long  duration, 


526  DISEASES  OF   THE  HEART 

the  attack  commonly  passes  away  before  the  morphine  has  an  opportunity 
to  exercise  its  pain-reheving  influences.  If  the  patient  can  swallow,  a  very 
useful  remedy  is  1  or  2  drachms  of  Hoffmann's  anodyne  given  in  a  little 
cracked  ice  and  water;  or,  if  this  is  not  at  hand,  ^  to  1  drachm  of  spirit 
of  chloroform  may  be  given  in  a  similar  manner.  The  employment  of 
nitrite  of  amyl,  nitroglycerin,  and  chloroform  is  useful  in  direct  proportion  to 
the  degree  of  arterial  spasm  which  is  present.  In  that  somewhat  unusual 
class  of  cases  in  which  attacks  of  angina  occur  with  a  state  of  low  arterial 
tension,  these  drugs,  manifestly,  cannot  be  of  the  same  value  as  in  those 
patients  in  which  the  systemic  arteries  are  tightly  contracted.  Should  the 
patient  be  seen  in  a  paroxysm  and  the  physician  possesses  none  of  the 
remedies  just  named  for  his  relief,  a  drink  of  hot  water,  containing  some 
capsicum,  or  some  brandy,  may  be  given,  since  this  not  infrequently  causes 
the  belching  up  of  a  considerable  quantity  of  gas  followed  by  some  degree 
of  relief  to  the  patient. 

The  treatment  between  the  paroxysms  is  dietetic,  hygienic,  and  medicinal. 
The  patient  must  take  a  sufficient  quantity  of  food  for  the  purpose  of 
maintaining  his  nutrition,  and  must  be  forbidden  to  eat  anything  more 
than  is  absolutely  necessary  for  this  purpose.  Sweet  and  fatty  articles  of 
diet  should  be  entirely  avoided,  as  should  be  champagne  and  all  sweet 
wines.  If  any  alcoholic  stimulant  is  required,  Scotch  or  rye  whiskey,  or 
a  dry  gin  with  lime-juice  and  sparkling  water  should  be  ordered.  There 
is  no  objection  to  the  diet  being  largely  one  of  meat,  if  the  kidneys  are  in 
a  fairly  healthy  state;  the  more  so,  as  starchy  foods  are  prone  to  cause  the 
formation  of  gas  in  the  stomach  and  bowels,  which  may  reflexly  upset  the 
cardiac  balance  and  precipitate  an  attack. 

The  hygienic  treatment  consists  in  having  the  patient  take  as  much 
sunshine  and  fresh  air  as  possible;  in  forbidding  him  to  expose  himself 
to  blustering  winds,  and  to  warn  him  that  if  his  peripheral  circulation  is 
chilled  the  consequent  contraction  of  his  capillaries  may  result  in  an  attack 
of  heart  pang.  Flannel  should  be  worn  next  the  skin  both  winter  and 
summer.  Sudden  effort,  as  going  up  stairs  rapidly  or  running  for  a  car, 
or  entering  into  any  heated  debate,  either  in  court  or  in  a  business  argument, 
should  be  avoided. 

As  distention  in  the  stomach  sometimes  causes  an  attack,  it  is  often 
necessary  to  feed  the  patient  with  small  quantities  of  food  four  or  five 
times  a  day  rather  than  to  permit  him  to  eat  two  or  three  hearty  meals. 

Care  must  be  taken  that  the  bowels  do  not  become  overloaded  with 
feces,  and  that  they  be  moved  every  day  by  some  vegetable  laxative  or  one 
of  the  mild  saline  waters. 

The  medicinal  treatment  consists  in  the  administration  of  iodides  in  as 
large  doses  as  the  patient  can  readily  bear  without  danger  of  disordering 
his  digestion.  If  there  is  a  history  of  syphilis  in  the  case,  larger  doses  are 
needed  than  if  the  history  is  not  specific.  The  patient  should  take  at  least 
60  grains  a  day  of  the  iodide  of  sodium  or  iodide  of  strontium  if  possible, 
divided  into  four  doses,  which  should  be  taken  one  hour  after  food.  In 
some  cases  syrup  of  hydriodic  acid,  in  the  dose  of  ^  to  2  drachms  three  or 
four  times  a  day,  may  be  given  with  advantage,  well  diluted  with  water. 


CONGENITAL   CARDIAC  DEFECTS  527 

The  iodides  under  these  circumstances  lower  arterial  tension  and  do  wliat- 
ever  can  be  done  toward  arresting  the  process  of  fibroid  overgrowth  in  the 
bloodvessels.  The  patient  will  also  be  much  benefited  if  he  receives  nitro- 
glycerin in  the  dose  of  y^^  of  a  grain  four  or  five  times  through  the  twenty- 
four  hours,  the  dose  being  controlled,  not  by  the  number  of  doses  admin- 
istered, but  by  the  effects  which  it  produces  upon  arterial  tension.  In 
some  instances  it  is  wise  to  alternate  the  nitroglycerin  and  iodide.  If  the 
heart  muscle  is  very  feeble,  full  doses  of  nux  vomica,  10  or  20  drops  of  the 
tincture,  or  moderate  doses  of  digitalis — say,  5  minims  of  the  tincture — 
may  be  given  three  times  a  day;  the  nitroglycerin  being  actively  employed 
at  the  same  time  to  prevent  these  drugs  from  raising  arterial  tension  while 
they  are  stimulating  the  heart.  The  patient  should  be  instructed  to  carry 
glass  pearls  of  nitrite  of  amyl  in  his  pocket  and  to  crush  one  and  inhale 
its  contents  if  at  any  time  he  feels  threatened  by  an  attack. 

Symptoms  of  gastrointestinal  dyspepsia  are  to  be  relieved  not  only'  by 
regulating  the  diet  in  the  way  indicated,  but  by  the  use  of  pancreatin  and 
taka-diastase  to  aid  digestion.  A  very  useful  capsule  under  these  circum- 
stances is  one  which  contains  2  grains  of  taka-diastase,  2  grains  of  pancreatin, 
1  grain  of  capsicum,  and  \  grain  of  extract  of  nux  vomica.  This  should 
be  taken  thrice  daily. 


CONGENITAL  CARDIAC  DEFECTS. 

Two  abnormal  conditions  may  arise  in  the  heart  of  the  foetus  and  persist 
after  birth,  namely,  defects  of  development  and  defects  produced  by  an 
attack  of  endocarditis.  In  some  instances  the  endocarditis  is  responsible 
for  the  defect  in  development.  The  most  common  of  these  defects  is  the 
persistence  of  the  foramen  ovale,  which  permits  the  blood  to  make  a  short 
circuit  through  the  interauricular  septum  instead  of  passing  into  the  right 
ventricle  and  thence  through  the  lungs.  Sometimes  this  opening  is  partly 
guarded  by  a  membrane,  but  in  other  cases  no  such  membrane  is  present. 
If  the  opening  is  large  and  entirely  unguarded  by  a  membrane  the  patient 
is  apt  to  present  intense  cyanosis,  particularly  if  any  effort  is  made;  but 
in  some  cases  the  defect  does  not  produce  this  symptom  and  the  patient 
lives  to  adult  years,  no  one  suspecting  the  presence  of  such  a  defect,  the 
existence  of  which  is  revealed  only  at  autopsy.  Thus,  my  colleague, 
Coplin,  made  an  autopsy  upon  a  woman,  dead  of  croupous  pneumonia. 
During  her  life  and  in  her  final  illness  there  were  no  signs  of  cardiac  dis- 
ease, but  at  the  autopsy  a  twenty-five-cent  piece  could  be  dropped  flatwise 
through  the  foramen  ovale.  More  or  less  oblique  communications  between 
right  and  left  auricles  are  present  in  about  2  to  5  per  cent,  of  adult  hearts. 

A  much  more  rare  condition  is  that  in  which  there  is  an  absence  of  the 
septum  between  the  right  and  left  sides  of  the  heart,  and  as  a  result  "bilocular 
heart"  is  present.  In  others  again  the  absence  of  an  interventricular  septum 
produces  a  "trilocular  heart."  At  times  a  condition  is  met  with  in  which 
a  perforation  exists  in  the  upper  part  of  the  ventricular  septum,  in  the 
so-called  "undefended  space." 


528  DISEASES  OF  THE  ARTERIES 

Valvular  anomalies  also  occur.  The  three  aortic  semilunar  valves  may  be 
replaced  by  two  leaflets.  This  state  v^rhile  not  at  all  incompatible  with  Hfe 
is,  nevertheless,  prone  to  become  grave,  in  that  the  semilunar  valves  usually 
become  thickened  and  distorted.  The  pulmonary  valves  are  much  more 
rarely  abnormal,  and  the  valves  protecting  the  auriculoventricular  orifices 
on  both  sides  of  the  heart  are  even  more  rarely  anomalous  from  defective 
development.  These  valves  may,  however,  be  the  subject  of  endocardial 
disease  prior  to  birth,  and  the  result  is,  in  one  sense,  not  very  different 
from  that  met  with  in  the  heart  of  the  ordinary  individual  who  suffers 
from  rheumatic  endocarditis;  for  we  find  the  auriculoventricular  valves 
thickened  and  the  chordae  tendinege  broadened  and  shortened  so  that  they 
interfere  with  the  free  action  of  the  valves.  That  form  of  acute  or  chronic 
endocarditis  which  results  in  the  production  of  granular  or  warty  nodules 
on  the  valves  is  rarely  encountered  in  fetal  endocarditis. 

The  orifice  of  the  pulmonary  artery  is  very  commonly  found  to  be  in  a 
state  of  stenosis,  as  a  result  of  gluing  together  of  the  valves  and  contraction 
of  the  ring  around  the  orifice  itself.  The  agglutination  of  the  segments 
may  be  so  perfectly  accomplished  as  to  leave  a  smooth,  funnel-like  open- 
ing, or  the  valves  may  be  roughened  by  vegetations.  Patients  with  this 
defect  may  hve  for  years,  but  it  is  a  curious  fact  that  they  are  very  prone 
to  die  of  pulmonary  tuberculosis. 

Stenosis  of  the  right  conus  arteriosus,  of  the  pulmonary  artery,  and 
of  the  pulmonary  orifice  are  often  associated,  and  form  a  large  propor- 
tion of  the  congenital  lesions  seen  at  autopsy  in  persons  who  have  suffered 
from  these  defects,  but  lived  for  years.  It  is  a  noteworthy  fact  that  these 
lesions  are  not  rarely  complicated  by  a  patulous  interventricular  septum, 
an  open  foramen  ovale,  and  an  open  ductus  arteriosus.  Considerable 
hypertrophy  of  the  right  ventricle  is  naturally  found  in  these  cases  if  life 
is  prolonged. 

Narrowing  of  the  aortic  orifice  is  a  rare  congenital  defect.  INIalposi- 
tion  or  transposition  of  the  heart  is  sometimes  seen.  Transposition  is 
always  associated  with  transposition  of  the  other  viscera. 

Occasionally  ectopia  cordis,  a  state  in  which  the  heart  is  not  protected 
by  the  chest  wall,  is  met  with.  The  heart  has  also  been  found  in  the  abdom- 
inal cavity.  Peacock  reported  one  such  case  in  a  man  of  forty-seven 
years,  and  Rezek  one  in  a  man  of  thirty-two  years. 


DISEASES  OP  THE  ARTERIES. 

The  tubes  carrying  blood  are  subject  to  many  alterations,  some  of  which 
depend  upon  changes  in  the  perivascular  tissues,  including  with  these 
para-arterial  inflammations,  infection,  trauma,  etc.  The  most  important 
group  of  vascular  changes,  however,  result  from  alterations  in  stress  and 


ARTERIOSCLEROSIS  529 

tension  under  which  the  circulation  is  maintained,  and,  to  a  greater  degree, 
are  the  results  of  the  irritant  action  of  poisons  circulating  in  the  blood.  The 
intravascular  irritants  may  be  bacterial  or  of  bacterial  origin  (toxins), 
unusual  quantities  of  normal  salts,  or  the  presence  of  abnormal  compounds 
that  irritate  the  endothelium. 

Of  the  acute  and  subacute  inflammations  involving  the  intima  (end- 
arteritis), and  the  relation  of  this  change  to  later  alterations  in  the  vessels, 
we  are  at  present,  through  the  studies  of  Thayer  and  others,  becoming 
more  famihar.  The  clinical  importance,  however,  of  these  alterations  is 
not  as  yet  fully  appreciated.  Hyaline  and  fatty  degenerative  changes  occur 
in  the  intima  and  subintimal  tissues  in  a  number  of  pathological  processes. 
The  deposit  of  pigment  in  the  vessel  walls,  infiltration  by  lime  salts  (calcifi- 
cation), and  amyloid  disease  are  rarely,  if  ever,  primary  in  the  vessels,  but 
depend  upon  a  number  of  primary  conditions,  and  therefore  are  rarely,  if 
ever,  recognized  independently  of  the  conditions  by  which  they  are  caused. 
Infections  acting  within  the  vessels  give  rise  to  proliferative  or  necrotic 
changes  in  the  endothelium  with  the  formation  of  thrombi  (thrombo- 
arteritis  and  thrombophlebitis),  which,  by  mechanical  interference  of  the 
circulation,  influence  the  nutrition  of  the  organs,  or,  by  causing  embolism 
and  distribution  of  infectious  material  through  the  system  at  large,  constitute 
the  basis  of  septicaemia  and  pysemia  as  already  considered, 

ARTERIOSCLEROSIS. 

Definition. — Arteriosclerosis,  as  we  understand  it  to-day,  evidently  com- 
prises a  number  of  pathological  processes,  the  exact  relation  of  which,  one 
to  the  other,  is  still  somewhat  uncertain.  Two  important  processes,  often  if 
not  constantly  associated,  are,  first,  an  affection  involving  particularly  the 
smaller  arteries  (arterioles),  and  commonly  termed  arteriocapillary  fibrosis; 
and,  second,  a  type  of  arterial  change  involving  particularly  the  larger  vessels 
and  called  atheroma,  or,  on  account  of  the  changes  in  the  conformation  of 
the  affected  vessels,  arteritis  deformans.  Writers  are  not  agreed  that  these 
two  processes  are  independent,  but  they  are  very  constantly  associated,  and 
the  clinical  picture  embraced  under  the  term  arteriosclerosis  includes  them 
both. 

Etiology. — Certain  individuals,  and  often  whole  families,  seem  peculiarly 
liable  to  arteriosclerosis.  The  change  is  often  a  manifestation  of  age,  and 
the  trite  but  true  saying  "that  a  man  is  as  old  as  his  vessels"  indicates  the 
belief  in  preliminary  aging  of  those  in  whom  arterial  change  occurs  in  early 
life.  Alcohol,  and  intemperance  in  work  and  eating,  and  overexertion, 
mental  or  physical,  are  also  causes.  The  autointoxications,  lead  poisoning, 
syphilis,  and  gout  are  important  factors  in  the  production  of  arterial 
disease.  Certain  forms  of  chronic  interstitial  nephritis  may  precede,  ac- 
company, or  follow  arterial  change.  (See  Etiology  of  Chronic  Interstitial 
Nephritis.) 

Recent  studies,  experimental  and  pathological,  seem  to  indicate  that 
possibly  arteriosclerosis  may  bear  some  definite  relation  to  morbid  processes 
affecting  the  adrenals.  Josu^,  Ziegler,  Erb,  Pearce,  and  others  have 
34 


530 


DISEASES   OF   THE   ARTERIES 


produced  atheroma,  or  a  closely  allied  lesion,  by  the  intravenous  injection 
of  adrenalin.  Vaquez  reported  an  instance  of  adenoma  of  the  adrenal  asso- 
ciated with  heightened  arterial  tension,  and  Josu6  and  Bernard,  and,  more 
recently,  my  colleague,  Coplin,  have  shown  that  in  patients  having  arterio- 
sclerosis the  adrenal  is  rarely,  if  ever,  a  normal  organ.  The  observations 
are  not,  however,  as  yet  conclusive. 

The  relation  of  heightened  stress  to  arteriosclerosis  is  one  of  the  problems 
upon  which  authorities  are  not  agreed.  Allbutt  recognizes  a  mechanical 
arteriosclerosis  depending  upon  prolonged  high  tension  of  whatsoever  origin. 
There  can  be  no  doubt  that  in  some  cases  prolonged  stress  is  an  important 
etiological  factor,  as  is  shown  by  the  fact  that  typical  arteriosclerosis  is  rare 
in  the  pulmonary  artery  and  its  branches,  except  when  mitral  disease  or  pul- 
monary lesions  increase  the  tension  in  this  vessel,  under  which  circumstance 
sclerotic  changes  are  not  of  infrequent  occurrence.  Heightened  stress  in  the 
veins  also  tends  toward  the  development  of  phlebosclerosis,  as  is  shown  by 
the  occurrence  of  this  lesion  in  the  veins  of  the  lower  extremity,  when  for 
any  reason  the  tension  in  these  tubes  is  heightened,  and  also  by  the  develop- 
ment of  similar  changes  in  the  portal  area  in  cirrhosis  of  the  liver  with 
venous  obstruction. 

Pathology  and  Morbid  Anatomy.  Lesions  in  the  Terminal  or  Small 
Arteries. ~T\ie  change  in  the  arterioles  is  characterized  by  proliferation  of 
the  endothelium  and  subendothelial  tissues,  fragmentation  of  the  elastica, 
and  alterations  in  the  media.  There  has  been  much  dispute  as  to  the 
primary  alteration  in  the  muscle  layer,  some  holding  that  there  is  evidence 
of  a  distinct  hypertrophy,  which  others  fail  to  recognize.  Whether  or  not 
there  be  an  initial  increase  in  the  muscle  layer  of  the  arteriole,  there  is, 
sooner  or  later,  if  the  condition  persists,  a  degenerative  change,  hyaline  in 
tendency,  with  loss  of  elasticity,  thickening  of  the  intimal  and  subintimal 
tissues,  and  narrowing  of  the  lumen,  and  hence  increased  peripheral 
resistance. 

Lesions  in  the  Larger  Arterial  Trunks.— In  the  second  conspicuous  alter- 
ation of  arteriosclerosis  there  develops  in  the  larger  arteries  a  succession  of 
changes  greatly  influencing  the  elasticity  of  these  structures.  Councilman 
recognizes  at  least  three  divisions  of  this  type  of  arterial  change.  In  the 
nodular  form  a  cellular  infiltration  occurs  around  the  vasovasorum,  as 
originally  pointed  out  by  Martin,  extending  into  the  media  and  subintimal 
layers.  Fragmentation  of  the  elastica  with  efforts  at  production  of  new 
elastic  tissue  occurs.  Later  necrotic  and  degenerative  changes  weaken  the 
wall  and,  as  pointed  out  by  Thoma,  endothelial  proliferation  tends  to 
restore  the  smooth  lumen.  The  cells  forming  the  node  undergo  hyaline 
and  fatty  degeneration,  giving  rise  to  a  mass  of  cellular  detritus  constituting 
the  so-called  atheromatous  abscess.  Should  the  overlying  endothelium  give 
way  an  atheromatous  ulcer  is  formed;  these  areas  are  particularly  prone 
to  develop  around  smaller  branches  given  off  by  relatively  large  trunks, 
and  lessen  the  blood-carrying  capacity  of  the  affected  branches. 

The  nodules,  seen  on  the  vascular  surface  of  the  larger  arteries,  are  elevated, 
yellowish,  and  often  soft  from  degenerative  changes,  and,  later,  are  infil- 
trated by  calcareous  material,  becoming  rigid  so  that  they  break  when  bent. 


ARTERIOSCLEROSIS 


531 


Often  associated  with  this  nodular  form  is  a  diffuse  arteriosclerosis,  which 
may  also  occur  independently.  The  affected  vessels  are  dilated,  thin- 
walled,  with  irregular  elevations  at  points,  taking  on  more  or  less  fully  the 
character  of  the  nodules  already  described.  Sometimes  the  intima  is  almost 
unchanged. 


Fig.  75 


Left  coronary  artery.  Advanced  arteriosclerosis,  from  a  case  of  fatal  angina  pectoris.  Magnified  30 
diameters.  But  little  of  the  adventitia  is  shown.  The  media  is  thinned  and  at  points  encroached 
upon,  but  the  most  conspicuous  change  is  in  the  intima,  beneath  the  endothelial  layer  of  which  there 
has  been  extensive  proliferation  and  leukocytic  accumulation,  most  marked  in  the  upper  segment, 
greatly  altering  the  lumen  of  the  vessel,  lessening  its  carrying  capacity,  and  rendering  it  practically 
inelastic.     There  was  a  marked  fibroid  myocarditis  in  the  area  supplied  by  the  vessel. 


The  senile  arteriosclerosis  so  classified  by  Councilman  would  appear  to 
represent  that  late  stage  of  the  nodular  type  in  which  so-called  atheromatous 
ulcers  and  abscesses  form  with  calcareous  scales,  giving  rise  to  rigid  "pipe- 
stem"  or  "slate-pencil"  vessels  that  can  be  rolled  under  the  fingers  as 
tortuous,  inelastic,  rigid  tubes.  The  blood-carrying  capacity  of  such  vessels 
is  materially  diminished,  and  the  resistance  offered  to  the  circulation  pro- 
portionately increased. 

These  briefly  described  alterations  in  the  arteries  may  be  associated  with 


532 


DISEASES  OF   THE  ARTERIES 


similar,  though  usually  much  less  marked,  changes  in  the  veins  (phlebo- 
sclerosis),  the  combined  arterial  and  venous  lesions  constituting  what 
Thoma  has  called  angiosclerosis. 

The  thoracic  aorta  is  the  large  vessel  of  all  others  which  usually  presents 
the  greatest  atheromatous  change.  Its  entire  inner  surface  may  be  so 
roughened  that  it  no  longer  presents  any  of  the  appearances  seen  in  health. 
In  other  cases,  in  which  the  process  has  not  gone  so  far,  we  find  patches, 
or  plaques,  of  atheromatous  change  all  over  its  lining.  These  patches 
may  cover  areas  of  softening  or  areas  of  calcification,  and  on  them  thrombi 

Fig.  76 


Atheromatous  plaques  on  the  lining  of  the  aorta.     (Graupner  and  Zimmermann . ) 

may  form.  They  are  particularly  prone  to  appear  about  the  origin  of 
branch  vessels,  and  this  is  the  reason  that  fatal  disease  of  the  coronary 
arteries  so  often  occurs  as  part  of  the  aortic  changes. 

In  vessels  of  the  intermediate  class  and  in  the  aorta  these  changes  may 
so  weaken  the  resistance  of  the  vessel  wall  that  it  yields  to  pressure  and 
an  aneurysm  develops. 

When  changes  occur  in  the  small  vessels  their  intima  becomes  thickened 
by  an  outgrowth  of  the  endothelial  cells,  and  the  connective-tissue  cells 
in  the  media  also  proliferate,  so  that  the  vessel  becomes  fibroid,  the  elastic 
coat  being  rendered  rigid  and  the  calibre  of  the  vessel  diminished.  If  this 
process  proceeds  far  it  causes  an  obliterative  endarteritis. 

The  secondary  effects  of  these  vascular  changes  have  already  been  largely 
considered  when  discussing  the  causes  of  cardiac  hypertrophy  and  myo- 
cardial degeneration.    The  heart,  if  its  own  tissues  are  not  invaded,  under- 


ARTERIOSCLEROSIS  533 

goes  hypertrophy  to  enable  it  to  pump  blood  through  rigid,  unyielding 
vessels,*^  and  finally,  when  the  pressure  becomes  too  high,  develops  a  leak 
at  the  mitral  valve  to  relieve  pressure,  or  breaks  down  and  fails,  suddenly 
or  gradually,  under  the  strain  thrown  upon  it.  The  hypertrophy  chiefly 
affects  the  left  ventricle,  because  it  is  upon  this  part  that  the  strain  falls. 

Symptoms. — If  the  heart  is  examined  the  apex  will  be  found  displaced  a 
little  downward  and  to  the  left,  and  palpation  will  show  that  the  impulse 
against  the  chest  wall  is  forcible  if  hypertrophy  is  present. 

A  symptom  of  equally  great  importance  is  the  accentuation  of  the  aortic 
second  sound  at  the  second  right  costal  cartilage,  and,  indeed,  wherever 
it  is  heard  elsewhere  in  the  chest.  If  the  radial  or  temporal  arteries 
are  palpated  they  are  found  thickened  and  corded,  often  elongated  and 
tortuous  and  so  rigid  it  is  difficult  to  extinguish  the  pulse  by  pressure. 
This  high  arterial  tension  is  one  of  the  most  important  clinical  condi- 
tions that  can  be  estimated  by  the  physician. 

A  patient  presenting  these  signs  and  symptoms  may  continue  in  ap- 
parently excellent  health  for  several  years,  but  as  life  progresses  the  cardio- 
vascular changes  also  progress,  and  cardiac  failure,  attacks  of  angina  pec- 
toris, or  renal  disease  ensue.  Much  depends  in  these  cases  upon  how 
widespread  the  lesions  are  and  where  they  are  most  developed.  If  the 
coronary  arteries  are  the  parts  chiefly  affected,  anginoid  attacks  soon 
come  on.  If  the  cerebral  arteries  are  calcareous  apoplexy  ends  existence, 
or,  if  the  stroke  be  mild,  it  were  better  for  the  patient  if  death  ensued. 
Not  rarely  attacks  of  vertigo,  of  fleeting  monoplegia  or  hemiplegia,  and 
aphasia  may  take  place  as  the  result  of  the  arteriocapillary  fibrosis,  with- 
out being  due  necessarily  to  rupture  of  a  cerebral  vessel.  If,  again,  the 
renal  vessels  are  involved,  then  the  general  manifestations  of  chronic  con- 
tracted kidney  are  produced. 

Among  the  complications  may  be  named  cerebral  and  pulmonary  embolus, 
and  gangrene  of  the  extremities  from  the  same  cause. 

Treatment. — The  treatment  consists  in  the  use  of  the  iodides,  whether 
there  be  a  history  of  syphilis  or  not,  in  the  administration  of  nitroglycerin 
to  lower  arterial  tension  and  relieve  the  heart  of  labor,  and  in  the  use  of 
gentle  exercise  and  warm  bathing  in  moderation  to  flush  the  capillaries 
with  blood.  After  the  circulation  begins  to  fail  in  the  advanced  stages  of 
the  disease  strychnine  and  digitalis  may  be  urgently  required.  Alcohol  in 
any  form  must  be  avoided  as  if  it  were  poison.  Highly  seasoned  dishes 
are  also  to  be  avoided.  If  the  heart  is  tired,  strophanthus  is  to  be  given 
to  support  this  organ.  High  altitudes  are  dangerous  for  such  patients.  Great 
muscular  and  mental  strain  are  dangerous  because  the  increased  arterial 
pressure  may  rupture  a  vessel  or  weary  the  heart. 

As  chronic  interstitial  nephritis  is  nearly  always  present  the  treatment  for 
that  state  should  be  instituted  if  any  sign  of  renal  disease  can  be  discovered. 
(See  Chronic  Interstitial  Nephritis.) 


534  DISEASES  OF   THE  ARTERIES 


ANEURYSM. 

Definition. — An  aneurysm  is  a  localized  dilatation  of  an  artery  and  depends 
upon  a  weakening  of  its  wall  so  that  it  is  unable  to  withstand  the  pressure 
of  the  blood.  This  dilatation  may  involve  the  entire  circumference  of  the 
vessel,  forming  a  cylindrical  or  fusiform  aneurysm,  or  it  may  chiefly  affect  only 
a  part  of  the  circumference,  forming  a  sacculated  aneurysm.  The  walls 
of  the  aneurysm  are  composed  of  the  thinned  coats  of  the  vessel,  but  as  the 
sac  develops  some  of  these  may  in  part  disappear. 

The  term  "dissecting  aneurysm"  is  applied  to  that  form  in  which  the 
blood  escapes  through  the  intima  and  forces  a  passage  for  itself  into  the 
middle  area  of  the  vessel  wall,  between  the  media  and  the  adventitia.  By 
"false  aneurysm"  is  meant  a  state  in  which  all  the  coats  of  the  vessel  give 
way  so  that  the  blood  escapes  into  the  surrounding  tissues,  where  a  pulsating 
sac  usually  forms,  owing  to  the  development  of  fibrous  tissue  around  it. 
An  "aneurysmal  varix,"  or  "varicose  aneurysm,"  is  one  in  which  the 
artery  communicates  with  a  vein  through  an  abnormal  opening,  so  that 
the  vein  and  its  neighboring  veins  are  distended  with  pulsating  blood. 
An  "embolic  aneurysm"  is  one  in  which  a  vessel  is  plugged  by  an  embolus 
and  then  undergoes  dilatation  in  its  proximal  part.  "Mycotic  aneurysm" 
is  often  multiple  and  occurs  as  a  result  of  the  infection  of  the  vessel  by 
micro-organisms,  as  in  ulcerative  endocarditis. 

Etiology. — Aneurysm  is  due  to  arterial  degenerative  changes  whereby  the 
normal  elasticity  of  the  vessel  is  impaired  and  its  lining  membrane  injured. 
(See  Arteriosclerosis.)  The  primary  causes  of  aneurysm  are,  therefore,  identi- 
cal with  those  of  ordinary  arterial  disease,  and  consist  in  syphilis,  alcoholism, 
and  excessive  toil  or  sudden  strain.  Thus  syphilis,  for  example,  weakens 
the  vessel  and  a  strain  causes  it  to  give  way.  There  are  also  cases,  not  so 
commonly  met  with,  in  which  congenital  defects  seem  to  exist  in  the  vessel 
walls.  Thus,  I  saw  a  few  years  ago  a  young  man  of  about  twenty-eight 
years,  who  developed  a  popliteal  aneurysm  and  then  a  thoracic  aneurysm 
and  finally  died  of  cerebral  aneurysm,  but  who  at  no  time  suffered  from 
syphilis  or  from  strain.  It  may  also  arise  from  injury,  as  when  a  vessel 
is  damaged  by  a  stab  wound  or  by  a  bullet,  and  these  injuries  may  result 
in  the  development  of  the  aneurysm  many  years  after  the  injury,  and  only 
when  the  arterial  changes  of  advancing  age  still  further  weaken  the  area 
which  was  damaged.  In  other  cases  the  acute  infectious  diseases,  without 
acusing  general  or  widespread  arterial  change,  may  produce  localized 
vascular  inflammation  and  necrosis. 

Pathology  and  Morbid  Anatomy. — In  fusiform  aneurysm  the  wall  of  the 
vessel  dilates  in  its  full  circumference,  but  certain  spots  give  way  more 
rapidly  than  others,  so  that  the  surface  of  the  dilated  vessel  is  slightly  nodular 
or  uneven.  As  it  increases  in  size  its  walls  become  thinner,  but  if  an  inflam- 
matory process  is  set  up  in  the  surrounding  tissues  the  actual  thickness  of 
the  wall  may  be  increased,  and  finally  a  marked  deposit  of  lime  salts  may 
take  place. 

In  sacculated  aneurysm  the  dilatation  may  originate  in  at  least  two  ways. 


ANEURYSM 


535 


In  one,  the  entire  vessel  having  become  weakened,  dilates,  and  the  middle 
coat  atrophies.  This  process  of  atrophy  becomes  further  advanced  in  one 
area  than  in  another,  and  here  bulging  rapidly  progresses.  In  other  cases 
the  low-grade  inflammatory  process  results  in  degeneration  of  the  tissues 
lying  under  the  intima,  thereby  greatly  weakening  the  sustaining  lamina, 


Fig.  77 


Zcttii 


Double  sacculated  aneurysm  of  the  thoracic  aorta,  the  upper  sac  rupturing  into  the  pleura.  On  the 
right  is  the  aorta,  in  which  can  be  seen  the  two  oval  openings  communicating  with  the  aneurysmal  sacs. 
The  inferior  margin  of  the  lower  sac  has  been  pushed  upward,  showing  the  erosion  of  the  body  of  the 
vertebra,  which,  above  the  point  shown,  has  exposed  the  spinal  canal,  but  had  not,  in  this  case,  com- 
pressed the  cord. 

which  eventually  yields,  so  that  the  fibrous  sheath  of  the  vessel  may  be 
all  that  is  left  of  the  arterial  wall.  In  either  case,  however,  a  process 
of  compensation  or  repair  may  develop  and  the  sac  become  filled  with 
a  clot  which  is  usually  laminated  and  remarkably  tough.  Such  aneurysmal 
sacs  often  grow  to  an  enormous  size,  becoming  as  large  as  a  child's  head. 

Frequency. — The  relative  frequency  of  aneurysm  as  compared  to  other 
diseases  is  not  of  much  interest,  and  there  are  no  very  large  statistics  which 


536  DISEASES  OF  THE  ARTERIES 

deal  with  this  point.  There  is,  however,  interesting  information  at  hand 
in  regard  to  the  relative  frequency  of  the  most  frequent  and  important 
forms  of  aneurysm.  Thus,  at  St.  Bartholomew's  Hospital,  Browne  found 
that  in  thirty  years  there  were  468  cases  of  aortic  aneurysm,  80  of  popliteal 
aneurysm,  21  of  femoral  aneurysm,  14  of  subclavian  aneurysm,  8  of  carotid 
aneurysm,  and  6  of  external  iliac  aneurysm. 

Aneurysm  of  the  Thoracic  Aorta. — Not  only  is  aortic  aneurysm  the  most 
common  lesion,  but  it  is,  by  reason  of  the  importance  of  this  vessel  and  of 
the  tissues  about  it,  capable  of  causing  very  characteristic  and  also  very 
obscure  symptoms,  both  by  disturbing  the  circulation  and  by  pressure  on 
neighboring  organs. 

For  convenience  of  study  the  aorta  is  usually  divided  into  three  parts : 
the  ascending,  the  transverse,  and  the  descending.  Each  of  these  may  be 
the  seat  of  an  aneurysm,  but  the  ascending  portion  is  most  frequently 
affected.  Some  years  ago  one  of  my  assistants,  Holder,  and  myself  studied 
the  statistics  derived  from  953  cases  of  aortic  aneurysm,  and  obtained  the 
following  results.  No  less  than  570  of  these  were  cases  of  aneurysm  of 
the  ascending  portion  of  the  arch.  Of  these,  544  were  sacculated  and  466 
occurred  in  males  and  78  in  females.  The  remaining  26  cases  were  fusi- 
form, and  all  of  these  26  cases  occurred  in  males.  These  statistics  em- 
phasize very  forcibly  the  far  greater  frequency  of  sacculated  aneurysm  than 
the  fusiform  variety.  When  we  consider  that  of  nearly  1000  cases  analyzed, 
aneurysm  of  the  ascending  aorta  occurred  no  less  than  570  times,  while 
aneurysm  of  the  transverse  portion  occurred  only  104  times,  and  of  the 
descending  portion  110  times,  the  great  difference  in  the  relative  frequency 
of  the  lesion  in  different  parts  of  the  aorta  is  also  marked. 

Of  the  466  cases  of  sacculated  aneurysm  occurring  in  males,  it  is  inter- 
esting to  note  that  the  great  majority  of  them  occurred  in  persons  between 
thirty-five  and  forty-five  years  of  age,  that  the  next  greatest  frequency  was 
in  persons  between  twenty-five  and  thirty-five',  then  between  forty-five  and 
fifty-five. 

When  we  come  to  the  consideration  of  aneurysms  involving  the  second 
or  transverse  portion  of  the  aorta  we  find,  once  again,  that  the  most  com- 
mon age  for  the  development  of  this  lesion  is  between  thirty-five  and 
forty-five;  for  out  of  88  males  suffering  from  this  lesion  37  were  between 
these  ages,  21  between  forty-five  and  fifty-five,  14  between  twenty-five  and 
thirty-five,  10  between  fifty-five  and  seventy,  and  2  between  fifteen  and 
twenty-five.  The  same  facts  as  to  age  also  hold  true  for  aneurysm  of  the 
descending  arch.  It  is  evident,  therefore,  that  aneurysm  is  not  a  disease 
of  old  age,  but  of  the  middle  period  of  life.  As  Coats  has  well  expressed 
it,  "aneurysm  occurs  when  the  period  of  greatest  bodily  vigor  overlaps 
the  period  of  occurrence  of  atheroma." 

Symptoms. — Aneurysm  of  the  aortic  arch  not  infrequently  lasts  for  some 
time  before  producing  any  symptoms,  and  is  then  spoken  of  as  a  "latent 
aneurysm."  In  other  instances  it  causes  symptoms  almost  as  soon  as  it 
develops,  and  the  difference  in  the  promptness  with  which  the  signs 
appear  depend  largely  upon  the  site  of  the  growth  and  the  parts  pressed 
upon. 


ANEURYSM  537 

When  the  convex  surface  of  the  ascending  arch  is  involved  we  find  the 
patient  presenting  engorgement  of  the  veins  of  the  head,  neck,  and  arm 
on  the  right  side,  and  the  voice  is  often  altered  or  lost  from  the  pressure 
upon  the  recurrent  laryngeal  nerve  of  the  right  side.  The  fwpil  of  the 
right  eye  may  be  dilated,  due  to  irritation  of  the  sympathetic;  or  it  may 
be  contracted  because  the  ciliospinal  nerves  are  paralyzed  by  pressure. 
There  is  often  severe  fain  due  to  pressure,  and  attacks  of  anginoid  pain 
may  be  present. 

The  physical  signs  are  dulness  on  percussion  over  the  second  right  inter- 
space, a  bruit,  or  roaring  sound,  produced  by  the  passage  of  blood  through 
the  sac,  and  perhaps  bulging  of  the  first,  second,  or  third  interspace  on  the 
right  side.  If  the  hand  is  placed  over  the  area  of  bulging,  a  distinct,  expansile, 
heaving  movement  is  felt.  Some  displacement  and  hypertrophy  of  the 
heart  is  often  present,  and,  if  the  sac  is  a  large  one,  the  apex  beat  of  the 
heart  may  be  far  below  and  outside  the  normal  spot  near  the  nipple.  If 
the  sac  develops  on  the  concave  part  of  the  arch,  then  the  downward  dis- 
placement of  the  heart  is  still  greater,  for  obvious  reasons. 

Hypertrophy  of  the  heart  is  by  no  means  a  constant  sequence  to  aneurysm. 
Not  rarely  the  heart  is  not  increased  in  size  at  all,  but  its  apex  may  be 
displaced  and  the  impulse  transmitted  to  the  chest  wall  more  markedly 
than  normal  because  of  the  pressure  produced  by  the  aneurysmal  sac. 

When  we  come  to  the  consideration  of  the  direction  in  which  sacculated 
aneurysms  of  the  ascending  arch  most  commonly  rupture,  or,  in  other 
words,  when  we  study  the  neighboring  tissues  into  which  the  blood  forces 
its  way  when  the  wall  of  the  aneurysm  bursts,  we  find  that  the  vast  majority 
rupture  into  the  pericardium.  Thus,  out  of  289  cases  in  which  death  was 
stated  to  have  been  due  to  rupture  in  males,  75  ruptured  into  the  peri- 
cardium and  58  into  the  pulmonary  artery;  23  ruptured  into  the  right 
auricle,  3  of  these  taking  place  some  time  before  death;  23  ruptured  exter- 
nally; 14  ruptured  into  the  superior  vena  cava;  11  into  the  oesophagus; 
9  into  the  left  auricle;  8  into  the  right  ventricle;  8  into  the  trachea;  6  into 
the  left  ventricle;  6  into  the  left  pleura,  and  5  into  the  right  lung;  3  burst 
in  the  posterior  mediastinum  and  1  burst  simultaneously  into  the  trachea 
and  oesophagus;  in  20  others  no  statement  was  made  as  to  the  direction  of 
the  rupture.  It  is,  however,  a  fact  that  death  is  much  more  commonly  due 
to  pressure  symptoms  than  to  rupture. 

Aneurysm  of  the  transverse  'portion  of  the  arch  usually  causes  a  ringing, 
brassy  cough,  dysphagia,  expansile  pulsation  in  the  suprasternal  notch,  and 
dulness  on  percussion  on  the  first  and  second  left  intercostal  spaces.  Its 
pressure  on  the  innominate  vein  may  cause  congestion  of  the  left  side  of 
the  face  and  neck.  Dyspnoea  from  tracheal  pressure  may  be  present,  and 
there  may  be  aphonia  from  paralysis  of  the  left  vocal  cord,  arising  from 
pressure  on  the  left  recurrent  laryngeal  nerve.  If  the  growth  is  so  situated 
that  it  passes  from  the  left  bronchus  it  may  cause  bronchiectasis  and  even 
bronchial  suppuration  by  preventing  drainage.  Again,  if  the  sac  be  a  large 
one,  it  may  involve  the  innominate  artery,  the  left  carotid,  and  even  the 
subclavian,  and  in  this  manner  the  radial  pulse  may  be  absent  on  one  side. 
Even  the  pulse  in  the  arteries  of  the  trunk  and  lower  extremities  maybe  greatly 


538 


DISEASES  OF  THE  ARTERIES 


lessened  in  vigor.  The  hruit  may  be  loud  and  angry,  but  if  the  laminated 
clot  be  large  it  is  often  absent.  The  aortic  second  sound  is  usually  accent- 
uated or  ringing  in  character  unless  aortic  regurgitation  is  present. 

When  the  descending  arch  is  affected  it  often  occurs  that  the  aneurysm 
extends  posteriorly,  and  the  bruit  and  pulsation  are  found  in  the  back, 
between  the  scapula  and  the  spinal  column  on  the  left  side.  In  these 
cases  severe  pain  due  to  pressure  on  the  intercostal  nerves  is  often  present, 
and  the  pressure  on  the  vertebrae  may  cause  erosion  and  even  paraplegia 
by  destroying  the  spinal  cord. 


Fig.  78 


Aneurysm  of  the  ascending  and  transverse  part  of  the  aortic  arch,  with  erosion  of  the  chest  wall. 

Aneurysms  of  the  ascending  and  transverse  portion  of  the  aorta  often 
produce  an  extraordinary  degree  of  erosion,  and  so  pass  through  the  wall 
of  the  chest  by  causing  the  absorption  of  the  bony  tissues,  and  by  pushing 
the  fragments  of  the  ribs  to  one  side.  This  is  well  shown  in  the  accompany- 
ing cut.  The  surface  of  this  tumor  is  often  shining  from  distention  of  the 
skin,  it  is  discolored  by  blood,  and  the  surface  may  weep  bloody  serum  for 
days  as  the  end  approaches. 

Under  the  name  tracheal  tugging  a  symptom  of  aortic  aneurysm,  which 
consists  in  the  transmission  of  a  tugging  sensation  to  the  trachea,  has  been 


ANEURYSM  539 

described  by  Oliver  and  studied  by  MacDonnell.  To  make  this  test,  the 
patient  stands  erect  with  his  head  sHghtly  tipped  backward,  so  as  to  stretch 
the  tissues  of  the  front  of  the  neck.  The  cricoid  cartilage  is  now  grasped 
by  the  thumb  and  finger  and  drawn  toward  the  chin,  when  if  aneurysm  is 
present  a  tugging  sensation  will  sometimes  be  felt  with  each  beat  of  the 
heart.  Sewall  has  shown  that  this  sign  is  present  in  cases  which  have 
adhesions  in  the  left  pleura,  and  in  some  healthy  persons  when  they  take  a 
deep  inspiration. 

(Occasionally  in  aortic  aneurysm  incurvation  of  the  finger-nails  and 
clubbing  of  the  finger-tips  on  one  side  may  be  present. 

Blood-spitting  is  due  to  the  formation  of  an  erosion  of  the  mucosa  at  the 
spot  in  the  bronchial  tube  where  the  tumor  causes  pressure.  Such  a  cause 
produces  only  a  slight  blood  stain  of  the  sputum.  When  the  blood  passes 
by  a  process  of  leakage  through  the  wall  of  the  sac  and  escapes  into  a 
bronchus  it  may  be  in  considerable  amount,  and  death  may  be  due  to  a 
free  hemorrhage  of  this  sort. 

Very  rarely  there  develops  in  the  chest,  as  the  result  of  aortic  aneurysm, 
an  adhesion  between  the  sac  and  the  superior  vena  cava,  so  that  on  the 
development  of  ulceration  a  communication  between  the  two  vessels  is 
established,  forming  on  a  large  scale  an  arteriovenous  aneurysm.  The 
most  exhaustive  study  of  this  state  has  been  made  by  Pepper  and  Griffith, 
and  was  reported  to  the  Association  of  American  Physicians  in  1890.  They 
could  find  only  28  cases  in  literature  in  addition  to  the  one  they  observed. 
Less  commonly  the  aneurysm  communicates  with  the  pulmonary  artery. 

Diagnosis. — The  symptoms  of  aneurysm,  on  which  the  diagnosis  must 
be  chiefiy  based,  have  already  been  mentioned.  They  may  be  briefly 
named  as  follows:  The  presence  of  bruit,  expansile  pulsation,  pressure 
symptoms,  dulness  on  percussion  over  the  second  and  third  interspace 
anteriorly  on  either  side,  unilateral  sweating,  and  mydriasis  or  myosis,  and 
thoracic  pain.  Swellings  due  to  aneurysm  nearly  always  are  expansile, 
but  care  must  be  taken  that  swellings  which  pulsate  by  reason  of  transmitted 
impulse  are  not  mistaken  for  a  true  dilated  vessel. 

Nothing  is  more  difficult  to  diagnosticate  correctly  than  the  early  mani- 
festations of  aortic  aneurysm.  Scarcely  a  physician  of  experience  can  look 
back  and  not  recall  cases  in  which  its  early  signs  completely  misled  him.  The 
inconstant  pain  in  the  chest  is  often  thought  to  be  rheumatic  or  neuralgic. 
In  other  instances  dyspnoeic  seizures  are  thought  to  be  asthmatic,  or  attacks 
of  severe  cardiac  pain  are  considered  to  be  due  to  true  angina  pectoris. 
The  persistence  of  symptoms  like  these,  despite  treatment,  the  age  of  the 
patient,  the  degenerated  state  of  the  palpable  arteries,  the  sounds  of  the 
heart,  and  the  history  of  syphilis,  of  alcoholism,  and  of  strain  or  blow  or 
wounds,  are  all  at  least  capable  of  arousing  suspicion  of  the  real  condition. 
The  pain  of  aneurysm  is  often  dull,  gnawing,  and  constant,  but  in  some  cases 
pain  may  be  absent.  Occasionally  an  unsuspected  aneurysm  may  cause 
an  attack  of  stridor  or  paroxysmal  dyspnoea,  resembling  somewhat  a  laryngeal 
crisis  in  locomotor  ataxia.  This  should  excite  suspicion  of  aneurysm  causing 
pressure  on  the  recurrent  laryngeal  nerves.  A  hemorrhage  from  the  lungs 
in  the  absence  of  tuberculosis  should  also  be  regarded  as  significant.    This 


540  DISEASES  OF  THE  ARTERIES 

haemoptysis  may  be  frothy  and  mucoid,  or  rusty,  like  that  of  pneumonia, 
or  prune-juice  in  hue. 

A  very  valuable  aid  in  the  diagnosis  of  thoracic  aneurysm  is  the  use  of 
the  x-rays,  either  the  fluoroscope  being  used  or  x-ray  pictures  being  taken. 
The  advantage  of  the  fluoroscope  is  the  fact  that  the  physician  can  see 
the  expansile  movement  of  the  mass. 

Prognosis. — ^The  prognosis  of  aortic  aneurysm  is,  in  the  vast  majority  of 
cases,  inevitably  fatal,  but  in  some  cases  life  is  preserved  for  many  years 
if  nature  succeeds,  by  the  deposition  of  laminated  clot,  in  walling  off  the 
sac.  An  old  scrub-woman  has  presented  herself  to  my  clinic  during  the 
past  thirteen  years,  each  season,  with  a  massive  aneurysm  of  the  aorta 
which  eroded  the  sternum  years  ago,  and  which  has  not  grown  since 
to  any  extent.  She  works  hard  for  her  living  and  has  little  discomfort. 
Her  case  is  the  exception  that  proves  the  rule,  however.  If  the  growth  is 
of  any  size,  life  rarely  lasts  more  than  a  few  months.  Even  when  it  is  small 
a  rupture  may  occur.  As  already  stated,  death  from  aortic  aneurysm  is 
usually  due  to  pressure  on  adjacent  parts,  and  not  most  commonly  to 
rupture,  as  is  generally  thought. 

Treatment. — Aneurysm  of  the  peripheral  arteries  is  best  treated  by 
compression  and  ligation,  and  the  methods  to  be  employed  will  be  found 
discussed  in  works  devoted  to  surgery. 

In  aortic  aneurysm  there  are  two  plans  of  treatment  which  may  be  insti- 
tuted, namely,  medicinal  and  dietetic,  on  the  one  hand,  and  operative  on 
the  other. 

The  medicinal  treatment  depends  to  some  extent  upon  the  underlying 
cause  of  the  aneurysm.  If  it  be  due  to  syphilis,  in  the  sense  that  this  disease 
is  chiefly  responsible  for  the  vascular  degeneration,  it  is  hardly  necessary 
to  state  that  the  iodides  in  full  doses  are  advisable,  not  that  they  can  cure 
the  aneurysm  in  the  sense  of  regenerating  an  old  vessel,  but  that  they  may, 
by  their  specific  influence,  arrest  the  degenerative  influence  in  the  vessel 
wall,  and  so  delay  the  progress  of  the  malady.  Even  if  there  is  no  history 
of  syphilis  in  the  case,  the  iodides  are  often  of  value  in  that  they  seem  to 
arrest  in  some  unknown  manner  degenerative  changes  in  the  vessels.  They 
should  be  given  in  sufficiently  large  dose  to  produce  some  evidence  of 
iodism,  but  not  in  sufficient  dose  to  seriously  disorder  digestion. 

The  second  point  in  the  treatment  of  the  case  is  the  institution  of  the 
greatest  degree  of  rest  which  is  compatible  with  comfortable  existence. 
The  patient  should  be  placed  in  bed  and  required  to  use  a  bedpan  in 
order  that  he  may  not  disturb  his  circulatory  equilibrium  by  getting  up. 
He  should  also  be  given  small  doses  of  the  bromides,  if  necessary,  to 
overcome  nervous  irritation  and  restlessness,  and  if  the  action  of  his  heart 
is  exceedingly  tumultuous  and  fails  to  become  more  quiet,  by  rest  in  bed, 
I  have  known  small  doses  of  aconite,  such  as  2  minims  of  the  tincture,  three 
or  four  times  a  day,  to  be  advantageous.  In  other  cases  veratrum  viride  is 
useful  in  the  same  dose.  Such  a  plan  of  rest  treatment  is  useless  unless  it 
is  carried  out  for  weeks,  and  sufficient  time  must  be  allowed  for  a  laminated 
clot  to  form  in  the  aneurysm  and  reinforce  its  walls. 

The  so-called  Tufnell  treatment  of  aneurysm  consists  in  a  more  rigorous 


ANEURYSM  541 

method  than  that  just  described.  The  patient  is  not  only  put  at  absolute 
rest,  but  he  is  also  given  considerable  quantities  of  iodide  of  potassium  and 
as  low  a  diet  as  is  compatible  with  existence.  Indeed,  the  treatment  may 
be  called  the  starvation  plan  of  treatment,  for  it  is  the  deliberate  purpose, 
when  this  plan  is  instituted,  to  lower  the  activity  of  the  circulation  by  the 
depression  which  is  associated  with  semi-starvation.  I  have  seen  this  plan 
instituted  in  a  few  cases  only,  and  I  have  never  seen  good  results  from  it. 
Surely,  no  advantage  can  accrue  except  by  diminishing  the  activity  of  the 
circulation,  and  this  can  be  obtained  by  the  use  of  aconite  or  veratrum  viride. 

The  use  of  digitalis  in  these  cases  is  not  advisable  because,  while  the  drug 
steadies  the  heart,  it  increases  arterial  tension  and  so  tends  to  increase  the 
pressure  upon  the  aneurysmal  sac 

The  operative  treatment  of  thoracic  aneurysm  is  only  possible  when  the 
tumor  is  of  the  sacculated  type.  The  fusiform  type  of  aneurysm  contra- 
indicates  its  employment.  A  large  number  of  operative  procedures  have 
been  suggested,  but  there  is  only  one  which  has  at  the  present  time  received 
general  recognition  by  the  profession,  namely,  the  so-called  Corradi  method, 
in  which  there  is  introduced  into  the  aneurysmal  sac  several  feet  of  fine 
gold  wire  which  has  been  previously  twisted  about  a  glass  spool,  both  the 
spool  and  the  wire  being  carefully  sterilized  by  boiling  before  they  are 
used.  After  the  skin  over  the  sac  has  been  carefully  sterilized,  the  greatest 
gentleness  being  used  lest  it  be  damaged,  a  hollow  needle,  which  is  insulated 
by  being  coated  with  porcelain,  is  pushed  into  the  sac,  and  then  through  it  is 
passed  from  ten  to  thirty  feet  of  wire,  according  to  the  size  of  the  growth.  A 
larger  number  of  feet  have  been  used,  but  ten  or  fifteen  feet  will  be  sufficient 
in  the  vast  majority  of  cases.  As  soon  as  all  the  wire,  save  about  six  inches 
has  passed  into  the  sac,  the  external  end  of  the  wire  is  made  fast  to  an 
electrode  which  is  attached  to  the  positive  pole  of  a  galvanic  battery.  A  large, 
wet,  clay  electrode  attached  to  the  negative  pole  is  placed  under  the  back  to 
complete  the  circuit  and  by  means  of  a  "current  controller"  the  electricity 
is  gently  turned  on.  At  first  about  5  milliamperes  are  used ;  at  the  end  of  five 
minutes  the  current  is  raised  to  10  milliamperes,  and  after  this  the  current 
is  increased  every  five  minutes  by  5  milliamperes  until  about  50  milliamperes 
are  employed.  A  higher  number  of  milliamperes  have  been  used,  but  with 
increasing  experience  I  am  confident  that  they  are  unnecessary  and  perhaps 
harmful.  As  the  result  of  this  method  of  procedure  it  not  infrequently 
happens  that  by  the  end  of  the  first  twenty  minutes  or  half-hour  the  sac 
is  found  to  be  somewhat  more  firm  than  before,  and  that  pulsation  in  it 
has  diminished  owing  to  the  fact  that  the  acid  reaction  produced  by  elec- 
trolysis about  the  gold  wire  has  resulted  in  the  formation  of  a  clot,  which, 
as  time  goes  by,  becjomes  more  and  more  firm  and  solid.  At  the  end  of 
from  thirty  minutes  to  an  hour  the  wire  is  disconnected  from  the  battery, 
its  external  end  is  pushed  underneath  the  skin,  and  the  external  wound  is 
closed  by  collodion.  Absolute  quiet  must  be  maintained  for  ten  days  or 
two  weeks  after  the  operation,  in  order  that  the  clot  may  become  thoroughly 
consolidated. 

I  have  now  performed  this  operation  thirteen  times,  and  my  experience 
has  been  that  in    no  instance  did    the    patient    suffer  much  pain.      In 


542  DISEASES  OF   THE   ARTERIES 

several  instances  the  patient  has  stated  during  the  operation  that  he 
was  much  improved,  and  in  every  instance  he  has  vohmtarily  expressed 
his  pleasure  at  the  subsequent  improvement.  Unfortunately,  the  condi- 
tion of  the  aorta  is  such  that  when  we  close  one  bulging  spot  in  this  way, 
it  is  not  long  before  another  area  gives  way  under  pressure,  and  so  another 
aneurysm  is  formed.  In  all  of  my  cases  this  accident  has  ultimately  occurred. 
Tlie  greatest  duration  of  life  after  any  one  of  the  operations  which  I  have 
performed  has  been  a  little  over  six  months.  But  in  one  case  operated  on 
by  Stewart  some  years  ago  the  patient  lived  in  comparative  health  for  a 
period  of  three  years,  and  then  died  from  pneumonia  following  an  alcoholic 
debauch,  although  at  the  time  of  operation  the  aneurysm  could  be  seen  as 
large  as  a  fist  outside  the  chest  wall.  Considering  the  slight  pain  of  the 
operation,  it  is  indicated  in  many  cases,  if  only  for  the  temporary  relief  which 
it  gives. 

Aneurysm  of  the  Abdominal  Aorta. — Aneurysm  of  the  abdominal  aorta 
usually  occurs  near  the  diaphragm,  and  it  is  far  more  rare  than  aneurysm 
of  the  thoracic  aorta.  Out  of  325  cases  of  aortic  aneurysm  collected  at 
Guy's  Hospital  in  forty-six  years,  54  involved  the  abdominal  aorta.  Of  these 
63  per  cent,  occurred  between  the  ages  of  twenty-one  and  forty  years  and  77 
per  cent,  between  twenty-one  and  fifty  years;  over  90  per  cent,  occurred 
in  men.  The  growth  usually  arises  from  the  neighborhood  of  the  coeliac 
axis.  Like  that  in  the  thorax,  its  sacculated  form  is  more  common  than  its 
fusiform  type.  It  usually  projects  forward,  but  it  may  extend  backward 
and  cause  erosion  of  the  vertebrae,  followed  by  pressure  on  the  spinal  cord. 
Pain  is  usually  a  constant  symptom,  which  is  often  referred  to  the  region 
of  the  heart  or  to  the  back.  On  inspecting  the  abdomen  distinct  pulsation 
may  be  seen  at  once,  but  care  must  be  taken  that  the  transmitted  pulsation 
of  the  aorta  in  a  state  of  health  is  not  mistaken  for  true  expansion.  These 
two  states  can  be  separated  by  careful  palpation.  In  some  instances  the 
aorta  can  be  clearly  felt  through  the  belly  wall;  in  other  cases  a  morbid 
growth  in  the  stomach  or  in  the  omentum  can  be  felt,  but  although  it 
pulsates  it  is  not  expansile.  If  the  patient  is  placed  in  the  knee-elbow 
position  so  that  the  growth  falls  away  from  the  aorta,  the  diagnosis  may  be 
readily  made.  Auscultation  may  reveal  a  bruit  if  aneurysm  is  present,  but 
if  a  stethoscope  is  used  it  is  easy  by  pressure  on  the  aorta  to  narrow  its 
lumen  and  cause  a  humming  Sound,  which  is  not  a  sign  of  aneurysm. 
Again,  in  hysterical  persons  a  very  marked  pulsation  of  the  aorta  may  be 
complained  of  by  the  patient  and  felt  by  the  physician.  I  saw  not  long  since 
an  hysterical  male  who  had  rhythmical  contraction  of  his  abdominal  rectus 
muscles  synchronous  with  his  pulse.  It  was  only  possible  to  diagnose  his 
case  by  giving  him  ether  to  the  point  of  relaxation. 

A  larger  proportion  of  these  cases  end  by  rupture  than  is  the  case  in 
aneurysm  of  the  thoracic  aorta.  Thus,  out  of  these  54  cases  no  less  than 
43  died  from  rupture. 

Aneurysm  of  the  abdominal  aorta  may  rupture  into  the  retroperitoneal 
tissues,  through  the  diaphragm  into  the  pleural  spaces,  or  into  the  general 
peritoneal  cavity,  or  more  rarely  into  an  intraperitoneal  viscus,  as,  for 


ANEURYSM  543 

example,  the  stomach.  Rarely  death  ensues  from  the  vessel  becoming 
closed  by  a  thrombus. 

Even  more  rare  than  aneurysm  of  the  abdominal  aorta  is  aneurysm  of 
its  branches.  Cases  have  been  recorded  in  which  a  blow  upon  the  belly 
has  caused  aneurysm  of  the  hepatic  artery,  and  in  a  case  seen  by  the  writer 
it  followed  ulceration  produced  by  a  malignant  growth  of  the  gall-bladder. 
That  this  condition  is  very  rare  is  shown  by  the  fact  that  up  to  1898  only  26 
cases  had  been  recorded.  The  symptoms  are  usually  mistaken  for  hepatic 
colic,  and  this  error  is  all  the  more  easy  because  jaundice  from  pressure 
is  often  present.  In  most  of  the  recorded  cases  the  antemortem  diagnosis 
has  been  "gallstones"  or  "duodenal  ulcer." 

Aneurysm  of  the  splenic  artery  is  rarer  than  aneurysm  of  the  hepatic 
artery,  and  causes  symptoms  like  those  of  gastric  ulcer. 

Aneurysm  of  the  superior  mesenteric  artery  is  also  rare.  Rolleston  has 
collected  20  cases.  Embolism  is  the  usual  cause,  and  injury  may  be  respon- 
sible for  it.  This  growth  may  cause  jaundice  by  pressure  on  the  gall-duct, 
as  in  a  case  reported  by  J.  A.  Wilson;  or  it  may  press  on  the  renal  arteries 
and  cause  uraemia,  as  in  a  case  recorded  by  Burney  Yeo.  Aneurysm  of  the 
inferior  mesenteric  artery  is  practically  unknown. 

Aneurysm  of  the  renal  artery  is  also  rare,  although  small  multiple  sacs 
are  sometimes  seen.  If  the  sac  be  very  large  haematuria  may  occur,  or 
wasting  of  the  kidney  may  ensue.  Sometimes  by  the  sjjdden  rupture  of 
an  aneurysm  of  this  vessel  the  retroperitoneal  space  hasoeen  filled  with 
blood.  In  the  surgical  clinic  of  the  Jefferson  College  Hospital,  my  colleague, 
Dr.  W.  W.  Keen,  recently  cut  down  on  a  kidney  because  of  severe  renal 
symptoms,  and  found  a  large  aneurysm  of  the  artery.  He  was  forced  to 
remove  the  aneurysm  and  the  kidney. 


DISEASES  OF  THE  DIGESTIVE  TEACT. 


DISEASES  OF  THE  MOUTH. 

STOMATITIS. 

Definition. — As  its  name  implies,  stomatitis  is  an  inflammation  of  the 
mouth.  Of  the  many  forms  that  have  been  described  three  are  important: 
catarrhal  stomatitis,  aphthous  stomatitis,  and  ulcerative  stomatitis.  All 
these  forms  of  stomatitis  usually  occur  in  childhood.  The  catarrhal  and 
aphthous  forms  are  more  common  in  early  infancy,  but  the  ulcerative  type 
is  practically  never  met  with  in  children  who  have  not  as  yet  gotten  teeth, 
and  is  more  common  in  those  past  puberty  than  are  the  other  forms. 

Catarrhal  Stomatitis. — In  catarrhal  stomatitis  there  is  hypersemia  of  the 
mucous  membrane  of  the  tongue  and  cheeks,  with  an  increase  in  secretion 
on  the  part  of  the  mucous  and  salivary  glands.  It  arises  from  injury,  as  by 
some  foreign  body  being  taken  into  the  mouth  which  acts  as  a  mechanical 
irritant,  or  by  hot  or  irritating  liquids.  These  are,  however,  only  predis- 
posing causes.  Difficult  dentition,  or  the  use  of  a  rubber  nursing  nipple 
which  is  dirty,  are  more  common  factors.  It  also  occurs  as  one  of  the  mani- 
festations of  the  acute  eruptive  diseases,  as  in  scarlet  fever  and  measles, 
and  it  may  be  a  symptom  of  some  metallic  poisoning,  as  mercury,  lead,  or 
arsenic. 

Symptoms. — The  symptoms  of  catarrhal  stomatitis  are  intense  hyper- 
cemia  of  the  mucous  membrane  of  the  mouth  with  some  swelling  which  is 
particularly  visible  on  the  gums.  If  the  finger  be  placed  in  the  mouth  a 
sense  of  increased  heat  is  felt.  The  child  evidently  suffers  a  good  deal  of 
pain.  When  given  the  breast  or  bottle  it  eagerly  seizes  it  because  of  hunger 
and  thirst,  and  then,  as  the  nipple  touches  the  tender  mucous  membrane, 
gives  a  cry  of  pain  and  disappointment.  Cool  water  is  usually  taken  with 
avidity  if  given  from  a  cup.  The  flow  of  saliva  is  so  free  that  constant 
dribbling  on  the  chin  is  present  or  the  excess  of  saliva  is  swallowed  and 
disturbs  digestion.  If  the  mouth  be  very  carefully  examined  it  may  be  that 
tiny  blisters  at  the  opening  of  the  mucous  glands  will  be  seen  and  the  papilla 
of  the  tongue  will  be  found  enlarged,  swollen,  and  unduly  red  in  hue.  Some 
digestive  disturbance  and  diarrhoea  are  nearly  always  present.  Whether 
these  symptoms  are  the  result  of  the  condition  of  the  mouth,  or  whether  the 
state  of  the  mouth  is  secondary  to  disturbed  digestion,  is  often  difficult  to 
determine. 

35  (545) 


546  DISEASES  OF   THE  MOUTH 

Prognosis. — Recovery  from  catarrhal  stomatitis  is  usually  rapid,  the  con- 
dition rarely  lasting  for  more  than  a  few  days  after  the  disordered  digestion 
is  corrected  and  proper  cleanliness  of  the  mouth  is  obtained. 

Aphthous  Stomatitis. — The  aphthous  form  of  stomatitis,  sometimes  called 
follicular  or  vesicular  stomatitis  or  canker,  may  be  considered  as  a  still  fur- 
ther development  of  the  catarrhal  form.  In  this  condition  we  not  only  have 
a  diffuse  hypersemia  of  the  mucous  membrane  of  the  mouth,  but  in  addi- 
tion small  spots  appear  which  look  as  if  the  superficial  epithelium  had  been 
snipped  off  with  curved  scissors.  These  spots  are,  of  course,  exquisitely 
sensitive.  All  the  symptoms  of  the  catarrhal  form  are  much  exaggerated, 
and  in  addition  to  more  marked  digestive  disturbance  the  patient  often 
has  systemic  disturbance,  as  is  shown  by  some  fever  and  general  wTetched- 
ness.  Nutrition  is  interfered  with  materially  only  by  the  inability  to  take 
food. 

Ulcerative  Stomatitis. — The  ulcerative  form  of  stomatitis,  sometimes 
called  fetid  stomatitis,  or  putrid  sore  mouth,  is  a  much  more  serious  type, 
but  it  is  often  so  mild  that  the  dividing  line  between  it  and  the  aphthous 
form  is  not  readily  made.  When  well  developed,  the  mucous  membrane 
is  seen  to  be  studded  by  small  ulcers  which  may  coalesce,  forming  rather 
large  areas  of  superficial  necrosis.  If  the  child  is  badly  nourished,  or  suffer- 
ing from  some  malady  which  impairs  its  general  nutrition,  ulcerative  stom- 
atitis mav  become  a  very  serious  affection,  causing  great  suffering,  inter- 
fering seriously  with  proper  feeding  and  rapidly  undermining  the  strength 
of  the  patient.  The  ulcers  are  situated  chiefly  along  the  edges  of  the  gums 
which  recede  from  the  teeth,  or  on  the  margins  of  the  tongue,  on  the  buccal 
membrane,  and  even  on  the  lips.  The  breath  is  often  very  foul  and  the 
corners  of  the  mouth  become  excoriated  from  the  salivary  flow.  When  the 
patient  is  a  sufferer  from  scurvy  and  bad  hygienic  surroundings,  it  may  be 
an  important  factor  in  preventing  recovery. 

In  many  cases  the  condition  arises  from  carious  teeth  and  occasionally 
the  disease  occurs  epidemically.  On  the  other  hand,  I  have  repeatedly 
seen  mild  ulcerative  stomatitis  occur  in  otherwise  healthy  young  girls  past 
puberty,  in  whom  none  of  these  causes  were  apparent. 

In  severe  cases  the  ulceration  may  be  very  deep  and  may  even  cause 
loosening  of  the  teeth  or  superficial  necrosis  of  the  lower  jaw. 

Treatment. — The  treatment  of  all  these  forms  of  stomatitis  may  be  con- 
sidered simultaneously.  All  of  them  are  to  be  treated  by  careful  attention 
to  cleanliness  of  the  mouth  itself  and  of  all  objects  entering  the  mouth,  by 
careful  regulation  of  the  bowels  and  the  food,  and  by  a  mouth-wash  of 
chlorate  of  potash  and  myrrh  in  the  following  formula: 

R. — Potassii  chlorat.  .......     gr.  xxx. 

Tinct.  myrrhge  .         .  .  .  .  .  .     TJl  x. 

Elix.  calisayge    .......    f  ^iij. — M 

Sig. — Dilute  one  tablespoonful  with  two  of  water,  and  use  as  a  mouth-wash 

When  very  young  children  are  treated  this  solution  may  be  applied  to 
the  mucous  membrane  by  means  of  a  swab  tied  to  a  small  stick  or  pencil 
These  measures  are  usually  efficient  in  the  catarrhal  and  aphthous  type. 


STOMATITIS  547 

In  the  ulcerative  form  it  may  be  necessary  in  addition  to  touch  each  ulcer 
with  a  solid  stick  of  nitrate  of  silver  or  with  a  solution  of  this  drug  of  the 
strength  of  60  grains  to  the  ounce.  This  is  painful,  but  efficacious.  Only  a 
few  spots  should  be  touched  at  each  sitting.  When  the  teeth  are  not  carious 
peroxide  of  hydrogen  may  be  used  locally.  The  system  should  be  well  sup- 
ported by  nutritious  foods  such  as  cold  consomme  or  cold  chicken -jelly,  by 
ordinary  foods  if  they  can  be  taken  into  the  mouth,  and,  if  anaemia  is 
present,  by  the  use  of  iron  and  quinine  in  moderate  doses. 

When  for  any  reasoh  chlorate  of  potash  cannot  be  applied  locally  the, 
physician  may  give  the  drug  internally  in  the  dose  of  2  grains  every  three 
hours,  since,  as  it  is  eliminated  by  the  salivary  glands,  the  saliva  bathes 
the  diseased  mucous  membrane  with  the  drug.  This  plan  of  treatment  is 
contraindicated  if  any  renal  irritation  or  marked  gastric  disturbance  is 
present. 

In  scorbutic  cases  fresh  vegetables,  fruit,  and  beef-juice  are  absolutely 
needful  in  the  treatment  of  the  patient. 

There  still  remains  to  be  discussed  in  this  connection  three  forms  of  sore 
mouth  which  do  not,  strictly  speaking,  fall  under  any  of  the  headings  just 
given,  since  in  all  of  them  definite  specific  causes  have  been  isolated, 
namely,  so-called  thrush  or  parasitic  stomatitis,  gangrenous  stomatitis, 
and  mercurial  stomatitis. 

Thrush. — Thrush,  or  parasitic  stomatitis  (Soor  or  Muguet),  is  due  to 
the  presence  in  the  mouth  of  a  parasite  variously  named  Saccharomyces  albi- 
cans, Monilia  Candida,  or  Oidium  albicans.  This  parasite  has  been  classed 
with  yeasts,  and  grows  with  branching  filaments  at  the  ends  of  which  egg- 
shaped,  torula  cells  are  produced.  Thrush  is  distinctly  associated  with 
impaired  health  of  the  mucous  membrane,  and  in  children,  in  whom  it  is 
most  commonly  met  with,  it  is  due,  as  a  rule,  to  the  use  of  dirty  nursing  nipples 
or  nursing  bottles,  or  to  general  impairment  of  health.  When  the  latter 
cause  is  present,  thrush  may  appear  in  the  mouth  of  adults,  and  for  this 
reason  it  sometimes  aids  in  increasing  the  miseries  of  those  whose  vitality 
is  impaired  by  tuberculosis,  diabetes,  and  by  prolonged  exhausting  fevers. 
It  is  also  seen  in  children  suffering  from  marasmus.  The  parasite  can  be 
readily  conveyed  from  one  person  to  another  by  utensils. 

Symptoms. — The  subjective  symptoms  of  thrush  consist  in  the  same 
discomfort  in  the  mouth  which  is  met  with  in  aphthous  stomatitis.  The 
objective  symptoms  are,  however,  to  be  carefully  separated  from  that  state. 
Instead  of  denudation  or  depression  of  the  surface  of  the  mucous  membrane 
there  is  seen  on  the  tongue  small  particles  or  specks  in  the  form  of  tiny  pearly 
white  spots,  which  are  raised  and  may  gradually  coalesce  and  seem  to  from 
a  membrane  that  is  usually  easily  removed,  although  its  removal  may  leave 
a  bleeding  surface.  From  the  tongue  the  growth  may  extend  to  the  entire 
mucous  membrane  of  the  mouth  and  the  soft  and  hard  palate.  Very  rarely 
it  even  spreads  to  the  pharynx  and  oesophagus,  and  even  into  the  stomach 
and  small  intestines.  Holt  states  that  the  fungus  has  been  found  in  the 
lungs  of  babies  suffering  from  bronchopneumonia.  Thrush  is  separated 
from  aphthous  stomatitis  by  the   fact  that  the  profuse    salivation  of  the 


548  DISEASES  OF   THE  MOUTH 

latter  is  replaced  by  great  dryness  of  the  mouth,  and  by  the  aid  of  a 
microscopic  examination  of  the  growth. 

Prognosis. — The  prognosis  depends  upon  the  health  of  the  patient.  In 
the  robust  the  condition  may  last  but  a  few  days,  but  in  the  feeble  and 
impoverished  it  may  persist  for  weeks.  It  does  not  materially  influence 
the  general  health  except  by  interfering  with  the  taking  of  nourishment. 

Treatment.— The  treatment  consists  in  cleanliness,  good  feeding,  the  use 
of  a  mouth-wash  of  borax  in  the  strength  of  10  grains  to  the  ounce,  or  of  a 
mouth-wash  of  permanganate  of  potash,  1  grain  in  8  ounces  of  water, 
or  by  diluting  peroxide  of  hydrogen,  1  part  in  o  of  water.  Any  under- 
lying disorder  of  nutrition  should  be  carefully  removed  if  it  be  possible. 
All  sweets  and  syrups  should  be  carefully  avoided. 

Gangrenous  Stomatitis,  Cancram  Oris,  or  Noma. — Noma  is  a  term 
applied  to  all  forms  of  severe  ulceration  of  a  localized  character  attacking 
mucous  membranes,  but  the  state  may  be  present  without  the  mucous 
membrane  being  broken,  the  tissues  of  the  cheek  being  chiefly  affected. 
The  condition  occurs  so  rarely  in  those  who  are  past  puberty  that  it  may 
be  said  to  be  a  disease  of  early  childhood.  It  affects  the  buccal  mucous 
membrane  and  cheek  so  constantly  that  the  word  "noma"  has  come  to 
mean  a  malignant  and  sometimes  a  perforating  gangrenous  process  involv- 
ing the  cheek,  although,  strictly  speaking,  noma  may  affect  the  ear,  the 
vagina,  the  buttock,  the  nose,  or  the  external  genitalia. 

In  the  vast  majority  of  cases  noma  results  in  the  death  of  the  patient, 
not  so  much  because  it  is  in  itself  a  fatal  disease  as  that  it  is  a  terminal 
infection;  that  is,  one  which  develops  only  in  a  child  or  adult  whose  vital 
resistance  is  so  lowered  by  disease  or  poor  nutrition  that  the  pathological 
process  known  as  noma  is  possible. 

The  disease  is  rarely  seen  in  private  practice,  but  has  its  greatest  fre- 
quency in  institutions  for  poor  children,  where  because  of  mismanagement, 
or  of  the  wretched  state  of  the  child  on  admission,  it  readily  falls  a  victim 
to  infections  of  all  kinds. 

Noma  more  commonly  follows  measles  than  any  of  the  other  eruptive 
diseases,  but  it  also  sometimes  complicates  or  follows  scarlet  fever,  typhoid 
fever,  or  whooping-cough.  It  is  practically  never  a  primary  lesion  at  the 
point  of  development,  but  begins  in  a  solution  of  continuity  such  as  an 
^  ulcer  due  to  a  carious  tooth  or  as  a  sequence  of  ulcerative  stomatitis.  In 
all  probability  it  is  not  due  to  an  infection  by  any  single  micro-organism, 
but  to  several  organisms  which  may  be  associated.  Cases  have  recently 
been  recorded  in  which  the  ulceration  seemed  to  be  due  to  the  bacillus  of 
diphtheria,  but  mixed  infection  is  the  rule.  An  attempt  to  establish  speci- 
ficity for  any  single  organism  has  been  futile. 

Not  only  has  the  ulcerative  process  a  tendency  to  rapidly  become  deep 
and  so  to  perforate  the  cheek,  but  it  lacks  the  sharp  line  of  demarcation 
marking  the  wall  often  built  by  nature  to  prevent  the  spread  of  gan- 
grene. That  is  to  say,  the  ulcer  is  bounded  by  an  extending  area  of 
necrosis,  often  branching  and  discolored,  which  spreads  from  day  to  day, 
with  no  apparent  effort  on  the  part  of  the  system  to  limit  its  progress. 
The  soft  parts  melt  into  the  fetid  ulcer,  and  cartilage  and  bone  undergo 


ECZEMA   OF   THE   TONGUE  549 

necrosis.  When  recovery  does  occur,  which  is  exceedingly  rare,  a  line  of 
demarcation  forms,  and  the  extension  of  the  disease  is  arrested  in  this  way; 
the  ulcer  clears  up  and  repair  slowly  takes  place. 

Symptoms.— The  local  symptoms  of  noma  are  a  foul  breath,  a  state  of 
localized  ulceration  with  deejp  induration  of  the  tissues  near  by,  and  the 
speedy  development  in  the  centre  of  the  ulcer,  of  a  dirty-looking  slough  of 
necrotic  tissue.  The  side  of  the  face  is  usually  much  swollen  and  distorted, 
and  when  felt  by  the  fingers  the  tissues  feel  brawny  and  hard.  If  the  ulcera- 
tion extends  to  the  gums,  the  teeth  become  loosened.  So  great  may  be  the 
destructive  process  that  the  teeth  and  alveoli  may  be  seen  through  the  per- 
forated cheek. 

The  systemic  symptoms  are  not  characteristic  of  any  specific  state,  but 
are  those  of  frofound  systemic  poisoning,  depression,  and  exhaustion.  The 
pulse  is  rapid  and  feeble,  the  appearance  of  the  patient  markedly  septic  and 
cachectic,  and  the  temperature  mildly  febrile.  The  height  of  the  tempera- 
ture depends,  however,  to  a  considerable  degree,  upon  the  vitality  of  the 
patient.  When  the  sufferer  is  profoundly  exhausted  and  the  vital  state  is 
very  low  marked  febrile  movement  does  not  occur. 

Treatment. — From  the  description  just  given  it  is  evident  that  the  treat- 
ment of  noma,  to  be  successful,  must  depend  upon  its  early  institution  and 
thorough  character.  It  must  also  consist  in  the  use  of  such  nutritious  food 
and  such  medicines  as  will  serve  to  support  the  strength  of  the  patient. 
The  local  treatment  consists  in  the  early  and  complete  cauterization  of  the 
part  affected  by  the  electrocautery  or  its  excision  by  the  knife,  so  that  the 
necrotic  mass  is  at  once  destroyed  and  removed.  The  physician  must  not 
limit  the  operation  to  the  dead  tissues,  but  extend  the  excision  to  the  li\'ing 
tissues  as  well  in  order  that  none  of  the  infected  tissue  may  remain.  The 
local  process  may  be  temporarily  treated  by  swabbing  the  part  with  peroxide 
of  hydrogen  or  by  using  permanganate  of  potash.  In  cases  in  which  the 
streptococcus  or  the  bacillus  of  diphtheria  are  present,  the  serum  therapy 
needed  for  these  specific  infections  should  be  used. 


ECZEMA  OF  THE  TONGUE. 

Under  this  distinctly  erroneous  term  is  described  a  condition  in  which 
there  is  a  superficial  overgrowth  and  desquamation  of  the  epithelium  cover- 
ing the  tongue.  As  a  rule,  the  centre  of  each  spot  of  desquamation  begins  to 
heal  while  the  periphery  is  still  spreading,  so  that  the  appearance  of  the 
inflammatory  zone  is  distinctly  circinate.  Its  irregular  outline  has  given  it 
the  name  of  "  geographical  tongue."  In  other  instances  the  appearance  of  the 
tongue  is  that  of  a  worm-eaten  leaf.  In  some  patients  it  produces  no  dis- 
comfort whatever.  In  others  the  patient  may  have  some  itching  and  tingling, 
and  on  examining  the  tongue  is  surprised  to  find  the  curious  outlines  which 
have  been  described.  Not  infrequently  nervous  patients  are  wont  to  con- 
sider that  it  is  an  evidence  of  syphilis,  or  perhaps  of  a  malignant  growth.  A 
modified  form  of  this  condition  is  very  frequently  seen  in  children  as  a  result 
of  a  catarrhal  condition  of  the  stomach  and  bowels. 


550  DISEASES  OF   THE  SALIVARY  GLANDS 

Treatment. — In  adults  it  is  best  treated  by  the  local  application  of  nitrate 
of  silver,  20  grains  to  the  ounce.  In  children  the  correction  of  the  gastrointes- 
tinal disorder  usually  results  in  a  normal  growth  of  epithelium,  so  that  the 
condition  is  relieved.  As  a  rule,  such  children  require  some  simple  bitter 
such  as  tincture  of  gentian  with  5  or  10  grains  of  bicarbonate  of  soda. 


LEUKOPLAKIA  BUCCALIS. 

Leukoplakia  buccalis  is  sometimes  called  smoker's  tongue,  ichthyosis  lin- 
gualis,  and  buccal  psoriasis.  It  is  characterized  by  the  development  of  white 
spots  of  considerable  size  on  the  mucous  membrane  of  the  mouth  and  tongue, 
which  are  due  to  cellular  infiltration  of  the  subepithelial  connective  tissue 
and  a  thickening  of  the  epithelium.  When  the  spots  occur  on  the  edge  of 
the  tongue  and  are  indented  by  the  teeth  they  sometimes  look  like  the  scars 
or  puckerings  which  are  seen  on  the  edges  of  the  tongue  in  cases  of  advanced 
syphilis.  Occasionally  these  areas  may  be  slightly  ulcerated,  and  in  some 
cases  are  thought  to  be  the  seat  of  epitheliomatous  degeneration.  In  the 
majority  of  instances,  however,  they  are  benign,  and  after  removal  of  the 
cause  require  no  treatment  unless  the  surface  is  ulcerated,  in  which  case  they 
may  be  touched  with  nitrate  of  silver  and  the  patient  directed  to  avoid  taking 
hot,  irritating  substances  into  the  mouth,  and  particularly  to  avoid  smoking 
or  chewing.  Leukoplakia  is  sometimes  looked  upon  as  a  precancerous 
condition,  and  this  is  probably  true  in  the  sense  that  the  state  if  per- 
mitted to  continue  may  lead  to  cancer. 


MUCOUS  PATCHES. 

Mucous  patches  are  opaque,  white,  flattened  swellings  on  the  mucous 
membrane  of  the  mouth  and  lips,  and  are  characteristic  of  secondary  syphilis. 
(See  Syphilis.)  From  them  the  virus  of  syphilis  is  readily  communicated. 
Not  infrequently  their  surface  is  somewhat  ulcerated. 

Treatment. — The  treatment,  of  course,  consists  in  the  active  employment 
of  mercury  internally  and  the  use  of  nitrate  of  silver  locally. 


DISEASES  OF  THE  SALTY AKY  GLANDS 

FUNCTIONAL  DISORDERS  OF  THE  SALIVARY  GLANDS, 

Ptyalism. — Ptyalism,  or  salivation,  occurs  as  the  result  of  poisoning  by 
mercury  or  the  iodides.  It  is  also  produced  by  such  drugs  as  jaborandi, 
and  occasionally  occurs  because  of  irritation  of  the  mucous  membrane  of 


INFLAMMATION  OF   THE  SALIVARY  GLANDS  551 

the  mouth  by  the  development  of  stomatitis  in  one  of  its  several  forms. 
Rarely  a  form  of  idiopathic  ptyalism  is  met  with  in  young  children.  Under 
these  conditions  the  salivation  is  probably  the  result  of  a  neurosis. 

When  due  to  the  influence  of  a  drug,  the  condition  is  to  be  arrested  by 
stopping  the  use  of  that  substance  and  aiding  in  its  elimination  by  the 
employment  of  sodium  bicarbonate  if  the  iodides  have  been  taken,  and  mild 
saline  purgatives  if  mercury  has  been  used.  A  mouth-wash  containing  10 
grains  of  chlorate  of  potassium  and  2  drachms  of  fluid  extract  of  rhus  glabra 
in  an  ounce  of  water  will  be  useful  to  improve  the  condition  of  the  mucous 
membrane  and  arrest  the  flow  of  saliva.  Sometimes  moderate  doses  of 
atropine  are  useful.  In  other  cases,  10  to  15  grain  doses  of  camphoric  acid 
given  thrice  a  day  may  be  used. 


DRY  MOUTH. 

Dry  mouth,  or  xerostomia,  is  frequently  met  with  in  all  fevers,  but  some- 
times occurs  as  an  independent  condition.  Under  these  circumstances  the 
tongue  is  seen  to  be  red  and  dry,  with  lessened  superficial  epithelium,  so  that 
it  is  smooth  and  shiny.  It  is  said  to  be  most  frequent  in  women  after  great 
nervous  excitement  or  in  those  suffering  from  hysteria. 

Treatment. — Temporary  relief  from  dryness  of  the  mouth  may  be  pro- 
duced by  washing  it  with  a  mixture  of  1  part  of  glycerin  to  2  of  water,  to 
which  has  been  added  a  little  lemon-juice. 


INFLAMMATION  OF  THE  SALIVARY  GLANDS. 

The  most  important  and  most  common  inflammation  of  the  salivary  glands 
is  the  swelling  of  the  parotid  gland  in  mumps,  which  has  already  been  con- 
sidered. The  next  most  frequent  cause  of  inflammation  of  the  salivary 
glands  is  a  septic  condition  of  the  mouth  in  the  course  of  one  of  the  prolonged 
adynamic  fevers,  such  as  typhoid  fever,  and  in  persons  who  are  suffering 
from  cerebral  softening.  In  these  cases  it  would  seem  that  infection  may 
pass  through  the  salivary  duct,  and  so  cause  inflammation  of  the  gland  itself. 
Occasionally  a  similar  accident  occurs  in  pytemia,  pneumonia,  syphilis,  and 
scarlet  fever.  In  some  of  these  diseases  the  infection  undoubtedly  enters 
the  glands  by  way  of  the  bloodvessels  and  lymphatics.  Pyogenic  infection 
of  the  parotid,  whether  hsemal,  lymphatic,  or  by  a  duct,  produces  a  suppura- 
tive interstitial  parotitis,  or  parotid  abscess,  also  called  "  parotid  bubo."  A 
curious  form  of  inflammation  of  the  parotid  gland  with  stenosis  of  Steno's 
duct  is  sometimes  seen  in  cases  of  sulphuric  acid  poisoning.  While  it  is  pos- 
sible for  the  sublingual  and  submaxillary  glands  to  be  involved,  the  parotid 
is  the  gland  which  nearly  always  suffers. 

The  inflammation  may  be  treated  in  its  early  stages  by  cold  compresses, 
by  the  application  of  leeches,  and  by  the  administration  of  circulatory 
sedatives  like  aconite,  provided  the  patient  is  not  already  depressed  by  dis- 
ease.   So  far  as  possible  the  treatment  should  also  be  addressed  to  the  relief 


552  DISEASES  OF   THE  PHARYNX 

of  the  underlying  cause  of  the  condition.  If  the  gland  is  suffering  from 
a  subacute  inflammation,  mercurial  ointment,  iodine  ointment,  or  ichthyol 
ointment  may  be  thoroughly  rubbed  into  the  skin  over  it,  unless  perchance 
the  gland  is  swollen  as  the  result  of  mercurial  or  iodide  influence.  WTien  an 
abscess  forms  it  must  not  be  forgotten  that  it  should  be  opened  promptly, 
but  with  great  care.  Not  infrequently  a  parotid  abscess  is  so  closely  asso- 
ciated with  an  important  bloodvessel,  or  indeed  with  the  external  carotid 
artery,  that  a  careless  incision  may  produce  disaster.  Such  an  abscess  should 
always  be  opened  by  careful  dissection. 

Chronic  indurative  or  sclerosing  parotitis  is  a  well-known  pathological 
condition  the  clinical  features  of  which  are  still  obscure.  It  has  been  observed 
in  diabetes  with  and  without  pancreatic  disease,  but  the  exact  relationship, 
if  any,  is  not  known. 

Ludvig's  Angina. — This  condition,  sometimes  called  Angina  Ludovici,  is 
a  ceUulitis  of  the  neck  which  begins  as  an  inflammation  of  the  floor  of 
the  mouth,  usually  in  the  area  of  the  submaxillary  gland.  As  a  rule  it  begins 
on  one  side  and  then  spreads  to  the  opposite  side.  In  malignant  cases  it 
rapidly  involves  not  only  the  floor  of  the  mouth,  but  the  tissues  about  the  root 
of  the  tongue  and  under  the  angles  of  the  jaw,  so  causing  oedema  of  the 
glottis.  In  some  cases  these  tissues  slough,  forming  what  is  known  as 
cijnanche  gangrcenosa.     In  still  others,  an  abscess  points  externally. 

Symptoms. — ^The  symptoms  are  brawny  swelling,  great  pain,  rigors,  fevers, 
and,  if  the  infection  is  severe,  general  septicaemia  and  death. 

Treatment. — In  the  very  early  stages  the  use  of  cold  and  of  leeches  to  the 
skin  under  the  jaw  may  be  of  advantage.  After  the  inflammation  is  well 
developed,  drainage  should  be  established  by  the  surgeon. 


DISEASES  OF  THE  PHARYNX. 

ACUTE  PHARYNGITIS. 

Definition. — Acute  pharyngitis  is  an  acute  catarrhal  inflammation  of  the 
mucous  membrane  hning  the  pharynx  in  which  there  is  hyperaemia  and 
congestion,  with  some  infiltration  of  the  submucous  tissues,  and,  later,  an 
increased  secretion  of  mucus. 

Etiology. — Acute  pharyngitis  is  caused,  as  a  rule,  by  simultaneous  exposure 
to  cold  and  infectious  dust.  Cold  and  damp  air  first  impair  the  vital  resist- 
ance of  the  pharyngeal  mucous  membrane,  and  then  dust,  laden  with  micro- 
organisms, falling  upon  it  speedily  produces  infection.  There  can  be  no 
doubt   that   systemic  conditions   also  favor  the  development  of _  this  state. 

Aside  from  the  fact  that  lowered  vitality  always  permits  infection  to  take 
place  readily,  there  can  be  no  doubt  that  the  excessive   use  of  alcohol, 


ACUTE  PHARYNGITIS  553 

tobacco,  or  rich  foods,  or  the  presence  of  a  torpid  Kver,  or  a  catarrh  of 
the  nose,  mouth,  or  stomach  aid  materially  in  permitting  the  condition 
to  arise.  Pharyngitis  also  arises  as  a  result  of  lithaemic  states.  Sometimes 
infection  seems  to  come  from  a  chronic  tonsillitis  or  is  an  extension  from 
the  nares.  The  condition  is  particularly  prone  to  arise  in  those  who  work 
for  a  number  of  hours  a  day  in  imperfectly  ventilated  rooms.  Sometimes 
irritating  fumes  and  dust  seem  capable  of  producing  this  condition. 

Pathology. — ^After  a  prehminary  dry  stage  the  engorgement  of  the  blood- ' 
vessels  of  the  mucous  membrane  and  the  inflammation  of  the  mucous  glands 
results  in  the  pouring  out  of  considerable  quantities  of  mucus,  marked 
epithelial  desquamation,  and  in  severe  cases  some  fibrin.  If  pyogenic 
organisms  are  present  the  secretion  may  be  distinctly  mucopurulent.  In 
some  instances  the  swelling  of  the  submucous  tissues  is  very  marked.  In 
others,  although  severe,  it  may  be  superficial.  In  very  rare  cases  the  exudate 
may  be  so  fibrinous  as  to  form  a  false  membrane  which  is  not  always  due 
to  the  presence  of  the  bacillus  of  diphtheria.  Not  rarely  in  such  cases  the 
uvula  and  the  tonsils  are  also  involved. 

Symptoms. — Acute  pharyngitis  usually  comes  on  suddenly,  with  the  symp- 
toms of  what  is  popularly  called  "sore  throat,"  so  that  the  patient  feels  that 
the  mucous  membrane  is  swollen  and  sore,  and  there  is  some  pain  on  swal- 
lowing. On  inspection  it  will  be  found  that  the  posterior  wall  of  the  pharynx 
and  neighboring  parts  are  dry  and  red,  with  the  capillaries  injected.  After 
secretion  is  established  the  parts  are  thoroughly  moistened  by  serum  and 
mucus.  In  some  instances,  if  the  infiltration  of  the  submucous  tissues  is 
marked,  the  patient  may  complain  of  a  sense  of  constriction  in  the  throat, 
and  at  times  a  good  deal  of  pain  may  extend  along  the  Eustachian  tube  into 
the  ear.  If  the  pain  is  not  too  great,  the  patient  may  continually  clear  his 
throat  in  an  efi^ort  to  relieve  the  irritation.  Constitutional  symptoms  are 
usually  mild,  but  the  tongue  is  coated  and  the  patient  may  be  somewhat 
depressed. 

Prognosis. — Recovery  always  ensues  unless  some  unforeseen  complica- 
tion arises. 

Treatment. — The  treatment  consists,  if  the  patient  is  seen  in  the  early 
stages,  in  the  application  of  a  cold  compress  to  the  neck  below  the  angle 
of  the  jaw.  This  compress  is  made  by  dipping  cloths  in  ice-water,  wringing 
them  out,  and  then  binding  them  against  the  part.  They  should  not  be 
allowed  to  become  warm  and  so  produce  the  relaxing  effects  of  a  poultice. 
Internally,  if  the  patient  is  an  adult,  he  may  be  given  from  1  to  5  drops  of 
the  tincture  of  aconite  with  a  drachm  of  sweet  spirit  of  nitre  in  a  glassful  of 
hot  lemonade.  Before  taking  this  he  should  be  put  to  bed  in  order  that  when 
perspiration  develops  he  will  not  catch  cold.  Small  pieces  of  ice  may  be  held 
in  the  mouth,  but,  as  a  rule,  better  results  will  be  obtained  if  the  patient  gar- 
gles with  as  hot  water  as  he  can  bear.  This  water  may  be  fortified  by  adding 
to  it  an  equal  quantity  of  the  distilled  extract  of  witch-hazel.  If  the  bowels 
are  at  all  constipated,  saline  purgatives,  such  as  citrate  of  magnesia,  should 
be  used  to  unload  them.  If  there  is  any  rheumatic  or  gouty  tendency,  the 
patient  will  do  best  if,  in  addition  to  the  purgatives,  he  is  given  20  grains  of 
bicarbonate  of  potash  in  large  draughts  of  water  every  four  or  five  hours; 


554  DISEASES  OF   THE  PHARYNX 

or,  instead,  10  grains  of  salol  may  be  given  every  three  hours  until  40  grains 
have  been  used. 

Local  treatment  aside  from  the  use  of  the  gargle  is  usually  unnecessary. 
If  the  condition  is  due  to  a  gouty  tendency,  the  use  of  any  one  of  the  oily 
substances  commonly  employed  in  atomizers  produces  increased  discomfort, 
in  the  writer's  experience.'  If  it  is  not  due  to  this  cause,  some  relief  may 
be  obtained  by  spraying  the  parts  with  3  drops  each  of  oil  of  sandal-wood 
and  oil  of  sassafras  in  an  ounce  of  liquid  albolene.  In  other  cases,  when  the 
oils  cause  discomfort,  my  colleague.  Dr.  Kyle,  strongly  recommends  apply- 
ing hydrochloric  acid,  in  the  proportion  of  5  to  10  drops  of  the  dilute  acid 
in  an  ounce  of  water,  for  the  purpose  of  contracting  the  dilated  bloodvessels. 

The  salicylates  are  useful  if  lithsemia  is  present. 

When  the  second  stage  is  reached  5  to  10  grains  of  chloride  of  ammonium 
may  be  given  in  equal  parts  of  fluid  extract  of  licorice  and  water  four  or 
five  times  a  day.  Or,  instead,  10  grains  of  benzoate  of  ammonium  may 
be  given  in  capsule  four  times  a  day. 


ULCERATIVE  OR  PHLEGMONOUS  PHARYNGITIS. 

Etiology. — This  condition,  sometimes  called  ulcerated  sore  throat,  or 
phlegmonous  pharyngitis,  is  due  to  an  infection  of  the  mucous  membrane 
of  the  throat  by  micro-organisms.  It  is  not  uncommonly  seen  in  physicians 
and  nurses  who  are  attending  children  suffering  from  scarlet  fever  and 
diphtheria.  Many  years  ago  it  was  frequently  met  with  in  medical  students 
who  were  dissecting  cadavers  which  had  been  imperfectly  preserved.  This 
form  of  pharyngitis  is  exceedingly  painful  in  its  early  stages,  and  is  charac- 
terized by  changes  much  like  those  just  described  in  acute  catarrhal  pharyn- 
gitis, except  that  a  superficial  necrosis  of  the  mucous  membrane  rapidly 
occurs,  so  that  in  a  few  hours  small,  irregular  ulcers  may  be  seen  upon  the 
soft  palate,  the  half  arches,  and  the  pharyngeal  wall.  If  the  infection  is 
severe,  so  that  the  submucous  tissues  are  involved,  it  becomes  a  phlegmon- 
ous pharyngitis. 

Symptoms. — A  patient  with  infectious  pharyngitis  usually  complains  of 
much  pain  in  the  throat  and  in  the  muscles  of  the  neck.  This  is  greatly 
increased  when  he  attempts  to  swallow.  There  may  be  slight  febrile  move- 
ment and  depression. 

Treatment. — The  treatment  consists  in  spraying  the  inflamed  mucous  mem- 
brane with  a  normal  salt  solution,  and  following  this  by  a  gargle  or  spray 
of  1  per  cent,  solution  of  carbolic  acid  and  water  or  albolene.  This  in  turn 
is  followed  by  a  spray  of  menthol,  4  grains  to  the  ounce.  Cold  compresses 
applied  under  the  jaw  are  advantageous.  If  one  or  two  ulcers  are  par- 
ticularly active,  they  may  be  touched  with  nitrate  of  silver.  Usually  it  is 
advisable  to  give  the  patient  a  moderate  purgative  dose  of  calomel  and  to 
follow  it  by  a  saline  purge,  such  as  a  Seidlitz  powder. 


CHRONIC  PHARYNGITIS  555 


CROUPOUS  PHARYNGITIS. 

Etiology. — Croupous  pharyngitis  occurs  in  two  forms  as  diphtheria,  which 
has  already  been  described,  and  as  a  simple  membranous  pharyngitis,  which 
commonly  is  due  to  infection  by  the  pneumococcus  or  Streptococcus  pyogenes. 
The  chief  difference  between  this  form  of  pharyngitis  and  diphtheria  is  that 
the  mucous  membrane  is  not  deeply  involved,  that  true  ulceration  never 
occurs,  and  the  Klebs-LoefHer  bacillus  is  absent.  The  inflammation  is, 
however,  of  such  a  character  that  a  false  membrane  develops  with  desquama- 
tion of  the  epithelium.  If  the  membrane  is  removed,  the  tissues  beneath 
may  bleed,  very  much  as  they  do  in  diphtheria.  Although  there  is  usually  a 
slight  chill  and  some  fever,  the  degree  of  systemic  disturbance  is  by  no  means 
as  marked  as  in  the  well-developed  case  of  true  diphtheria. 

Treatment. — The  treatment  consists  in  washing  the  infected  parts  thor- 
oughly by  a  spray  of  normal  salt  solution,  and  following  this  by  a  solution 
of  hydrogen  peroxide  and  water  half  and  half,  and  this  in  turn  by  gargling 
and  spraying  with  distilled  extract  of  witch-hazel.  Usually  this  treatment 
is  sufficient.  If  the  condition  persists,  Loeflfler's  solution  may  be  applied 
locally.    Antitoxin  is  to  be  used  if  diphtheria  is  present.     (See  Diphtheria.) 


CHRONIC  PHARYNGITIS. 

Etiology. — A  condition  of  chronic  inflammation  of  the  pharyngeal  mucous 
membrane  is  frequently  met  with  in  certain  climates,  particularly  that  of 
the  Atlantic  seaboard.  It  is  also  found  in  persons  who  continually  use  the 
voice,  and  so  it  has  obtained  the  name  of  "auctioneer's"  or  "clergymen's" 
sore  throat.  It  is  also  met  with  in  persons  who  use  tobacco  to  excess,  and 
sometimes  in  those  who  take  too  much  alcohol.  Obstructions  in  the  nasal 
passages  seem  distinctly  to  predispose  to  this  state. 

Pathology. — The  pathological  condition  consists  in  a  thickening  of  the 
mucous  membrane  of  the  pharynx  and  an  increase  in  the  connective  tissues 
of  the  mucous  membrane  itself,  and  of  the  submucous  tissues.  This  may 
result  in  a  secondary  atrophy  of  the  glands  in  the  mucous  membrane. 

Symptoms. — The  symptoms  consist  in  a  thickening  of  the  pharyngeal 
secretions  and  irritation  of  the  mucous  membrane,  so  that  the  patient  is 
continually  attempting  to  clear  the  throat,  which  often  feels  dry  and  harsh. 
The  cough  is  spasmodic,  unproductive  in  its  result,  and  is  made  much  worse 
by  exposure  to  cold  and  dust. 

Treatment. — The  treatment  consists  in  a  regulation  of  the  digestive  sys- 
tem, in  giving  tone  to  the  circulation  if  it  is  feeble,  in  rest  for  the  nervous 
system  if  the  patient  is  overworked,  and  in  the  internal  administration  of 
benzoate  of  ammonium  in  10  grain  doses  several  times  a  day.  Before  going 
to  bed  at  night  the  patient  should  gargle  his  throat  with  hot  water  or  with 
hot  salt  solution,  and  if  the  bloodvessels  are  much  dilated  a  spray  of  dilute 
hydrochloric  acid,  10  drops  to  the  ounce  of  water,  should  be  used. 


556  DISEASES  OF   THE   TONSILS 


FOLLICULAR  PHARYNGITIS. 

Etiology. — Under  the  name  of  follicular  pharyngitis  a  closely  related 
condition  to  that  just  described  exists,  in  which  an  annoying  cough  is  per- 
sistent, and  in  which  a  considerable  number  of  enlarged  follicles,  surrounded 
by  an  injected  mucous  membrane,  can  be  seen  on  the  posterior  wall  of  the 
pharynx. 

Treatment. — ^The  treatment  is  of  the  same  character  as  that  just  described 
for  chronic  pharyngitis.  Occasionally  it  is  necessary  to  cauterize  the  follicles. 
An  excellent  application  is  tincture  of  iodine  1  part  in  2  parts  of  glycerin. 


DISEASES  OF  THE  TONSILS. 

ACUTE  TONSILLITIS. 

Definition. — As  its  name  implies,  this  disease  consists  in  an  acute  inflam- 
mation of  the  tonsils,  accompanied  by  great  swelling  of  their  tissues,  and 
an  associated  pharyngitis.  It  occurs  in  two  forms,  the  follicular  and 
diffuse.    The  follicular  form  is  distinctly  infectious. 

Etiology. — Acute  tonsillitis  is  the  result  of  an  infection  by  pathogenic 
micro-organisms,  which  are  practically  always  present  in  the  crypts  of 
the  tonsils,  but  do  not  penetrate  the  mucous  membrane  until  its  per- 
meability is  increased  by  congestion,  or  by  general  causes  affecting  perhaps 
the  vital  resistance  of  the  entire  body.  In  many  instances  the  suppurating 
form  arises  because  the  organisms  attempt  to  enter  the  general  system  by 
way  of  the  tonsils,  and  the  suppurative  process  is  the  result  of  an  effort  to 
prevent  such  an  entrance.  The  streptococcus  is  a  cause  in  some  cases. 
In  other  cases  the  organism  which  Poynton  and  Payne  think  is  the  cause  of 
acute  articular  rheumatism  is  responsible,  and  the  bacillus  of  diphtheria  is 
also  a  common  factor. 

Follicular  tonsillitis  is  more  common  in  the  period  of  life  from  five  to 
twenty  years  than  at  any  other  time,  and  is  rare  in  infancy.  Some  indi- 
viduals suffer  from  frequent  attacks  until  they  reach  forty  or  fifty  years 
of  age.     After  this  time  of  life  it  is  very  rare. 

Although  follicular  tonsillitis  is  rare  in  adults,  the  suppurating  form  is 
frequently  met  with  in  this  class  of  patients.  Persons  who  have  a  lymphatic 
temperament  are  far  more  susceptible  than  persons  of  the  wiry  type,  and  it 
is  particularly  prone  to  occur  in  those  who,  because  of  obstruction  of  the 
nasal  passages,  are  "mouth  breathers,"  or  who  suffer  from  subacute  or 
chronic  hypertrophic  catarrh  of  the  nasopharynx.  One  attack  distinctly 
predisposes  to  another.  My  experience  leads  me  to  believe  that  it  is  dis- 
tinctly infectious,  for  I  have  repeatedly  seen  healthy  persons  develop  the 


ACUTE   TONSILLITIS  557 

malady  after  being  exposed  to  the  breath  of  those  who  were  ill  with  it. 
Another  predisposing  cause  is  the  breathing  of  vitiated  air,  and  air  that  is 
contaminated  by  sewer  gas  or  smoke.  How  much  these  influences  act 
directly  as  sources  of  infection  and  how  much  as  agents  which,  by  dimin- 
ishing vital  resistance,  make  infection  possible,  is  difficult  to  determine. 

Pathology  and  Morbid  Anatomy. — In  acute  folUcular  tonsillitis  there  is  an 
inflammatory  swelling  of  the  parenchyma  of  the  gland.  The  mucous  mem- 
brane covering  the  gland  is  intensely  hypersemic  and  may  even  show  vesicles 
on  its  surface.  Each  follicle  exudes  a  cheesy-looking  mass,  and  these  masses 
dot  the  surface  of  the  tonsil  or  coalesce  and  produce  a  tonsillar  coating, 
which  at  first  glance  closely  resembles  the  false  membrane  of  diphtheria. 
If  some  of  this  material  is  examined  microscopically  it  is  found  to  consist 
of  dead  epithelial  cells,  micro-organisms,  and  pus  cells.  In  addition  to 
these  superficial  changes  there  is  hyperemia  of  the  tonsillar  capillaries,  and 
proliferation  of  the  lymphoid  cells  in  the  deeper  tissues  of  the  glands.  In 
the  more  deeply  situated  and  intense  inflammations  of  the  gland,  sometimes 
called  quinsy,  there  is  a  necrosis  of  the  tissues,  suppuration  takes  place,  and 
the  pus  escapes  from  the  tonsillar  abscess,  either  by  the  aid  of  the  surgeon's 
knife  or  by  rupture  of  the  abscess  wall.  In  any  of  these  conditions  the 
passage  of  bacteria  or  their  toxins  into  the  lymphatics  may  produce  glandular, 
enlargement  in  the  neck. 

Symptoms. — A  patient  suffering  from  the  earliest  stages  of  acute  tonsillitis 
may  first  feel  soreness  of  the  throat,  with  a  sense  of  local  swelling  or  con- 
striction, or  the  systemic  signs  of  the  infection  may  first  be  manifested. 
Creeping,  chilly  sensations,  or  even  a  true  rigor,  may  develop,  and  there  is 
very  frequently  an  amount  of  aching  and  fain  in  the  limbs  which  is  extraor- 
dinarily severe,  so  that  the  patient  complains  most  bitterly,  not  only  of  this 
symptom,  but  of  the  degree  of  illness,  so  that  he  fears  a  serious  malady. 
Violent  headache  is  often  a  prominent  symptom,  and  the  temperature 
soon  becomes  very  high,  mounting  to  103°  or  104°  or  even  105°  in  a  few 
hours.  Rarely  nattsea  and  vomiting  may  occur.  An  examination  of  the 
throat  will  show  the  presence  of  distinct  swellings  of  the  tonsils,  which 
not  rarely  extend  as  far  across  the  fauces  as  the  uvula,  and  even  press  against 
one  another.  These  swellings  are  intensely  congested  and  frequently  covered 
with  exudate,  and  are  often  very  foul  in  appearance.  The  breath  of  the 
patient  is  exceedingly  foul,  and  unless  ventilation  is  very  good  the  odor  may 
fill  the  room.  Owing  to  the  swelling  of  the  tonsils  and  adjacent  glands  and 
stiffness  of  the  muscles  of  the  sides  of  the  neck,  an  examination  of  the  patient's 
throat  may  be  very  painful. 

As  general  systemic  infection  often  enters  the  body  by  way  of  the  tonsils 
it  is  wise  to  be  on  the  watch  for  signs  of  endocarditis.  Doubtless  the  asso- 
ciation of  rheumatism  with  tonsillitis  by  many  practitioners  is  due  more  to 
the  development  of  septic  arthritis  from  the  entrance  of  pathogenic  germs  by 
these  pathways  than  to  any  real  relationship  between  acute  rheumatism  and 
tonsillitis.  I  have  seen  several  cases  of  severe  ulcerative  endocarditis  and 
acute  arthritis  follow  an  acute  tonsillitis.  It  is  a  noteworthy  fact  that  acute 
follicular  tonsillitis  is  practically  always  bilateral,  while  the  deeper  form, 
sometimes  called  quinsy,  is  often  unilateral. 


558  DISEASES  OF   THE   TONSILS 

In  the  suppurating  form  of  the  disease  the  systemic  manifestations  are 
often  less  severe  than  in  the  folHcular  types  just  described,  but  the  local  pain 
is  often  very  severe,  and  opening  the  mouth  may  be  very  painful.  The  tonsil 
is  often  enormously  enlarged,  but  is  rarely  dotted  with  follicular  spots. 
Instead  it  may  be  smooth  and  shining  in  appearance.  The  inflammation 
often  extends  to  the  uvula,  which  may  be  so  swollen  and  elongated  as  to 
cause  great  distress. 

Treatment. — The  treatment  of  both  forms  of  tonsillitis  is  largely  identical. 
To  the  surface  of  the  tonsil,  in  the  first  twenty-four  hours  of  the  inflam- 
mation, there  is  nothing  better  to  arrest  the  process  and  relieve  pain  than 
pure  guaiacol  applied  by  a  cotton  applicator.  This  often  causes  great  pain 
for  the  moment,  but  it  is  remarkably  efficacious.  Externally,  over  the 
gland,  a  small  ice-bag  is  a  valuable  application.  It  should  be  kept  con- 
stantly applied  for  several  days.  Internally  in  the  very  early  stages  the  use 
of  biniodide  of  mercury  is  very  useful  in  the  dose  of  5^  of  a  grain  every 
half -hour  till  -^  grain  has  been  taken. 

After  the  stage  of  onset  is  past  the  best  internal  treatment  is  10  to  20 
minims  of  tincture  of  iron  chloride  well  diluted  with  water  every  three  or 
four  hours  and  potassium  bicarbonate,  or  citrate,  in  copious  draughts  of 
water  to  flush  the  kidneys  and  diminish  the  backache. 

Many  practitioners  rely  largely  on  salol  or  salicin  at  this  time,  giving  them 
in  full  "doses.  They  are  efficacious,  but  they  increase  headache,  disorder 
the  digestion,  and  may  irritate  the  kidneys,  which  are  prone  to  irritation  in 
this  disease. 

Some  cases  get  relief  from  gargling  with  very  hot  water  or  by  holding  ice 
in  the  mouth. 

When  the  tonsils  are  chronically  enlarged  and  repeated  attacks  of  tonsil- 
litis occur  they  should  be  removed  between  attacks  by  the  tonsillotome.  The 
application  of  caustics  like  nitrate  of  silver  often  makes  them  larger  than  before. 

In  the  suppurating  form  the  pus  should  be  evacuated  as  soon  as  it  is 
formed,  the  tonsils  being  punctured  by  a  bistoury  or  a  tenotome,  the  tip  of 
which  is  exposed  after  being  run  through  a  small  cork  so  as  to  guard  it  and 
prevent  any  movement  of  the  patient  from  causing  the  physician  to  injure 
an  important  bloodvessel. 

In  all  cases  of  follicular  tonsillitis  cultures  of  the  secretions  from  the  throat 
should  be  examined  for  the  Klebs-Loeffler  bacillus,  for  in  all  cases  before 
making  a  diagnosis  of  follicular  tonsillitis  the  physician  should  carefully 
exclude  diphtheria.  (See  Diphtheria.)  When  children  are  in  the  household 
the  patient  should  be  carefully  isolated. 


CHRONIC  HYPERTROPHIC  TONSILLITIS. 

Definition. — Chronic  hypertrophic  tonsillitis  is  a  condition  of  overgrowth, 
or  hyperplasia  of  the  tonsils,  which  affects  all  parts  of  both  tonsils  and 
usually  involves  the  so-called  pharyngeal  tonsil.  In  some  instances  the 
lymphoid  texture  of  the  glands  is  chiefly  affected,  while  in  others  the  connec- 
tive tissue  undergoes  the  greater  part  of  the  overgrowth.     In  the  one  instance 


CHRONIC  HYPERTROPHIC  TONSILLITIS  559 

the  enlarged  tonsils  present  themselves  as  projecting  masses,  soft  in  texture. 
In  the  other  they  are  remarkably  hard  and  cut  with  a  resistance  almost 
cartilaginous  in  character.  In  some  instances  there  is  overgrowth  of  the 
tonsils  without  the  adenoid  of  the  pharynx  being  involved.  Nearly  always 
patients  with  this  affection  suffer  from  associated  nasal  catarrh,  often  from 
secondary  middle-ear  disease,  and  they  present  a  peculiar  expression  of 
stupidity  or  lack  of  intelligence. 

Symptoms. — Aside  from  organic  disease  of  the  great  viscera  there  is  no 
chronic  malady  which  produces  such  extraordinary  changes  in  the  physical 
appearance,  growth,  and  mental  development  as  does  this  one.  The  obstruc- 
tion to  free  nasal  breathing  results  in  mouth  breathing,  and  this  in  turn 
causes  the  child  to  hold  the  mouth  open  in  a  silly  manner,  which  detracts 
from  its  facial  appearance.  So,  too,  the  lack  of  free  respiration  results  in  a 
failure  of  physical  development,  so  that  the  chest  is  often  foorly  developed, 
and  even  the  entire  body  is  dwarfed.  Finally,  this  same  cause  produces 
restless  nights  and  so  causes  loss  of  physical  rest,  which  may  be  empha- 
sized by  attacks  of  spasmodic  croup  or  night  screaming.  Constant  cough 
at  night  on  lying  dow^n  is  also  often  a  troublesome  symptom  and  is  due 
to  undue  dryness  of  the  nasopharynx  or  to  tickling  of  the  uvula  by  the 
edges  of  the  projecting  tonsils. 

After  the  disease  has  lasted  for  years  the  child  is  often  stupid,  morose, 
and  apathetic  to  a  degree,  and  the  open  mouth,  stunted  nose,  and  heavy  eyes 
make  a  diagnosis  of  the  tonsillar  state  easy.  When  the  child  is  stripped 
the  chest  is  often  found  to  be  barrel-shaped  or  the  patient  is  pigeon-breasted, 
or  it  presents  the  Trichterbrust  of  the  Germans,  or  the  so-called  funnel  chest 
of  English  -writers,  in  which  there  is  a  deep  depression  of  the  lower  part  of 
the  breast-bone.  These  thoracic  changes  are  due  to  two  chief  causes:  first, 
the  general  impairment  of  nutrition  produces  malnutrition  of  the  thoracic 
walls  as  in  rickets,  and,  second,  in  the  effort  at  sufficient  respiration  the 
chest  walls  undergo  faulty  development.  The  breath  is  often  quite  fetid, 
due  to  retained  secretions  and  particles  of  food  in  the  crypts  of  the  tonsils, 
and  if  the  tonsils  be  pressed  upon  a  surprisingly  large  amount  of  material 
can  be  expelled  from  their  cavities. 

The  nasopharyngeal  spaces  of  such  children  are  first-rate  culture  fields  for 
the  growth  of  bacteria  of  all  sorts  and  for  acute  infections,  such  as  diphtheria 
and  scarlet  fever. 

Treatment. — If  we  except  the  effects  produced  by  the  use  of  thyroid  gland 
in  cretinism  it  is  not  possible  to  find  any  state  in  which  the  physician  can 
cause  such  a  complete  metamorphosis  in  his  patient  as  to  health  of  mind 
and  body  as  in  this  malady.  The  removal  of  the  enlarged  tonsils  by  tonsil- 
lotomy and  the  scraping  away  or  curetting  of  the  pharyngeal  adenoid 
results  in  free  and  easy  breathing  and  in  an  extraordinary  change  in  growth 
and  spirits.  Children  who  have  been  stunted  in  mind  and  body  for  years 
gain,  it  may  be,  thirty  pounds  in  a  few  months,  become  rosy  and  bright- 
looking,  and  are  able  for  the  first  time  to  keep  up  with  their  fellows  in 
school  and  in  sport. 

The  use  of  cod-liver  oil  and  syrup  of  the  iodide  of  iron  after  the  operation 
is  a  great  aid  to  speedy  recovery. 


560  DISEASES  OF  THE  (ESOPHAGUS 

Physicians  and  parents  should  regard  it  as  a  duty  to  see  that  children  are 
relieved  from  this  trouble,  which  tlireatens  health  and  mental  power,  and 
which  exposes  the  patient  as  a  fair  mark  to  infectious  disease.  Chronic  middle- 
ear  disease  and  deafness  often  ensue  if  these  growths  are  not  removed. 

While  it  is  true  that  operation  often  gives  permanent  relief,  it  sometimes 
has  to  be  repeated,  as  the  tissues  redevelop  after  removal  of  the  primary 
hypertrophy. 

As  an  anaesthetic  ether  is  far  safer  than  chloroform  during  the  performance 
of  the  operation  of  tonsillotomy  or  curetting  the  pharyngeal  tonsil. 


DISEASES  OF  THE  (ESOPHAGUS. 

(ESOPHAGITIS. 

An  acute  inflammation  of  the  oesophagus  often  ensues  after  the  ingestion 
of  irritant  poisons,  such  as  concentrated  lye,  ammonia-water,  carbolic  acid, 
and  similar  substances.  Under  these  conditions  it  is  but  a  part  of  the 
general  inflammation  of  the  gastrointestinal  tract  which  all  irritant  poisons 
induce,  and  has  little  interest  except  from  a  toxicological  standpoint  and 
the  strictures  that  commonly  follow.  When  oesophagitis  is  due  to  disease 
it  may  arise  from  an  extension  of  a  diphtheria  from  the  pharynx  or  from 
an  extension  of  the  inflammation  in  the  pharynx  in  cases  of  scarlet  fever. 
So,  too,  in  certain  cases  of  typhoid  fever  the  oesophagus  may  undergo  inflam- 
matory changes,  and  these  may  progress  to  such  an  extent  that  ulceration 
ensues.  (See  Typhoid  Fever.)  Sometimes,  too,  the  oesophagus  is  involved 
in  cases  of  aphthous  stomatitis  and  in  thrush. 

A  membranous  oesophagitis  occurs,  but  it  is  rare.  It  may  follow  the  swal- 
lowing of  escharotics  and  is  occasionally  seen  after  prolonged  alcoholic 
excesses.    A  cast  of  the  entire  oesophagus  may  be  expelled. 

The  mucous  membrane  in  ordinary  inflammations  of  the  oesophagus  is 
reddened  and  hypersemic.  There  may  be  some  pain  beneath  the  breast- 
bone, which  is  increased  by  the  swallowing  of  food  or  drink,  but  in  the  milder 
types  no  symptoms  are  present,  and  unless  ulceration  is  followed  by  cica- 
trization, neither  the  physician  nor  the  patient  may  be  aware  of  the  fact  that 
the  oesophagus  has  suffered  from  an  inflammatory  process. 

Should  symptoms  of  pain  and  discomfort  exist,  they  may  be  relieved  by 
the  use  of  demulcent  drinks,  of  which  perhaps  the  best  is  emulsion  of 
sweet  almonds,  or  milk  with  arrowroot.  Sometimes  swallowing  small 
pieces  of  ice  gives  relief. 

In  cases  of  heart  disease  and  cirrhosis  of  the  liver  a  form  of  chronic 
oesophagitis  sometimes  develops,  in  which  the  mucous  membrane  suffers 
from  a  chronic  catarrh  and  the  smaller  bloodvessels  become  varicose  and 
rupture,  causing  the  vomiting  of  blood. 


DILATATION  OF  THE  (ESOPHAGUS  561 


ORGANIC  STRICTURE  OF  THE   (ESOPHAGUS. 

As  has  already  been  intimated,  stricture  of  the  oesophagus  usually  follows 
the  healing  of  an  ulcer  which  is  produced  by  the  ingestion  of  some  corrosive 
substance,  or  by  ulceration  developing  in  the  course  of  typhoid  fever  or 
syphilis.  Stricture  may  be  cylindrical  or  annular,  symmetrical  or  asym- 
metrical, single  or  multiple.  The  usual  sites  are  behind  the  cricoid  cartilage, 
opposite  the  bifurcation  of  the  trachea,  and  at  the  hiatixs  oesophagei. 
Occasionally  inflammation  of  a  lymphatic  gland,  the  pressure  of  a  tumor  in 
the  mediastinum,  or  of  an  aneurysm,  causes  a  narrowing  of  the  gullet,  and, 
more  rarely  still,  a  polypoid  tumor  may  grow  from  the  mucous  membrane. 
Malignant  stricture  will  be  discussed  later. 

Symptoms. — The  symptoms  consist  in  difficulty  in  swallowing  food,  the 
patient  stating  that  it  lodges  part  way  down  to  the  stomach,  and  that  if 
any  considerable  quantities  are  taken  regurgitation  takes  place,  the  regurgi- 
tated materials  containing  no  trace  of  gastric  juice  or  the  products  of 
digestion.  If  an  oesophageal  bougie  is  passed  it  is  found  to  be  arrested  at 
the  level  of  the  stricture,  and  it  may  be  impossible  to  push  it  past  this  point. 

Treatment. — The  treatment  consists  in  the  use  of  a  small  bougie  to  dilate 
the  stricture,  followed  by  the  employment  of  larger,  graduated  bougies.  If 
the  stricture  is  so  tight  that  food  cannot  pass  and  the  life  of  the  patient  is 
endangered  by  inanition,  and  if  the  use  of  a  bougie  fails  to  overcome  the 
obstruction,  surgical  interference  will  be  necessary.  Sometimes  stricture 
of  the  oesophagus  is  a  congenital  condition,  in  which  case  the  child  rarely 
lives,  and  little  can  be  done  for  its  relief. 


DILATATION  OF  THE   (ESOPHAGUS. 

Etiology. — Dilatation  of  the  oesophagus  occurs  in  two  forms,  namely, 
the  diffuse  and  the  localized.  In  the  diffuse  form  the  entire  tube  is  dilated, 
and  there  may  be  some  overgrowth  of  the  muscular  fibres,  which  has  occurred 
in  an  endeavor  on  the  part  of  the  oesophagus  to  force  food  past  an  obstruction 
which  exists  near  the  cardiac  orifice  of  the  stomach. 

When  a  localized  dilatation  occurs  it  takes  the  form  of  a  diverticulum, 
which  may  be  divided  into  two  types,  namely,  "pressure  diverticula"  and 
"traction  diverticula."  The  pressure  diverticula  are  very  rare  and  are 
found  usually  at  the  junction  of  the  pharynx  and  the  oesophagus,  where 
the  muscular  fibres  are  weakest.  Their  origin  is  supposed  to  depend  upon 
pressure  upon  this  point  of  the  gullet  in  deglutition,  and  they  are  thought 
to  develop  in  those  who  are  in  the  habit  of  bolting  their  food.  The  diver- 
ticulum arising  from  this  cause  is  lined  with  mucous  membrane,  its  sub- 
mucous tissues  are  thickened,  and  the  muscular  coat  is  atrophied  so  that 
the  mucous  coat  bulges  through  it  as  a  hernia-like  projection.  The  lesion 
always  occurs  in  the  posterior  or  posterolateral  wall  of  the  oesophagus. 

Traction  diverticula  occur  more  frequently  than  the  type  just  mentioned, 
but  are  very  seldom  recognized  during  life.  They  are  thought  to  be  due 
36 


562  DISEASES  OF  THE  (ESOPHAGUS 

to  contraction  of  tissues  which  have  become  attached  to  the  oesophagus  by 
inflammatory  adhesions,  as  in  cases  in  which  inflammation  of  the  bronchial 
lymph  glands  has  taken  place.  This  lesion  is  usually  found  in  the  anterior 
wall  of  the  gullet,  and  a  number  of  diverticula  may  be  present  in  a  single 
case. 

Atonic  dilatation  of  the  oesophagus  is  occasionally  observed;  the  dilated 
tube  may  be  fusiform  or  flask-shaped,  the  part  of  the  organ  corresponding 
to  the  neck  of  the  flask  being  upward.  Such  dilatation  occurs  indepen- 
dently of  organic  disease  below,  and  has  been  attributed  to  spasm  of  the 
cardia.  The  dilated  oesophagus  may  be  extremely  capacious,  holding  a 
pint  or  more  of  fluid. 

Symptoms. — The  symptoms  of  diffuse  dilatation  of  the  oesophagus  due  to 
stenosis  are  those  produced  by  stricture  of  the  gullet,  and  consist  chiefly  in 
difficulty  in  swallowing.  It  is  a  condition  rarely  recognized  during  life.  The 
small  diverticula  due  to  traction  by  adhesions  are  also  rarely  recognized, 
unless  one  of  them  becomes  so  large  that  it  forms  a  pocket  in  which  food 
accumulates,  until  by  reason  of  its  decomposition  or  fermentation  it  pro- 
duces so  much  irritation  and  inflammation  that  the  stomach,  oesophagus,  and 
all  the  muscles  of  the  chest  and  abdomen  endeavor  to  expel  it  by  a  process 
akin  to  that  of  vomiting.  Sometimes  a  diverticulum  of  this  character  is 
capable  of  holding  a  very  considerable  quantity  of  fluid. 

Diagnosis. — The  diagnosis  of  a  diverticulum  is  reached  by  the  use  of  a 
stomach  tube,  which  is  passed  as  far  as  it  will  go  and  then  used  as  it  would 
be  in  lavage,  or  as  a  stomach  pump  would  be  employed.  Under  these 
circumstances  milk  or  other  liquids  which  have  been  swallowed  are  brought 
up  when  the  tube  has  not  been  passed  far  enough  to  make  it  possible  that 
the  liquids  are  obtained  from  the  stomach.  Such  large  diverticula  are 
usually  of  the  traction  type.  A  diverticulum  or  dilatation  may  be  discovered 
by  filling  the  cavity  with  a  mixture  of  bismuth  and  syrup  of  acacia  and  using 
the  a'-rays. 

Treatment. — The  treatment  consists  in  the  use  of  a  stomach  tube  for  the 
purpose  of  feeding  the  patient,  provided  the  physician  or  the  patient  is  suc- 
cessful in  passing  the  tube  past  the  diverticulum.  In  those  cases  in  which 
the  diverticulum  is  so  large  that  it  prevents  the  ingestion  of  food,  by  pressure 
on  the  oesophagus,  and  so  interferes  with  the  patient's  nutrition,  the  only 
resort  is  a  surgical  operation  and  rectal  alimentation. 


SPASM  OF  THE   (ESOPHAGUS. 

This  affection,  sometimes  called  "  cesophagismus,"  is  rarely  met  with 
except  in  persons  suffering  from  hysteria  or  insanity.  It  is  sometimes 
seen  in  hydrophobia,  and  it  is  this  difficulty  in  swallowing  water,  rather 
than  an  actual  dread  of  water,  which  has  given  that  disease  its  name;  for 
with  the  thought  of  swallowing,  at  the  sight  of  water,  the  spasm  develops. 
The  difficulty  in  swallowing  usually  points  to  the  presence  of  spasm  or 
stricture,  and  if  there  is  no  history  of  the  ingestion  of  an  irritant  some  time 
before,  or  other  causes  which  would  be  likely  to  produce  ulceration  and 


CANCER  OF   THE  (ESOPHAGUS  563 

stricture,  the  strong  possibility  of  spasm  is  to  be  considered.  Usually  in 
spasm  it  is  much  easier  to  pass  an  oesophageal  bougie  than  it  is  in  cases  of 
stricture.  But  occasionally  the  spasm  is  sufficiently  tight  to  oppose  the 
passage  of  the  bougie,  and  to  give  to  the  hand  guiding  the  bougie  the  sensation 
which  is  produced  by  the  end  of  the  instrument  coming  in  contact  with  a 
true  organic  obstruction. 

Treatment. — The  treatment  consists  in  the  passage  of  a  bougie  once  or 
twice  a  day;  in  the  administration  of  nervous  sedatives  if  the  patient  is  in  a 
condition  of  nervous  excitation;  of  stimulants,  if  she  is  in  a  condition  of 
profound  depression,  and  of  measures  devoted  to  the  improvement  of  the 
general  health,  both  mental  and  physical,  if  it  is  impaired.  As  the  spasm 
may  be  due  to  a  fissure,  ulcer,  or  other  tender  spot  the  food  should  not  be 
bulky,  but  preferably  liquid  and  never  taken  in  large  amounts. 


CANCER  OF  THE   (ESOPHAGUS. 

Cancer  of  the  oesophagus  usually  occurs  in  the  form  of  squamous  epithe- 
lioma, and  affects  men  more  frequently  than  women.  Occasionally  a  medul- 
lary cancer  is  found  in  this  region.  The  growth  soon  undergoes  ulcera- 
tion, and  not  infrequently  the  entire  circumference  of  the  tube  may  be 
involved,  and  in  this  manner  a  stenosis  may  be  developed  with  dilatation 
of  the  oesophagus  above  the  point  of  growth.  The  disease  is  quite  rare,  for 
of  7290  cases  of  cancer  collected  by  Williams  but  6  per  cent,  were  primary 
in  the  oesophagus.  Tanchon  in  9118  cases  of  cancer  found  only  13  in  the 
oesophagus.  Cases  have  been  recorded  as  early  in  life  as  nineteen  years, 
but  most  patients  are  past  forty.  The  disease  is  about  equally  divided  as 
to  its  occurrence  in  different  levels  of  the  tube.  Thus,  if  the  statistics  of 
Kraus,  von  Hacker,  and  Newmann  are  added  together,  making  1477  cases, 
we  find  that  582  were  near  the  cardia,  453  near  the  middle  third,  and  440  at 
the  upper  third. 

Symptoms. — The  symptoms,  as  in  cases  of  ordinary  stenosis  due  to  stric- 
ture, consist  in  difficult  deglutition  and  not  infrequently  considerable  pain, 
both  at  the  time  of  swallowing  and  when  the  oesophagus  is  at  rest.  The 
food  is  often  regurgitated  almost  as  soon  as  it  leaves  the  pharynx,  and  some- 
times the  effort  at  regurgitation  is  followed  by  the  appearance  of  some  blood 
and  mucus.  Blood  and  mucu^  also  very  frequently  appear  if  a  bougie  is 
used  to  pass  the  stricture.  The  age  of  the  patient,  the  absence  of  a  history 
of  the  ingestion  of  a  corrosive  poison,  the  emaciation  and  weakness,  and 
the  presence  of  primary  or  secondary  growths  elsewhere  render  the  diagnosis 
possible.  Sometimes  an  aneurysm  of  the  thoracic  aorta  by  pressing  on  the 
oesophagus  may  produce  somewhat  similar  symptoms,  but  under  these 
circumstances  the    physical  signs  of  aneurysm  may  be  found. 

Prognosis. — The  prognosis  in  oesophageal  cancer  is,  of  course,  exceed- 
ingly bad.  Death  comes  from  exhaustion  and  starvation,  from  pneumonia 
due  to  the  inhalation  of  septic  materials,  or  to  ulceration  of  a  large  blood- 
vessel. Sometimes  the  lymphatic  glands  of  the  neck  are  secondarily  involved. 
Occasionally  the  physician  is  chagrined  at  the  autopsy  to  find  that  an  unsus- 


564  DISEASES  OF  THE  STOMACH 

pected  oesophageal  cancer  has  been  present  for  weeks  without  presenting 
symptoms,  and  without  his  having  recognized  its  existence. 

Treatment. — Medicinal  measures  are  of  course  fruitless  except  for  the 
relief  of  pain.  Surgical  measures  are  of  little  value,  since  the  patient  is 
usually  so  exhausted  by  the  time  that  the  diagnosis  is  confirmed  and  he  is 
willing  to  resort  to  an  operation,  that  life  is  prolonged  but  little  by  the  opera- 
tive interference.  Exner  has  recently  reported  a  case  in  which  improvement 
followed  the  use  of  radium  in  a  tube  attached  to  a  bougie. 


DISEASES  OF  THE  STOMACH. 

ACUTE  GASTRIC  CATARRH. 

Definition. — Acute  gastric  catarrh,  or  acute  catarrhal  gastritis,  as  its  name 
indicates,  is  a  state  in  which  the  mucous  membrane  of  the  stomach  becomes 
hypereemic  and  then  swollen,  with  lessened  secretion,  followed  by  excessive 
production  of  mucus  and  reduction  in  the  quantity  of  digestive  ferments. 
The  term  acute  gastritis  is  sometimes  employed  to  describe  this  state.  This 
is  unfortunate  because  a  true  inflammation  of  all  the  coats  of  the  stomach 
is  not  present  except  when  irritating  foods  have  been  taken  in  excess,  or 
when  some  irritant  poison  has  been  swallowed. 

Etiology. — ^The  causes  of  acute  gastric  catarrh  are  very  various.  In  chil- 
dren it  is  often  a  sequel  to  taking  cold,  with  some  resulting  interference 
with  the  activity  of  the  liver.  It  also  follows  the  excessive  use  of  sweets  in 
this  class  of  patients.  In  older  persons  it  is  nearly  always  due  to  the  takingof 
an  excessive  amount  of  indigestible  food  or  overloading  the  viscus  with 
ordinary  foodstuffs,  particularly  if  alcoholic  drinks  and  highly  seasoned 
articles  have  been  swallowed. 

}  Symptoms. — ^The  symptoms  of  acute  gastric  catarrh  in  children  are  quite 
different  from  those  met  with  in  adults  in  most  instances.  The  child  has 
nausea  and  vomiting,  and  some  epigastric  discomfort.  Fever,  varying  from 
100°  to  102°,  often  develops  and  persists  for  several  days.  The  bowels 
may  be  constipated  or  several  loose  movements  may  occur  daily.  The 
appearance  of  the  tongue  in  this  class  of  cases  is  very  characteristic.  It  is 
evenly  coated  by  a  thin  white  fur  which  is  dotted  by  many  tiny  red  spots 
where  the  enlarged  papillae  exist.  The  tongue  is  also  somewhat  drier  than 
normal  and  the  breath  slightly  foul  and  hot.  The  urine  is  usually  decreased 
in  amount  and  high  colored. 

In  adults  acute  gastric  catarrh  presents  somewhat  different  symptoms. 
There  is  often  some  pai7i  or  tenderness  on  pressure  in  the  epigastrium  and 
a  loss  of  appetite  amounting  to  disgust  for  food.  Nausea  may  be  quite  per- 
sistent and  vomiting  may  occur. 

In  both  children  and  adults  the  attacks  may  last  for  from  one  to  four  days. 


ACUTE   TOXIC  GASTRITIS  565 

Diagnosis. — When  the  physician  is  called  to  see  a  child  who  is  suffering 
from  moderate  fever,  a  somewhat  coated  tongue  and  epigastric  distress, 
he  must  not  be  hasty  in  stating  that  the  case  is  one  of  acute  gastric 
catarrh,  because  many  of  the  acute  infectious  diseases  begin  by  moderate 
gastric  disorder  and  a  coating  of  the  tongue.  Whenever  the  gastric  symp- 
toms persist  for  more  than  four  or  five  days,  enteric  fever  should  be  sus- 
pected as  being  the  cause  of  the  illness,  but  care  must  be  taken  that  the 
common  error  of  calling  mild  typhoid  fever  "gastric  fever"  is  not  made. 
Uncomplicated  acute  gastric  catarrh  is  so  rare  in  adults,  who  have  not 
abused  alcohol,  that  great  care  should  be  taken  before  the  physician  is 
satisfied  with  this  diagnosis. 

Treatment. — The  treatment  consists  in  unloading  the  portal  and  hepatic 
circulation,  which  is  nearly  always  disordered,  by  the  use  of  small  doses  of 
calomel,  giving  |  of  a  grain  every  half-hour  for  eight  doses,  and  following 
this  in  five  hours  by  a  Seidlitz  powder  or  some  other  mild  and  cooling  saline 
purge.  If  the  stomach  is  very  irritable  the  Seidlitz  powders  should  be 
divided  into  fourths  and  taken  at  fifteen-minute  intervals.  After  this  treat- 
ment has  acted  the  patient  should  receive  small  doses  of  bismuth  subnitrate 
and  oxalate  of  cerium.  For  a  child  2  grains  of  the  former  and  1  of  the  latter 
may  be  given  every  hour  for  five  or  six  doses.  Adults  may  take  5  grains  of 
the  bismuth  at  a  dose. 

The  rest  of  the  treatment  consists  in  the  use  of  small  quantities  of  liquid 
food,  such  as  whey  or  barley-water,  or  scalded  toast.  Small  quantities  of 
milk  and  lime-water  may  be  used.  In  some  instances  total  abstinence  from 
food  for  twelve  or  twenty-four  hours  gives  the  best  results.  Rest  in  bed  is 
also  very  advantageous  for  both  children  and  adults. 


ACUTE  TOXIC  GASTRITIS. 

Etiology. — Acute  toxic  gastritis  is  produced,  as  its  name  implies,  by  the 
entrance  into  the  stomach  of  any  poison  which  is  capable  of  acting  as  a 
severe  irritant  or  as  a  corrosive.  Some  of  these  irritants  act  with  only  suffi- 
cient severity  to  produce  hypersemia  and  moderate  superficial  inflamma- 
tion, but  others  corrode  the  stomach,  and  may  even  perforate  it.  Most 
of  the  metallic  poisons,  such  as  mercuric  chloride  and  mercuric  iodide; 
oxalic  acid,  carbolic  acid,  and  the  ordinary  mineral  acids,  such  as  sulphuric, 
hydrochloric,  and  nitric  acids,  belong  to  the  class  of  severe  corroding  irri- 
tants. Other  substances,  such  as  phosphorus  and  chlorate  of  potassium, 
not  only  act  as  irritants,  but  produce  fatty  degeneration.  Arsenic  differs 
in  its  action  on  the  stomach  from  that  of  the  mineral  acids  in  that  it  does 
not  coagulate  albumin  and  is  not  corrosive.  It  causes,  however,  a  peculiar 
exfoliation  of  the  mucous  membrane  lining  the  stomach  and  bowels,  partly 
by  its  local  effect  induced  by  direct  contact,  and  partly  by  the  elimination 
of  the  arsenic  by  the  gastric  walls,  whereby  the  mucous  membrane  is  shed. 
Among  the  vegetable  substances  which  may  cause  gastritis  may  be  men- 
tioned croton  oil,  elaterium,  and  castor-oil  beans. 


566  DISEASES  OF   THE  STOMACH 

Morbid  Anatomy. — As  the  result  of  the  violent  inflammation  of  the  stomach 
produced  by  these  drugs  death  may  ensue,  or,  if  the  patient  survives  the 
acute  stage,  extensive  exfoliation  of  the  superficial  part  of  the  mucosa 
occurs,  or  ulcers  may  form  which  ultimately  cause  death.  Free  and 
interstitial  hemorrhages  occur.  In  other  instances  there  is  so  much  destruc- 
tion of  the  peptic  tubules  that  the  gastric  mucosa  is  largely  destroyed  and 
cicatricial  contractions  ensue. 

Symptoms. — The  symptoms  of  toxic  gastritis  are  violent  burning  pain  in 
the  stomach,  thirst,  and  vomiting.  The  vomited  matters  may  be  stained 
with  blood,  and  usually  contain  an  excess  of  mucus  and  often  flakes  of 
the  mucosa  itself.  Sometimes  diarrhoea  develops.  The  pulse  is  rapid,  the 
patient's  expression  is  anxious,  and  death  may  occur  within  a  few  hours 
in  collapse. 

Diagnosis. — While  it  is  not  possible  to  make  a  positive  diagnosis  as  to  the 
character  of  the  poison  which  has  been  taken  by  the  appearance  of  the 
stomach  at  autopsy,  certain  poisons  nevertheless  produce  definite  lesions 
which  may  be  considered  almost  peculiar  in  themselves.  When  sulphuric 
acid  is  taken,  the  parts  are  blackened;  nitric  acid  makes  them  yellow.  Most 
of  the  alkalies  stain  them  brown  and  the  silver  salts  cause  intense  redness 
followed  by  a  brown  and  black  hue  on  exposure  to  light.  It  is  also  stated 
that  oxalic  acid  causes  a  peculiar  gelatinous  appearance  of  the  gastric 
mucous  membrane  and  that  ammonia  may  cause  a  suppurative  condition. 

Treatment. — The  treatment,  of  course,  depends  upon  the  character  of  the 
poison.  In  all  instances,  except  when  phosphorus  is  taken,  olive  oil  may  be 
given  to  protect  the  stomach;  morphine  should  be  used  hypodermically 
to  relieve  pain  and  irritation,  and  external  heat  should  be  applied  to  combat 
shock.  When  one  of  the  acids  has  been  taken,  any  alkali  such  as  lime- 
water,  plaster  from  the  walls  suspended  in  water,  very  dilute  ammonia,  or 
even  soap  and  water  may  be  used  to  antidote  the  acid  except  in  the  case  of 
oxalic  acid,  when  only  lime  or  chalk  should  be  used;  for  while  calcium 
oxalate  is  insoluble,  the  oxalates  of  potassium  and  sodium  are  not  insoluble, 
and  are  practically  as  poisonous  as  the  oxalic  acid  itself.  When  lead  in  one 
of  its  soluble  forms,  or  carbolic  acid  is  taken  as  a  poison  the  antidote  is  any 
soluble  sulphate,  of  which  magnesium  sulphate  and  sodium  sulphate  are 
the  best. 

]  The  after-treatment  of  acute  toxic  gastritis  consists  in  the  use  of  large 
doses  of  bismuth  subnitrate,  and  in  the  employment  of  rectal  feeding,  so 
that  the  stomach  may  be  put  at  rest  for  as  many  days  as  possible. 


PHLEGMONOUS  GASTRITIS. 

Definition. — The  term  "phlegmonous  gastritis"  is  apphed  to  a  condition 
in  which  the  inflammation  is  of  such  a  character  that  it  proceeds  to  suppura- 
tion, the  chief  part  of  the  suppurative  process  developing  in  the  submucous 
tissues,  and  sometimes  extending  to  the  muscular  coat  of  the  stomach  and 
even  to  the  peritoneum. 


PHLEGMONOUS  GASTRITIS  567 

Etiology. — The  disease  is  exceedingly  rare,  and  has  appeared  with  about 
equal  frequency  at  all  ages  from  ten  to  eighty  years.  In  some  instances 
it  is  primary,  the  seat  of  the  infection  beginning  in  an  ulcer  or  growth,  or 
more  rarely  from  some  direct  traumatism.  The  secondary  cases  are  those 
in  which  the  process  develops  during  the  course  of  one  of  the  acute 
infections,  such  as  typhoid  fever,  puerperal  fever,  pyaemia,  and  variola. 
Fifty  cases  have  been  gathered  by  Jacoby  and  85  by  Leith,  but  these  figures 
of  course  include  many  of  the  same  instances  of  the  disease.  Phlegmonous 
gastritis  is  of  two  kinds:  a  diffuse  form  with  a  rapid  course,  profound  sys- 
temic disturbances,  and  speedy  death,  and  a  circumscribed  form  in  which 
the  symptoms  are  much  less  severe;  the  patient  living,  it  may  be,  for  weeks, 
but  usually  dying  as  the  result  of  the  disease. 

The  pyloric  portion  of  the  stomach  is  chiefly  affected.  Its  walls  are 
greatly  thickened,  and  the  submucous  tissues  are  riddled  with  pus,  having 
undergone  almost  complete  necrosis.  Not  infrequently  many  perforations  of 
the  mucous  membrane  occur,  so  that  the  internal  surface  of  the  stomach  has 
a  sieve-like  appearance. 

Several  cases  of  suppurative  gastritis  have  been  reported  in  the  United 
States,  and  they  are  remarkable  enough  to  demand  notice.  In  Kinnicutt's 
case  the  disease  followed  an  alcoholic  debauch.  In  Hemmeter's  case  the 
patient  had  vomited  blood,  was  treated  for  gastric  ulcer,  and  did  not 
die  until  two  months  after  the  onset  of  severe  symptoms.  The  infection  had 
here  occurred  through  a  healed  ulcer.  In  Smith's  case  violent  epigastric 
pain  with  collapse  and  death  in  two  and  a  half  days  took  place,  the  entire 
submucosa  being  infiltrated  with  pus.  In  Loomis'  case  abdominal  pain, 
bilious  vomiting,  and  a  feeble  pulse  with  delirium  preceded  death,  which 
occurred  at  the  end  of  four  days.  In  Hun's  case  the  gastric  walls  were 
fully  one-half  inch  in  thickness  and  the  tissues  between  the  peritoneum 
and  the  mucous  membrane  were  purulent. 

In  the  circumscribed  form  of  phlegmonous  gastritis  the  abscess  may  be 
single,  or  multiple  abscesses  may  be  present. 

Symptoms. — The  symptoms  in  the  diffuse  form  consist  in  the  sudden 
development  of  violent  epigastric  pain,  followed  by  faintness  and  collapse, 
with  incessant  vomiting.  After  the  vomiting  has  continued  for  some  time, 
the  vomited  matter  may  be  stained  with  bile. 

When  the  disease  is  secondary  to  malignant  growth,  it  is  stated  that  vomit- 
ing does  not  often  develop.  Notwithstanding  the  severity  of  the  process, 
pus  is  never  found  in  the  vomit  in  the  acute  cases.  The  temperature 
varies  from  103°  to  105°.  The  pulse  is  rapid  and  feeble,  and  becomes 
more  and  more  so  until  death  occurs  in  collapse,  preceded  by  a  stage  of 
apathy. 

Diagnosis. — There  is  practically  no  array  of  diagnostic  symptoms  in  cases 
of  this  disease  save  the  onset  of  violent  epigastric  pain. 

The  pus  may  escape  into  the  general  peritoneal  cavity,  the  patient 
dying  with  symptoms  of  perforation  and  collapse.  The  most  extraordinary 
case  of  this  character  so  far  recorded  is  the  one  reported  by  Callow,  in 
which  the  patient  vomited  a  pint  of  pus,  pus  appeared  in  the  stools,  and 
there  were    seven  pints  of    it  in  the  peritoneal  cavity.      All  this  pus  was 


568  DISEASES  OF  THE  STOMACH 

traced  to  a  large  abscess  cavity  in  the  wall  of  the  stomach  which  had,  how- 
ever, not  been  accompanied  by  pain  during  its  formation. 

Treatment. — When  it  is  possible  to  make  a  diagnosis  prompt  operative 
interference  is  strongly  indicated.  So  far,  this  has  not  been  attempted 
early  enough  in  any  case  to  give  satisfactory  results.  The  parts  should  be 
drained  and  a  gastroenterostomy  performed.  (For  an  excellent  paper  on 
this  subject  see  Moynihan  in  the  Medical  Chronicle  for  November,  1903.) 


DIPHTHERITIC  GASTRITIS. 

Inflammation  of  the  stomach  with  the  formation  of  a  false  membrane  due 
to  the  Klebs-Loeffler  bacillus  is  very  rarely  encountered.  It  nearly  always 
follows  diphtheria  in  the  upper  air-passages.  Still  more  rarely  in  cases  of 
septicaemia,  scarlet  fever,  and  smallpox  a  false  membrane  may  develop  in 
the  stomach.  The  condition  is  of  interest  solely  from  a  pathological  stand- 
point. 

MYCOTIC  GASTRITIS. 

Inflammation  of  the  stomach  due  to  the  growth  of  specific  micro-organ- 
isms upon  its  mucous  membrane  is  very  rare.  The  thrush  fungus,  Oidiura 
albicans,  has  been  found  in  certain  cases.  Anthrax  of  the  stomach  has  also 
followed  anthrax  of  the  mouth.  The  yeast  fungus  is  not  infrequently 
present,  but  rarely  produces  severe  inflammation  of  the  stomach.  Cases 
which  are  in  the  nature  of  medical  curiosities  have  been  reported  in  which 
acute  inflammation  of  the  stomach  was  due  to  the  action  of  maggots  deposited 
about  the  mouth  by  the  common  fly,  or  swallowed  wnth  various  articles  of 
food.  In  all  such  instances  the  condition  of  the  stomach  has  been  profoundly 
depressed,  as  otherwise  the  ability  of  this  organ  to  destroy  invading  micro- 
organisms and  parasites  prevents  it  from  becoming  infected. 


CHRONIC  GASTRITIS. 

Definition. — By  chronic  gastritis  is  meant  a  state  in  which  the  gastric 
mucous  membrane  suffers  from  prolonged  and  persistent  inflammation  of  a 
low  grade,  or  repeated  acute  or  subacute  attacks,  which  result  in  more  or  less 
well-marked  pathological  changes.  The  term  "  chronic  gastric  catarrh"  is 
often  used  as  a  synonym  to  describe  this  condition. 

Etiology. — The  causes  of  chronic  gastritis  are  very  numerous.  In  the 
majority  of  cases  they  consist  in  the  frequent  entrance  into  the  stomach  of 
irritating  foods  or  drinks,  as  in  alcoholics,  or  in  persons  given  to  the  exces- 
sive use  of  highly  seasoned  foods.  In  these  cases  a  very  large  part  of  the 
disorder  in  the  gastric  mucosa  is  also  dependent  upon  the  engorged  portal 
circulation  and  the  hepatic  torpor  which  such  dietary  indiscretions  induce. 
Cardiac  diseases  which  lead  to  hepatic  congestion  very  frequently  induce 
gastric  catarrh.    Alcohol,  bad  food,  or  badly  chewed  food,  hepatic  cirrhosis, 


CHRONIC  GASTRITIS  569 

and  congestion  of  the  liver  are,  therefore,  the  chief  causes  of  this  con- 
dition. 

Pathology  and  Morbid  Anatomy. — The  changes  in  the  stomach  in  chronic 
gastritis  may  be  divided  into  two  classes :  In  the  first  there  is  a  proliferation 
of  the  connective-tissue  cells  and  formation  of  new  tissue,  which,  like  similar 
forms  of  overgrowth  elsewhere,  results  in  atrophy  or  degenerative  changes 
in  the  gastric  glands.  In  other  words,  the  lesions  are  not  limited  to  the 
superficial  portion  of  the  mucous  membrane,  but  extend  well  down  into 
the  deeper  layers.  As  the  contraction  of  the  overgrown  connective  tissue 
proceeds,  it  may  cause  the  projection  on  the  surface  of  the  inner  wall  of  the 
stomach  of  wart-like  masses,  so  that  broad,  raised  patches  of  mucous  mem- 
brane are  discernible,  or  even  polypoid  formations  appear  (gastritis  poly- 
posa).    The  entire  gastric  mucosa  may  be  contracted  or  plicated. 

In  other  cases  the  lesions  appear  to  be  more  of  a  degenerative  type;  the 
sclerosis  or  fibrosis  is  inconspicuous,  and  the  epithelial,  or  granular,  atrophy 
is  most  marked.  In  other  cases  cystic  alteration,  with  little  fibrous  hyper- 
plasia, may  be  the  dominant  alteration.  In  the  pyloric  end  of  the 
stomach  the  contraction  which  follows  the  overgrowth  of  connective  tissue 
may  produce  stenosis,  a  condition  which  is  emphasized  in  some  cases  by  the 
inflammatory  process  extending  to  the  muscular  layer  of  the  stomach,  by  which 
means  still  greater  thickening  takes  place.  The  closure  of  the  pyloric  orifice 
is,  therefore,  due  to  a  true  hyperplasia.  The  cause  of  the  nipple-like  projec- 
tions found  in  the  gastric  mucous  membrane  in  some  of  these  cases  is  un- 
known. It  may  be  due  to  the  constricting  influence  of  connective  tissue 
formed  between  the  tubules,  or  it  may  arise  from  overgrowth  of  the  submucous 
coat  of  the  stomach. 

The  second  type  of  chronic  gastritis  is  that  characterized,  not  by  over- 
growth of  connective  tissue,  as  has  just  been  described,  but  by  wasting  or 
atrophy  of  the  glands.  In  some  cases,  however,  there  is  at  first  some  hyper- 
plasia of  connective  tissue,  and  this  is  followed  by  atrophic  changes.  The 
mucous  membrane  becomes  thin  and  smooth  and  is  often  pigmented,  while 
the  epithelial  cells  lining  the  gastric  tubules  suffer  from  atrophic,  fatty  or 
necrotic  changes.  The  deeper  tissues  in  some  cases  escape,  but  in  others 
they  also  undergo  wasting,  so  that  even  the  submucous  coat  and  the  mus- 
cular coat  atrophy.  To  this  condition  has  been  given  the  unfortunate,  but 
etymologically  correct,  name  of  phthisis  ventriculi.  In  such  a  case  it  is  quite 
possible  for  gastric  dilatation  to  develop. 

Atrophic  gastritis  is  much  more  rare  than  the  hyperplastic  type,  and  is 
often,  if  not  always,  associated  with  another  grave  condition,  pernicious 
anaemia.  Finally,  in  very  rare  instances,  cases  of  atrophic  gastritis  may 
develop  into  ulceration  of  the  gastric  mucosa,  the  ulcers  being  small,  round 
or  irregular  in  shape,  and  rarely  penetrating  very  deeply  (erosive  gastritis). 
They  are  found  chiefly  near  the  pylorus  and  may  bleed  very  freely. 

Symptoms. — The  symptoms  of  chronic  gastritis  consist  in  loss  of  appetite, 
impairment  of  the  sense  of  taste,  and  nausea,  which  is  particularly  prone  to 
be  present  in  the  morning  and  may  often  amount  to  actual  vomiting — the 
"morning  vomiting  of  the  drunkard."  The  vomited  matters  are  but  partly 
digested  and  are  often  mixed  with  much  mucus.    Most  cases  frequently  helch 


570  DISEASES  OF  THE  STOMACH 

up  gas,  and  with  it  a  mouthful  of  acid  fluid  may  be  brought  up  which  scalds 
the  pharynx.  Hydrochloric  acid  may  be  lacking  in  the  gastric  contents,  but 
in  its  place  an  excess  of  butyric  and  acetic  acids  is  often  present,  particularly 
if  the  stomach  is  feeble  and  is  unable  to  expel  its  contents  into  the  bowel  with 
sufficient  promptness.  Lactic  acid  is  also  present  in  some  cases.  It  is  the 
presence  of  these  acids  that  causes  heartburn,  or  pyrosis.  In  some  cases, 
however,  ^n  excess,  or  at  least  a  normal  amount,  of  hydrochloric  acid  is 
secreted. 

The  tongue  is  moderately  coated,  the  bowels  are  prone  to  constipation, 
and  the  general  nutrition  is  slightly  impaired,  partly  because  of  poor  diges- 
tion, but  chiefly  because  of  the  fact  that  the  patient  has  cut  off  from  his 
diet  list  one  article  after  another,  with  the  thought  that  it  "disagrees"  with 
him.  There  is  not,  however,  an  impairment  of  nutrition  sufficient  to  cause 
great  loss  of  weight  in  many  cases,  because  the  digestive  function  of  the 
duodenum  is  not  always  impaired.  If  the  liver  is  diseased,  a  very  consider- 
able loss  of  weight  is  usually  present.  Digestion  is,  of  course,  as  is  clear  from 
a  consideration  of  the  state  of  the  gastric  mucous  membrane,  greatly  delayed 
and  very  imperfect,  and  as  a  result  the  patient  becomes  inert,  low-spirited, 
and  vitally  depressed,  so  that  he  presents  the  clinical  picture  of  what  is 
commonly  called  by  the  laity  "a  confirmed  dyspeptic." 

If  the  cause  of  the  gastric  disorder  is  alcoholic  cirrhosis  of  the  Hver,  the 
symptoms  of  cirrhosis  are  associated  with  those  of  gastric  catarrh, 

A  constant,  unproductive  cough  is  often  present  without  any  lesions  being 
found  in  the  lungs 

When  the  atrophic  form  of  chronic  gastritis  is  present,  a  very  profound 
degree  of  anaemia  is  often  developed,  as  already  stated. 

Diagnosis. — The  separation  of  chronic  gastritis  from  gastric  cancer  is  by 
no  means  easy  in  many  instances,  for  in  many  cases  of  cancer  gastritis  is 
also  present.  The  presence  of  a  mass,  of  considerable  pain,  of  coffee-ground 
vomit,  and  an  absence  of  HCl  in  the  gastric  fluids  would  point  to  the  diag- 
nosis of  cancer;  but  as  pain  is  not  always  present  in  cancer,  as  ulcers  of  the 
stomach  may  be  present  in  chronic  catarrh,  giving  rise  to  bloody  vomit, 
and  as  HCl  is  often  diminished  or  absent  in  this  state,  these  signs  are  not 
entirely  reliable.  Lactic  acid  is  not  commonly  present  in  large  amount  in 
chronic  gastritis,  but  it  is  usually  present  in  excess  in  cancer. 
\  Prognosis. — The  prognosis  in  a  case  of  chronic  gastritis  must  be  given 
guardedly,  for  while  one  patient  may  speedily  recover  under  proper  treatment, 
other  patients  remain  ill  for  long  periods,  even  with  the  most  skilful  treat- 
ment. Much  depends,  too,  upon  the  course  of  the  disease  and  upon  the 
general  heaUh  of  the  patient.  While,  on  the  one  hand,  the  malady  does 
not  cause  death,  on  the  other,  complete  recovery  may  seem  impossible.^ 

Treatment. — Theoretically,  chronic  gastritis  may  be  prevented  by  avoiding 
the  use  of  irritating  and  indigestible  foods  and  alcohohc  drinks,  but,  practi- 
cally, patients  are  not  seen  until  after  the  condition  has  been  developed  by 
the  various  causes  which  have  been  enumerated.  After  the  condition  has 
developed  the  treatment  must  be  devoted  to  the  removal  of  the  habits  which 
act  as  causes,  to  the  relief  of  the  conditions  which  exist  in  other  portions  of 
the  body,  and  to  the  cure  of  the  symptoms  already  present  in  the  stomach. 


CHRONIC  GASTRITIS  571 

In  cases  in  which  errors  in  diet  exist  these  must  be  rectified,  and  if  alcohol 
is  used  it  must  be  stopped.  If  an  examination  of  the  heart  shows  that  it  is 
feeble,  and  that  the  gastric  condition  is  due  to  an  impaired  circulation,  rest 
and  the  use  of  moderate  doses  of  digitalis  must  be  resorted  to,  but  it  must 
not  be  forgotten  that  digitalis  in  full  doses  is  capable  of  causing  gastric 
distress.  Usually  it  is  necessary,  in  order  to  get  the  best  results,  to  administer, 
every  few  days,  small  doses  of  blue  mass,  which  not  only  unloads  the  liver, 
but  seems  to  increase  the  efficiency  of  the  digitalis. 

The  local  treatment  of  the  stomach  consists  in  the  employment  of  lavage, 
by  means  of  which  the  excessive  quantities  of  mucus  and  undigested  food 
are  removed.  Emetics  should  not  be  employed,  as  they  are  too  violent  and 
apt  to  increase  the  inflammatory  process.  Not  infrequently  the  mucus  which 
is  secreted  is  so  thick  and  tenacious  that  there  is  some  difficulty  in  removing 
it  from  the  stomach.  Under  these  circumstances,  various  medicinal  sub- 
stances may  be  added  to  the  water  which  is  employed  for  the  lavage.  A  salt 
solution  may  be  used,  composed  of  |  ounce  of  sodium  chloride  and  1  ounce 
of  sodium  bicarbonate,  placed  in  a  quart  of  warm  water.  After  the  stomach 
has  been  thoroughly  cleansed,  it  may  be  washed  a  second  time  with  boric 
acid,  1:100;  salicylic  acid,  1:1000;  chloroform-water,  1:200;  hydrochloric 
acid,  1 :  200.  When  chloroform- water  is  used,  great  care  should  be  taken  that 
the  chloroform  is  thoroughly  mixed  with  water  and  that  the  mixture  is  then 
allowed  to  stand  for  a  sufficient  time  to  permit  of  the  separation  of  any  excess 
of  chloroform. 

Lavage  should  be  carried  out,  as  a  rule,  not  oftener  than  twice  in 
twenty-four  hours ;  in  many  cases  once  every  alternate  day  is  often  enough. 
The  best  time  to  perform  lavage  is  usually  in  the  evening  at  about  9  o'clock, 
so  that  the  stomach  may  have  complete  rest  for  the  next  ten  hours.  In  those 
cases,  however,  in  which  the  taking  of  food  in  the  morning  produces 
great  distress,  it  is  often  advantageous  to  use  lavage  on  first  arising,  in  order 
that  mucus  may  be  removed. 

In  regard  to  drugs,  it  may  be  said  that  the  one  which  has  the  greatest 
reputation  is  the  nitrate  of  silver  given  in  pills  containing  j  grain,  or  in  solution 
in  the  dose  of  from  |  to  1  grain  to  2  drachms  of  one  of  the  aromatic  waters, 
as  cinnamon-water  or  peppermint-water.  Another  drug  which  has  a  high 
reputation  is  the  subnitrate  of  bismuth,  which  should  be  given  in  large  doses, 
.about  1  drachm  twice  or  thrice  a  day.  Both  of  these  forms  of  treatment 
possess  the  disadvantage  that  they  are  constipating,  and  therefore  the  patient 
usually  has  to  take  a  small  dose  of  one  of  the  mild  laxative  saline  waters  on 
first  arising  in  the  morning. 

For  the  relief  of  loss  of  appetite  and  for  absence  of  hydrochloric  acid,  the 
various  simple  bitters,  such  as  cinchona,  quassia,  and  cardamom,  may  be 
given.  Of  the  compound  tincture  of  cardamom,  1  or  2  drachms  may  be 
given  once  or  twice  a  day  with  meals.  If,  in  addition,  it  is  believed  that  the 
stomach  lacks  motive  power,  strychnine  may  also  be  used,  and  the  fluid 
extract  of  condurango  may  be  given  in  the  dose  of  a  drachm  three  times  a 
day.  If  digestion  is  delayed  because  of  a  lack  of  hydrochloric  acid,  5  drops 
of  this  dilute  acid  may  be  given  with  each  meal,  combined  with  a  good 
essence  of  pepsin.    The  administration  of  nitrate  of  silver  one  hour  before 


572  DISEASES  OF   THE  STOMACH 

meals  usually  diminishes  pyrosis,  or  heartburn,  but,  if  it  does  not,  magnesium 
carbonate  or  bicarbonate  of  sodium  may  be  used  for  this  purpose.  These 
alkalies  frequently  diminish  pain  by  decreasing  acidity. 

The  diet  should  consist  of  easily  digested  foods,  and  it  is  to  be  remembered 
that  small  meals  given  five  or  six  times  a  day  are  better  than  large  meals 
given  three  times  a  day.  Chicken,  beef,  and  mutton  broths,  free  from  fat 
and  fortified  by  the  addition  of  barley  or  rice,  are  exceedingly  useful.  If 
solids  are  taken,  the  patient  must  be  instructed  to  chew  both  the  meats  and 
starches  thoroughly.  Often  it  is  advisable  to  have  the  meat  made  tender  by 
pounding  it,  or  by  cooking  it  in  such  a  way  that  its  fibres  are  readily  dis- 
solved by  the  gastric  juice. 

The  digestion  of  starches,  like  baked  potatoes,  toasted  bread,  Zweiback, 
and  pulled  bread,  should  be  aided  by  the  us'e  of  taka-diastase  or  pancreatin. 
Often  a  capsule  containing  both  of  these  digestive  ferments  will  be  advan- 
tageous in  its  effect. 

Milk  may  be  given  to  those  with  whom  it  agrees.  In  some  instances, 
when  it  cannot  be  taken  pure,  it  can  be  digested  readily  if  diluted  with  some 
sparkling  water,  particularly  Vichy  water.  In '  other  instances  the  addition 
of  a  small  quantity  of  salt  aids  in  its  digestion,  and  in  still  others  lime-water 
may  be  given  with  it. 

The  question  as  to  the  use  of  the  light  wines  by  a  patient  suffering  from 
chronic  gastritis  is  debatable.  If  any  fermentation  is  present,  they  must 
not  be  used.  If  patients  are  accustomed  to  drinking  wine  with  each  meal, 
it  may  be  advisable  to  permit  small  quantities,  particularly  with  luncheon 
and  dinner.    Champagnes  are  usually  distinctly  harmful. 


GASTRIC  DILATATION. 

Definition. — By  dilatation  of  the  stomach  is  meant  a  condition  in  which 
this  viscus  loses  its  propulsive  power  to  a  greater  or  less  degree  and  also 
undergoes  a  certain  amount  of  dilatation,  so  that  its  capacity  is  increased. 
It  is  sometimes  called  "  gastric  ectasy,"  or  "  gastrectasis." 

Etiology. — While  it  is  true  that  dilatation  is  the  state  which  impresses 
itself  most  forcibly  upon  the  clinician  when  a  patient  is  examined  who  is 
suffering  from  this  malady,  it  is  also  a  fact  that  the  dilatation  is  always  the 
result  of  some  primary  difficulty  in  expelling  the  contents  of  the  stomach 
into  the  duodenum.  In  some  instances  this  is  due  to  stenosis  of  the  pylorus 
produced  by  a  thickening,  as  in  chronic  gastric  catarrh;  in  others  it  may  be 
due  to  what  is  called  hypertrophic  stenosis  of  the  pylorus,  and  in  still  others 
the  obstruction  may  be  offered  by  a  tumor  at  this  point  or  by  a  cicatrix  or 
other  form  of  stricture.  Rarely  the  pylorus  becomes  so  glued  to  nearby 
tissues  that  it  is  held  abnormally  high,  and  is  so  fixed  that  it  is  almost 
impossible  for  the  stomach  to  force  its  contents  past  the  orifice. 

A  second  cause  of  difficulty  in  emptying  the  stomach  exists  in  a  weakness, 
congenital  or  acquired,  which  so  impairs  the  motor  power  of  the  viscus  that 
it  is  too  feeble  to  empty  itself.     Neither  obstruction  nor  inherent  weakness 


GASTRIC  DILATATION  573 

of  the  muscle  fibres  in  the  gastric  wall  are  necessarily  associated  with  dila- 
tation, but  it  can  be  readily  understood  that  these  causes  may  so  result. 
It  is  conceivable  that  in  the  obstructive  cases  the  stomach  may  undergo 
some  hypertrophy,  and  this  takes  place  in  a  considerable  number  of  cases 
as  a  primary  result  of  the  obstruction.  The  constant  endeavor  of  the 
stomach  to  empty  itself,  however,  ultimately  causes  fibroid  changes  in  the 
muscle  fibres  from  fatigue,  and  this  condition  is  emphasized  by  impaired 
nutrition  of  the  stomach,  and  perhaps  by  impaired  nerve  supply  as  well. 
Finally,  it  is  undoubtedly  true  that,  in  some  persons  at  least,  the  repeated 
distention  of  the  stomach  by  large  amounts  of  food  and  drink  may  cause 
permanent  dilatation,  particularly  if  these  materials  be  of  such  a  character 
that  they  produce  chronic  gastritis,  and  so  impair  the  tone  of  the  gastric 
walls.  Workmen  in  breweries  who  partake  of  large  amounts  of  beer,  and 
diabetics  who  eat  and  drink  to  excess  because  of  their  disease,  often  suffer 
from  gastrectasia.    . 

Dilatation  of  the  stomach  is  usually  a  disease  of  middle  age  or  of  adult 
life,  but  cases  are  not  uncommon  in  children.  The  youngest  case  I  ever  saw 
was  in  a  child  of  eighteen  months.  The  dilatation  due  to  obstruction  is  the 
type  in  which  the  greatest  enlargement  of  the  stomach  develops. 

Pathology  and  Morbid  Anatomy. — The  size  of  the  stomach  may  be  greatly 
increased,  so  that  the  average  capacity  of  a  quart  (1000  c.c.)  increased  to 
even  four  quarts.  Under  these  circumstances,  the  lower  border  of  the 
stomach  extends  far  below  the  normal  level.  Its  walls  are  decreased  in 
thickness,  there  is  atrophy  of  the  lining  mucous  membrane,  and  the  mus- 
cular fibres  are  even  more  wasted,  so  that  many  of  them  disappear  and 
are  replaced  by  connective  tissue.  When  primary  atrophy  of  the  muscularis 
has  been  present,  it  not  rarely  happens  that  an  excess  of  muscle  fibres  are 
found  in  the  pyloric  region,  although  advanced  secondary  wasting  has  oc- 
curred elsewhere.  In  some  cases  of  dilatation  the  gastric  walls  do  not  become 
thin,  but  may  appear  thicker  than  normal,  because  of  an  overgrowth  of 
connective  tissue  which  supplants  the  muscular  layer  of  the  organ. 

Gastric  dilatation  does  not  always  result  in  an  equally  well-developed 
increase  in  size.  In  some  instances  the  cardiac  orifice  and  the  pylorus  are 
near  one  another,  so  that  the  great  curvature  hangs  like  a  plumber's  trap;  in 
other  cases  cicatrices  distort  it  and  even  cause  an  hour-glass  form,  with  a 
dilatation  on  either  side. 

Symptoms. — The  symptoms  of  gastric  dilatation  are  usually  considered 
by  the  patient  to  be  those  of  "chronic  dyspepsia."  There  is  usually  loss  of 
appetite,  a  sense  of  gastric  discomfort  and  weight,  or  a  feeling  of  dragging 
down  in  the  abdomen  and  a  good  deal  of  belching  of  gas,  which  is  often 
accompanied  by  some  particles  of  food  mixed  with  fluid.  The  sense  of  dis- 
tention and  distress  gradually  increases  until  it  is  almost  insupportable,  and 
then  the  viscus  finding  the  burden  too  great,  unloads  itself  by  an  attack 
of  vomiting,  in  which  the  patient  is  surprised  to  find  articles  of  food  ingested, 
perhaps,  several  days  before.  Both  the  physician  and  the  patient  are,  not 
rarely,  amazed  at  the  quantity  expelled,  for  the  volume  shows  that  it  repre- 
sents the  ingested  fluids  and  solids  of  several  days.  Such  an  attack  of  vomit- 
ing, in  which  the  quantity  expelled  is  far  in  excess  of  the  amount  recently 


574  DISEASES  OF   THE  STOMACH 

swallowed,  is  a  very  important  diagnostic  point.  These  attacks  of  vomiting 
usually  occur  at  night.  When  the  dilatation  is  severe,  so  that  the  stomach 
cannot  completely  empty  itself,  the  rehef  given  by  vomiting  is  only  partial, 
and  perhaps  no  relief  follows. 

The  howels  are  constipated,  and  the  stools  when  passed  are  scanty,  because 
so  much  of  the  food  ingested  is  not  passed  on  into  the  duodenum.  The 
urine  is  also  scanty.  Not  rarely  it  is  decreased  to  one-third  the  normal 
quantity. 

Many  of  the  symptoms  are  due  to  stasis  of  the  food  in  the  stomach,  fermen- 
tation, and  the  absorption  of  toxic  materials  from  bacterial  growth. 

In  cases  in  which  bile  appears  in  the  urine,  the  cause  of  the  dilatation 
probably  does  not  depend  upon  gastric  dilatation  alone,  but  upon  some 
obstruction  in  the  duodenum,  which  dams  back  the  food  in  the  pyloric  orifice 
and  so  forces  the  stomach  to  undergo  distention. 

The  physical  signs  of  gastric  dilatation  are  as  follows:  On  inspection  in 
some  of  these  cases,  it  may  be  possible  to  outline  the  stomach  if  it  is  dis- 
tended with  food  and  gas.  This  determination  of  its  area  and  limitation  is, 
however,  much  better  accomplished  by  percussion  after  the  stomach  has  been 
emptied  by  the  use  of  the  stomach  tube  and  then  has  been  distended  by  gas. 
This  distention  may  be  produced  either  by  giving  the  halves  of  a  Seidlitz 
powder  separately  (or  by  the  use  of  30  grains  of  tartaric  acid  in  one-half  glass 
of  water  and  2  drachms  of  sodium  bicarbonate  in  another  half -glass  of  water), 
or  by  introducing  a  stomach  tube,  attaching  a  Davidson  syringe  to  it  and 
then  pumping  air  into  the  stomach  until  it  is  distended.  This  latter  plan  is 
probably  the  safer  of  the  two  if  ulcer  is  supposed  to  be  present,  but  if  the 
patient  is  not  accustomed  to  the  use  of  the  tube  its  presence  causes  so  much 
retching  and  gastric  unrest  that  it  is  usually  impossible  to  make  a  satisfactory 
examination  of  the  true  area  of  gastric  tympany. 

The  tympanitic  note  produced  by  the  percussion  of  a  stomach  so  dis- 
tended very  clearly  outlines  it  in  many  cases.  If  there  is  doubt  as  to  the 
presence  of  gas  in  the  colon,  which  may  cause  tympany,  the  large  intestine 
should  be  filled  with  fluid,  by  the  injection  of  a  large  clyster,  when  the 
areas  of  gastric  tympany  and  intestinal  flatness  on  percussion  can  be  readily 
defined.  In  other  cases  the  stomach  may  be  filled  with  fluid,  and,  if  need  be, 
the  bowel  filled  with  air  to  develop  the  same  outlines. 

It  has  been  held  by  some  clinicians  that  the  use  of  carbonic  acid  for  the 
purpose  of  dilating  the  stomach  for  diagnostic  purposes  is  dangerous,  but 
when  we  consider  the  hundreds  of  instances  in  which  it  has  been  used  in 
every  part  of  the  world  without  evil  effect,  we  must  conclude  that  it  rarely 
does  harm.  Behrend  has  recently  reported  3  cases,  however,  in  which 
death  followed  its  use,  the  patient  in  one  instance  suffering  from  a  profuse 
hemorrhage,  another  patient  bringing  up  froth  and  blood,  and  the  third, 
which  did  not  die  for  five  days,  suffering  from  great  distress  and  prostra- 
tion. Wharton  and  Musser  have  reported  a  perforation  of  the  stomach  after 
drinking  a  glass  of  carbonated  water.  All  of  these  cases  were  complicated 
by  gastric  ulcer. 

Auscultation  of  the  epigastrium  may  reveal  splashing,  or  succussion,  in 
many  cases  of  gastric  dilatation,  but  this  sign  should  never  be  regarded  of 


GASTRIC  DILATATION  575 

very  great  import,  for  not  rarely  the  same  sound  is  produced  by  fluid  in  the 
bowel. 

Some  years  ago  Einhorn  invented  the  electric  light  method  of  diagnosticat- 
ing dilatation  (gastrodiaphany).  This  consists  in  filling  the  stomach  with 
water  and  then  passing  a  small  electric  light  into  the  stomach,  the  patient 
and  physician  being  in  a  dark  room.  If  the  abdominal  wall  be  not  too  thick, 
the  area  of  light  can  be  readily  outlined  and  the  size  of  the  stomach  deter- 
mined. The  efficiency  of  this  method  of  determining  the  size  of  the  stomach 
can  be  much  increased  by  the  use  of  fluorescent  media.  The  best  of  these  is 
developed  by  the  use  of  two  solutions.  One  solution  consists  of  bicarbonate 
of  sodium,  40  grains,  dissolved  in  1  pint  of  distilled  water.  The  second  is 
composed  of  the  same  ingredients  plus  2  drachms  of  glycerin  and  ^  of  a 
grain  of  fluorescin  to  the  pint.  Before  the  test  is  used  the  patient  should 
take  2  grains  of  quinine  three  times  in  a  day.  He  then  swallows  ^  pint  of 
solution  No.  1  and  ^  pint  of  solution  No.  2,  when,  on  the  introduction  of 
the  gastrodiaphane,  the  illumination  of  the  stomach  becomes  very  marked. 

Another  means  of  diagnosis  is  the  use  of  the  a:-rays  after  the  patient  has 
received  a  large  dose  of  bismuth  subnitrate  (2  to  4  ounces).  By  this  means 
the  area  of  the  stomach  can  be  determined.  The  bismuth  must  always 
be  washed  out  after  the  test  to  prevent  poisoning. 

Another  aid  is  Turck's  gastric  sound,  the  end  of  which  can  be  felt  through 
the  abdominal  wall,  if  it  is  thin,  as  it  is  moved  about  in  the  stomach. 

The  use  of  drugs,  which  are  dissolved  only  in  the  intestine,  to  test  the 
motor  power  of  the  stomach  is  of  some  diagnostic  value.  Salol,  for  example, 
is  given  in  the  dose  of  15  or  20  grains,  and  the  urine  tested  after  five  hours 
for  salicyluric  acid  by  means  of  the  perchloride  of  iron  test,  which  consists 
in  adding  tincture  of  iron  chloride  to  the  urine,  when,  if  this  acid  is  present, 
a  purple  color  is  obtained.  When  dilatation  is  present  there  may  be  no 
response  for  twenty-four  hours. 

Finally,  as  a  means  of  determining  that  the  digestive  power  of  the  stomach 
is  greatly  impaired,  a  test  meal  should  be  used  after  the  stomach  has  been 
cleaned  by  lavage.  If  dilatation  is  present,  the  digestive  process  will  always 
be  very  slow  and  imperfect. 

Cases  of  gastric  dilatation  sometimes  develop  a  state  called  gastric  tetany, 
in  which  tetanic  spasms  develop  in  the  extremities.  This  is  preceded  by  a 
sensation  of  formication,  or  numbness,  associated  with  drowsiness.  It  has 
ensued,  as  a  rule,  upon  the  employment  of  lavage.  Following  the  sensory 
symptoms  the  patient  is  seized  with  violent  vomiting,  and  after  or  during 
this  attack  of  emesis  the  muscles  of  the  thumb  and  fingers  contract,  so  that 
the  thumb  is  drawn  into  the  palm  of  the  hand  and  the  fingers  are  flexed. 
The  wrist  is  also  strongly  flexed,  but  it  may  be  extended.  The  forearm  is 
flexed  on  the  arm,  and  the  biceps  is  hard  and  tense.  These  positions  may 
not  be  maintained,  but  be  changed  into  extension.  Both  sides  are  involved, 
but  one  side  usually  suffers  more  than  the  other.  When  the  legs  are  affected 
the  toes  are  flexed  and  the  knees  bent.  The  facial  muscles  may  be  in  spasm 
and  the  patient  may  have  explosive  speech,  as  if  in  a  shouting  delirium.  If 
the  affected  arm  be  pressed  upon  over  the  course  of  its  vessels  or  nerves,  the 
attacks  may  be  reproduced  (Trousseau's  sign);  if  the  point  of  exit  of  the 


576  DISEASES  OF  THE  STOMACH 

facial  nerve  be  tapped,  facial  spasm  develops  (Chvostek's  sign) ;  if  electricity 
is  used  it  is  found  that  the  muscles  are  excessively  irritable  (Erb's  sign). 
The  cramp-like  contractions  are  painful.  In  severe  cases  death  may  occur 
from  exhaustion.  Out  of  101  cases  reported  by  European  clinicians,  no  less 
than  75  died. 

Although  the  employment  of  the  stomach  tube  has  induced  attacks  of 
(^astric  tetany  in  some  cases,  attacks  not  due  to  this  cause  are  to  be  pre- 
vented by  frequent  and  thorough  lavage,  and  are  to  be  combated,  when 
present,  by  nerve  sedatives  such  as  morphine  or  hyoscine  hypodermically. 
Their  occurrence  in  a  mild  form  urges  upon  the  physician  the  need  of 
operation  for  the  gastric  state. 

Gastric  tetany  occurs  in  cases  of  dilatation  more  frequently  than  in  cases 
of  ulcer. 

Diagnosis. — As  a  rule,  the  diagnosis  of  gastric  dilatation,  in  its  well- 
developed  stage,  is  not  difficult.  Care  must  always  be  exercised,  however, 
that  dilatation  and  gastroptosis  are  not  confused,  for  in  both  affections  the 
lower  border  of  the  stomach  may  be  found  far  below  the  normal  level,  par- 
ticularly if  it  is  distended  with  liquid  or  gas.  The  use  of  any  of  the  methods 
of  percussion  and  palpation,  or  the  other  means  of  diagnosis  just  described, 
will  speedily  separate  the  one  state  from  the  other,  and  the  relatively  limited 
capacity  of  the  stomach  in  ptosis  and  its  large  capacity  in  dilatation  will 
be  another  factor  in  deciding  upon  the  real  state  which  is  present. 

Treatment. — The  treatment  of  gastric  dilatation  is  not  promising  unless 
the  patient  is  seen  and  his  condition  recognized  in  the  early  stages  of  the 
disease.  At  this  time,  and  later  on  as  well,  his  diet  should  be  most  carefully 
regulated.  He  should  be  instructed  to  avoid  all  fatty  articles  of  food  which 
may  give  rise  to  lactic  and  butyric  acid  fermentation,  and  should  also  avoid 
the  use  of  sweet  materials,  which  may  also  undergo  fermentative  changes. 
The  food  which  he  takes  should  be  thoroughly  masticated  and  insalivated, 
it  being  remembered  that  the  saliva  is  an  important  digestive  juice,  and  that 
much  may  be  done  in  aiding  the  digestion  by  thoroughly  moistening  the 
food  with  this  secretion.  The  patient  must  also  be  warned  not  to  eat  a  large 
amount  of  food  at  any  one  time,  but  rather  to  subsist  on  four  or  five  small 
meals  a  day.  He  should  also  be  instructed  not  to  take  large  quantities  of 
liquids  with  his  meals. 

As  to  the  articles  of  diet,  he  may  have  beef,  mutton,  chicken,  or  other 
simple  varieties  of  meats,  broiled  or  roasted,  but  not  fried.  Potatoes 
should  only  be  taken  when  baked,  and  then  in  moderation.  Zweiback, 
or  soda  biscuits  which  have  been  once  more  cooked  by  pouring  scald- 
ing water  over  them,  may  be  taken  in  moderation.  The  digestion  of  the 
starches  should  always  be  aided  by  the  simultaneous  ingestion  of  a  capsule 
containing  2  grains  of  taka-diastase  and  2  grains  of  pancreatin.  If  the 
diet  is  largely  a  meat  diet,  digestion  should  be  aided  by  the  use  of 
hydrochloric  acid  and  pepsin,  5  to  20  drops  of  the  dilute  acid  and  2  tea- 
spoonfuls  of  a  good  essence  of  pepsin  being  used.  Often  it  is  wise  to  add  to 
this  mixture  10  drops  of  the  tincture  of  nux  vomica,  or  -^Ig  of  a  grain  of 
strychnine,  for  its  effect  as  a  bitter  tonic  and  for  the  purpose  of  improving, 
if  possible,  the  activity  of  the  stomach. 


GASTRIC  DILATATION  577 

In  no  case  should  the  patient  be  allowed  to  accumulate  fluid  and  food 
in  the  stomach  for  more  than  twenty-four  hours.  In  other  words,  we  should 
not  wait  until  nature  relieves  the  stomach  by  an  attack  of  vomiting. 

As  in  chronic  gastric  catarrh,  lavage  should  be  performed  once  in  every 
twenty-four  hours,  preferably  at  night  before  going  to  bed,  and  in  all  cases 
it  should  be  remembered  that  it  is  not  only  futile  but  harmful  to  introduce 
food  into  a  stomach  which  is  already  partly  filled  with  fermenting  materials, 
and  which  is  therefore  incapable  of  dealing  with  new  food,  which  if  taken 
simply  adds  to  the  decomposing  mass  already  present. 

In  many  of  these  cases  it  is  advisable,  after  emptying  the  stomach  of  its 
contents,  to  wash  it  out  with  one  of  the  solutions  named  in  the  article  on 
the  Treatment  of  Chronic  Gastric  Catarrh. 

Emptying  the  stomach  by  means  of  the  stomach  tube  and  forbidding  the 
use  of  excessive  quantities  of  food  are  not  only  advantageous  in  that  they 
permit  digestion,  poor  as  it  may  be,  to  proceed,  but  also  do  good  in  that  they 
prevent  the  stomach  from  being  overloaded  and  distended,  and  so  further 
dilated,  by  its  contents.  It  seems  hardly  necessary  to  add  that  beer,  sweet 
wines,  and  champagnes  should  be  absolutely  forbidden  for  such  patients. 

The  medicinal  treatment  of  gastrectasy  consists  in  the  use  of  nux  vomica 
or  strychnine  in  full  doses  combined  with  physostigma,  the  object  being  to 
improve  the  tone  of  the  muscular  fibres  of  the  stomach.  A  pill  composed 
of  I  grain  of  extract  of  nux  vomica  and  I  grain  of  extract  of  physostigma 
may  be  given  three  or  four  times  a  day  with  advantage.  Gastrointestinal  anti- 
septics are  usually  not  particularly  useful.  From  2  to  5  minims  of  creosote  or 
guaiacol  may  be  given  in  capsule  one  or  two  hours  after  eating,  with  the  hope 
that  they  will  stop  fermentation.  In  other  instances  guaiacol  carbonate  may 
be  given  in  the  dose  of  2  to  5  grains  in  capsule.  In  still  other  instances 
naphthol  may  be  given  in  the  dose  of  2  to  5  grains  in  capsule  three  times 
a  day,  or  benzonaphthol  may  be  used  in  the  dose  of  10  grains,  in  the  same 
manner. 

Many  physicians  of  experience  resort  to  the  use  of  faradic  electricity  in 
these  cases,  introducing  a  stomach  tube  containing  the  positive  electrode 
and  applying  the  negative  electrode  to  some  point  on  the  surface  of  the  body. 

In  cases  in  which  the  dilatation  is  so  severe  and  the  symptoms  so  distress- 
ing that  none  of  the  measures  so  far  suggested  give  adequate  relief,  the 
question  of  operative  interference  must  be  considered.  Under  these  circum- 
stances, the  question  as  to  the  cause  of  the  dilatation  becomes  an  important 
factor.  If  it  is  dependent  upon  pyloric  stenosis,  a  gastroenterostomy  or 
pylorectomy  is  indicated.  But  if,  on  the  other  hand,  it  does  not  depend  upon 
this  cause,  but  upon  inherent  atony  and  failure  of  the  gastric  walls,  pylorec- 
tomy is,  of  course,  of  little  value,  and  a  gastroenterostomy  is  indicated. 
Before  proceeding  to  operation,  however,  it  must  be  remembered  that  there 
is  some  difference  between  an  operative  recovery  and  benefit  to  the  patient. 
Rarely  in  these  cases  the  patient  survives  the  operation  and  makes  a  sur- 
gical recovery,  but  abdominal  discomfort  persists,  either  because  of  the 
presence  of  adhesions,  irritation  of  nerve  fibres,  or  other  causes  which  it  is 
difficult  to  determine,  and  which  may  be  dependent  upon  the  altered  course 
of  food  from  the  stomach  to  the  bowel. 
37 


578  DISEASES  OF  THE  STOMACH 

Acute  Gastrectasis. — Under  the  names  acute  gastric  dilatation,  gastro- 
intestinal paralysis,  atonic  gastrectasis,  toxic  gastrectasis,  and  paralytic 
dilatation  of  the  stomach,  there  occurs  an  acute,  often  rapidly  fatal,  dila- 
tation of  the  stomach  alone  or  of  the  stomach  and  intestines. 

Etiology. — Some  cases  are  apparently  causeless,  and  even  at  autopsy  no 
cause  may  be  demonstrable.  Others  occur  in  the  course  of  acute  infectious 
processes,  some  of  which  are  systemic,  such  as  scarlet  fever  and  typhoid 
fever;  in  others  the  lesion  is  some  distance  from  the  affected  viscus,  as  in 
pneumonia  and  meningitis,  while  still  others  depend  for  their  development 
upon  infectious  processes  in  the  neighborhood  of  the  stomach  or  intestine, 
conspicuous  among  which  may  be  mentioned  peritonitis.  The  condition 
occasionally  follows  surgical  anaesthesia,  and  it  has  been  suggested  that 
swallowing  of  mucus  saturated  with  the  ansesthetic  may  be  the  cause  in  some 
cases.  It  has  been  attributed  to  acute  pyloric  obstruction,  as  by  foreign  bodies 
or  spasm,  but  that  this  is  not  always  the  cause  is  shown  by  the  reported 
instances  in  which  dilatation  extended  through  the  pylorus  and  first  and 
second  parts  of  the  duodenum  or  even  into  the  ileum.  It  has  been  thought 
to  depend  upon  obstruction  of  the  duodenum  by  the  superior  mesenteric 
vessels.  It  sometimes  follows  operation  involving  the  peritoneum,  and  may 
commence  after  labor.  Reynier  strongly  urges  the  influence  of  the  nervous 
system  in  the  production  of  acute  gastrointestinal  paralyses. 

Morbid  Anatomy. — At  autopsy  the  stomach  is  large,  thin,  and  flaccid;  it 
may  extend  almost  to  the  pubes.  It  contains  gas  and  fluid;  the  latter  may 
be  thick  and  viscid,  but  it  is  usually  thin,  watery,  greenish  or  occasionally 
brownish  in  color,  and  frequently  contains  flocculi.  The  gastric  mucosa 
may  weep  blood  and  the  vessels  be  widely  distended. 

Symptoms. — These  usually  come  on  rapidly.  In  operative  cases  they  may 
be  delayed  twenty-four  to  forty-eight  hours.  There  is  marked  abdominal 
distention  amounting  to  actual  hallooning;  the  dilated  organ  occupies  the 
middle  and  upper  left  areas  of  the  abdomen,  and  may  be  outlined  through 
the  abdominal  v/all.  Peristaltic  waves  are  rarely  recognizable.  Vomiting 
is  nearly  always  present.  In  the  few  reported  cases  in  which  vomiting  has 
been  absent,  it  has  been  suggested  that  the  associated  relaxation  in  the 
abdominal  wall  has  rendered  emesis  impossible.  The  vomited  fluid  is  thin, 
watery,  greenish  or  brownish.  Profound  degression  or  symptoms  border- 
ing on  colla'pse  quickly  appear.  The  jpidse  is  small,  rapid,  and  weak;  the 
respirations  shallow  and  frequent;  the  temperature,  in  the  absence  of  com- 
plications, is  usually  low  and  may  be  subnormal.  Thirst  is  intense,  and, 
on  account  of  suppressed  absorption  and  prompt  vomiting,  is  unrelieved  by 
drinks.     The  urine  is  scanty  or  even  suppressed. 

Diagnosis. — The  acuteness  of  the  symptoms  and  rapidly  progressing 
collapse  differentiate  the  condition  from  chronic  dilatation.  The  vomiting 
is  more  incessant  and  the  pain  less  than  in  volvulus  of  the  stomach,  w^hich 
in  some  respects  it  closely  resembles.  The  gastrorrhoea  that  accompanies  it 
and  the  character  of  the  vomit  is  unlike  acute  indigestion,  and,  ordinarily 
there  is  no  expulsion  of  fragments  of  the  mucosa  as  in  true  toxic  gastritis 
The  relaxed  abdominal  wall  is  quite  unlike  the  rigid  wall  of  perito- 
nitis. 


GASTRIC  ULCER  579 

Prognosis. — The  mortality  is  high;  in  Herff's  series  of  34  cases,  29  died. 
In  the  so-called  reflex  group — those  unassociated  with  any  intra-abdominal 
lesion — prompt  treatment  promises  some  relief. 

Treatment. — Its  prevention  after  operation  may  be  accomplished  by 
lavage  immediately  at  the  end  of  anaesthesia,  and  if  vomiting  appear  and 
persist,  lavage  should  be  repeated.  As  it  is  probable  that  the  condition  is 
of  toxic  origin,  free  lavage  should  repeatedly  be  practised,  and  the  stomach 
kept  empty  by  the  frec^uent  use  of  the  stomach  tube.  Water  and  food  had 
best  be  given  by  enema.  Strychnine  and  atropine  have  been  suggested. 
As  early  as  possible  saline  purgatives  should  be  administered  in  small,  but 
often  repeated,  doses.  As  relapses  are  possible  as  late  as  the  third  day, 
feeding,  and  even  the  administration  of  fluids,  must  be  begun  most  cau- 
tiously in  cases  fortunate  enough  to  survive. 


GASTRIC  ULCER. 

Definition. — Ulcer  of  the  stomach,  often  called  peptic  ulcer,  or  ulcus 
ventriculi,  is  due  to  necrosis  of  a  part  of  the  mucous  membrane  of  this  organ, 
so  that  an  exposure  of  the  submucous  tissue  is  present. 

Etiology. — Almost  ever  since  the  processes  of  gastric  digestion  have  been 
known,  animated  discussions  have  arisen  as  to  why  the  stomach  is  not 
digested  by  its  own  juices  and  a  large  number  of  explanations  have  been 
ofi^ered,  many  of  which  have  been  anything  but  satisfactory.  At  present 
the  conditions  which  result  in  gastric  ulcer  are  known  to  be  closely  con- 
nected with  the  inability  of  the  gastric  mucosa  to  resist  the  action  of  the  gas- 
tric juice.  If,  by  any  cause,  the  vital  resistance  of  the  mucous  membrane 
is  impaired,  at  the  point  of  greatest  impairment  an  ulcer  may  be  developed. 
In  very  rare  instances  an  injury  to  the  surface  of  the  abdomen  may  extend, 
or  be  transmitted,  deeply  enough  to  cause  a  lesion  in  the  gastric  wall;  but  it 
is  more  common  for  injuries  to  occur  by  internal  agents,  as  by  the  use  of 
certain  articles  of  food  which  may  interfere  with  the  circulation  in  the  wall 
of  the  stomach,  as,  for  example,  boiled  tea,  taken  very  hot,  which  contains 
an  excess  of  tannic  acid.  So,  too,  an  embolus  or  thrombus  in  a  branch  of 
a  gastric  artery  may  deprive  an  area  of  its  blood  supply,  and  subsequent 
digestion  remove  the  dead  tissue  and  so  form  an  ulcer.  Another  predis- 
posing cause  of  ulcer  is  the  secretion  of  superacid  juice  or  of  an  excess  of 
ordinary  juice,  and  finally,  in  some  cases,  a  local  necrosis  of  the  tissues  is 
produced  by  the  entrance  of  infecting  micro-organisms,  which,  however, 
cannot  enter  the  mucosa  if  normal  vital  resistance  is  maintained. 

Frequency. — The  frequency  of  gastric  ulcer  in  some  parts  of  the  world 
is  far  greater  than  in  others.  Even  between  England  and  the  United  States 
the  difference  is  extraordinary.  Out  of  59,762  medical  cases  in  the  London 
hospitals,  there  were  1649  cases  of  gastric  ulcer;  while  out  of  75,612  medical 
cases  in  hospitals  in  difl^erent  cities  in  the  United  States,  there  were  only  446 
cases.  According  to  these  figures  the  morbidity  of  gastric  ulcer  is  more  than 
four  times  as  great  in  England  as  it  is  in  the  United  States.  Since  these 
figures  were  compiled  Howard  has  confirmed  them  by  others. 


580  DISEASES  OF  THE  STOMACH 

In  regard  to  the  relationship  of  age  and  ulcer  statistics  vary  sHghtly,  but 
those  of  Welch  are  still  to  be  considered  the  most  competent.  He  found  that 
the  largest  number  of  cases  of  ulcer  occurred  between  twenty  and  thirty 
years  of  age,  and  Lebert  also  found  that  seven-tenths  of  252  cases  were 
between  twenty  and  forty  years  of  age.  A  case  of  ulcer  in  an  infant  only 
thirty  hours  old  has,  however,  been  recorded  by  Goodhart.  Cutler,  in  an 
exhaustive  search  in  literature,  found  only  24  cases  under  ten  years  of 
ao-e  with  autopsy  and  2  without  autopsy,  and  has  added  3  more  which  ^ 
occurred  in  the  Massachusetts  General  Hospital;  29  in  all. 

Women  suffer  from  ulcer  far  more  frequently  than  men.  This  is  shown 
by  all  statistics  and  is  illustrated  by  the  following  figures :  Of  1548  cases 
of  gastric  ulcer  collected  from  the  official  reports  of  hospitals  in  the  United 
States  and  England,  1273  occurred  in  women  and  275  in  men.  Of  1699 
cases  examined  postmortem  and  studied  by  Welch,  1020  were  in  women 
and  679  in  men.  Cantlie  states  that  out  of  20,586  cases  in  Montreal  there 
were  85  cases  of  gastric  ulcer,  and  of  these  82  were  women.  The  average  age 
was  twenty-seven  and  a  half  years. 

Other  etiological  factors  of  interest  are  occupation  and  associated  disease. 
Thus,  seamstresses  and  servant  girls  are  singularly  prone  to  ulcer,  as  are  also 
tailors  and  shoemakers.  Such  persons  are  usually  chlorotic  or  anaemic.  So, 
too,  ulcer  is  sometimes  a  complication  of  tuberculosis,  and  it  may  be  in 
itself  tuberculous. 

Gastric  ulcer  may  be  divided  into  four  classes:  In  the  first  the  lesion  is 
very  mild,  the  mucous  membrane  being  eroded  in  such  a  manner  that  its 
superficial  epithelium  is  destroyed.  All  authors  do  not  agree,  however,  that 
these  erosions  are  a  form  of  peptic  ulcer.  The  second  type  is  characterized 
by  an  ulcerative  process  which  penetrates  more  deeply,  so  that  the  submucous 
tissues  are  affected.  The  third  invades  the  submucous,  muscular,  and  even 
the  peritoneal  coat,  and  may  cause  perforation.  The  fourth  type  is  that  in 
which  as  a  result  of  cicatrization  and  contraction  scars  and  deformities 
develop,  which  produce  serious  consequences. 

Pathology  and  Morbid  Anatomy. — Gastric  ulcer  is  usually  single,  but  cases 
are  not  very  rare  in  which  the  ulcers  are  numerous.  When  acute  it  forms 
rapidly  and  presents  a  peculiar  punched-out  appearance.  In  the  usual 
chr(3nic  form  the  edges  are  more  shelving,  indurated,  and  not  so  sharply 
defined.  The  size  of  the  ulcer  varies  from  a  small  spot  scarcely  larger  than 
a  pinhead  to  an  enormous  excavation  covering  nearly  two-thirds  of  the 
gastric  surface.     These  large  ulcers  are,  however,  very  rarely  met  with. 

The  depth  to  which  the  ulcerative  process  extends  is  also  variable.  The 
mucous  membrane  nearly  always  suffers  most,  but  the  tissues  beneath  it  are 
affected  as  well,  and  the  destructive  process  may,  as  just  stated,  extend  as 
far  as  the  peritoneal  coat.  Undermined  ulcers  are  extremely  rare.  Around 
the  edge  of  the  ulcer  there  is  usually  marked  hypersemia,  and  the  surround- 
ing tissues,  especially  in  chronic  ulcers,  are  often  infiltrated  by  formative 
cells  or  by  the  development  of  connective  tissue.  Usually  the  rest  of  the 
stomach  exhibits  more  or  less  marked  chronic  gastritis. 

Ulcer  of  the  stomach  is  usually  found  on  the  posterior  wall  of  the  viscus 
near  the  pylorus  and  on  the  lesser  curvature  (75  per  cent.),  probably  because 


GASTRIC  ULCER  581 

this  is  the  part  of  the  stomach  which  carries  out  the  grinding  process  and 
urges  the  food  into  the  duodenum,  and  therefore  is  exposed  to  injury  and 
abrasion.  Armstrong  has,  however,  analyzed  240  cases  of  gastric  ulcer  and 
found  the  anterior  wall  affected  in  125  cases,  the  posterior  wall  in  only  32. 
If  the  healing  process  is  not  rapid  enough  to  arrest  the  ulcerative  process, 
the  wall  of  the  stomach  may  be  perforated  and  so  produce  severe  abdominal 
symptoms.  More  commonly,  however,  as  the  inflammatory  process  ap- 
proaches the  surface  of  the  stomach  it  causes  this  viscus  to  become  glued 
to  a  neighboring  organ,  and  so  it  happens  that  the  floor  of  the  ulcer  may  be 
formed  by  an  adjacent  viscus.  In  this  way  neighboring  organs  may  be 
involved  in  the  inflammatory  and  septic  process,  and  not  rarely  subphrenic 
abscess  is  due  to  this  cause.  Sometimes  a  perforation  takes  place  into  the 
colon  or  duodenum,  and  cases  have  been  recorded  in  which  the  pericardium 
and  pleura  have  been  involved  in  this  manner.  The  liver  is  also  sometimes 
infected,  Fenwick,  in  an  analysis  of  127  cases,  found  the  stomach  adherent 
to  the  pancreas  in  49,  to  the  liver  in  33,  and  to  the  liver  and  pancreas  in  10. 

Fig.  79 


Diagram  showing  the  situation  of  ulcers  of  the  stomach  on  the  lesser  curvature  and  near 
the  pylorus.     (Modified  from  English.) 

Ulcers  on  the  anterior  surface  of  the  stomach  are  less  common,  but 
more  prone  to  perforation  into  the  peritoneum  than  those  situated  poste- 
riorly. It  is  held  that  the  anterior  wall  is  more  movable  than  the  posterior, 
and  hence  time  for  adhesion  to  apposed  tissue  is  less. 

In  many  cases,  a  tendency  to  healing  asserts  itself  and  gradually,  the 
exposed  tissues  are  healed  by  the  formation  of  a  cicatrix  which  may  cause 
considerable  puckering  as  it  develops. 

If  the  ulcer  has  been  near  the  pylorus  this  may  cause  pyloric  stenosis,  or 
if  it  be  near  the  middle  of  the  stomach  and  the  ulcer  has  been  extensive  an 
hour-glass  contraction  may  result.     (See  Hour-glass  Stomach.) 

Symptoms. — Ulcer  of  the  stomach,  at  least  in  its  milder  forms,  may  exist 
for  years  without  its  presence  being  suspected,  the  patient  suffering  from  a 
train  of  moderate  gastric  symptoms,  generally  described  as  dyspeptic.  In 
most  cases,  however,  it  makes  its  presence  known  by  symptoms  which  sooner 
or  later  send  the  patient  to  her  physician  for  relief.     The  symptoms  now 


582  DISEASES  OF  THE  STOMACH 

complained  of  are  discomfort  and  fain  after  eating,  with  a  constant  gnawing 
between  meals  when  the  stomach  is  empty.  Not  infrequently  this  gastric  dis- 
tress is  relieved  by  taking  some  food,  and  then  increases  as  an  excess  of  gas- 
tric juice  is  poured  out  to  digest  the  food.  The  pain,  when  characteristic, 
is  peculiar  in  its  distribution,  for  it  radiates  from  the  epigastrium  back  to 
the  shoulder-blade,  or  to  a  spot  between  the  shoulder  blade  and  the  spine. 
Head  has  also  shown  that  in  gastric  ulcer  there  is  an  area  of  cutaneous  hyper- 
sesthesia  in  a  small  triangular  spot  in  the  left  epigastrium.  This  is  demon- 
strable by  a  light  touch,  and  not  on  deep  palpation.  At  times  the  pain  is 
exceedingly  severe,  and  it  may  require  active  medication  because  of  its  inten- 
sity. Oftentimes  the  patient  attempts  to  find  relief  by  lying  on  the  stomach 
or  placing  a  pillow  against  it,  but  as  a  rule  the  epigastrium  is  so  tender  that 
any  pressure  on  the  part  of  the  physician  makes  the  patient  wince.  Careful 
palpation  may,  however,  reveal  an  area  of  thickening  or  induration,  if  the 
ulcer  is  a  chronic  one.  Associated  with  these  symptoms  there  is  often 
vomiting  of  very  acid  fluid,  and  an  examination  of  the  gastric  contents  will 
show  an  excess  of  hydrochloric  acid  both  as  to  percentage  and  actual  quan- 
tity.    Constipation  is  usually  marked,  and  the  urinary  flow  is  scanty. 

It  is  important  to  remember  that  ulcer  of  the  stomach  does  not  by  any 
means  always  cause  the  same  train  of.  symptoms.  Attention  has  already 
been  called  to  the  fact  that  the  symptoms  may  be  latent.  In  other  cases 
there  may  develop,  with  great  suddenness,  a  profuse  hcematemesis  or  symp- 
toms of  collapse  from  perforation,  and  one  of  these  accidents  may  be  the 
first  symptom  of  any  importance.  In  other  instances  there  is  a  general  failure 
of  health,  marked  emaciation,  and  a  development  of  'profound  anoEmia.  In 
still  others  violent  neuralgic  pains  (gastralgia)  are  the  chief  manifestations. 
In  some  instances  the  disease  lasts  but  a  few  weeks ;  in  others  it  is  prolonged 
for  years. 

The  symptoms  so  far  described  are  chiefly  those  of  acute  or  subacute 
ulcer.  Chronic  idcer,  on  the  other  hand,  may  produce  none  of  these  symp- 
toms when  the  patient  presents  herself  for  treatment.  Beyond  a  history  of 
gastric  distress,  which  may  have  existed  for  many  years,  there  may  be  no 
pain  on  pressure  and  no  soreness,  in  the  sense  of  tenderness.  Indeed,  the 
symptoms  may  be  those  of  gastric  dilatation,  or  of  pyloric  stenosis.  The 
patient  is  emaciated  by  reason  of  voluntary  starvation,  to  decrease  discom- 
fort, and  by  the  loss  of  food  by  vomiting.  So,  too,  a  cicatrix  near  the 
middle  of  the  stomach  may  produce  an  hour-glass  stomach.  This  may 
become  evident  on  distending  the  stomach  with  gas  or  fluid,  but  it  is  to  be 
recalled  that  there  is  danger  that  rupture  may  ensue  from  this  practice, 
(See  Pyloric  Stenosis  and  Dilatation  of  the  Stomach.) 

In  no  other  disease,  save  pernicious  anaemia,  is  there  such  a  notable 
diminution  of  red  blood  cells  as  takes  place  in  many  cases  of  chronic  gastric 
ulcer.  Tliis  is  due  to  the  more  or  less  constant  loss  of  blood  which  escapes 
by  the  bowel,  the  loss  of  which  is  usually  not  recognized.  When  hemor- 
rhage does  not  occur  great  anaemia  is  rare,  although  the  patient  may  appear 
pallid. 

When  hemorrhage  from  the  stomach  takes  place  the  blood  may  be 
vomited  or  be  passed  by  the  bowel.    The  hemorrhage  may  follow  many 


GASTRIC  ULCER  533 

weeks  of  suffering  or  it  may  be  the  first  sign  that  the  gastric  mucous  mem- 
brane is  diseased.  The  quantity  of  blood  lost  may  be  very  small  or  so 
large  as  to  almost  exsanguinate  the  patient,  the  variation  depending  upon 
the  size  of  the  bloodvessel  which  is  eroded.  If  a  large  vessel  is  perforated 
by  a  small  ulcer  it  is  not  difficult  to  understand  why  it  is  that  hemorrhage 
may  be  the  first  symptom.  In  other  words,  the  hemorrhage  may  be  the  first 
symptom  of  ulcer.  On  the  other  hand,  not  infrequently  gastric  hemor- 
rhage, particularly  if  it  be  from  a  chronic  ulcer,  may  be  so  scanty  as  never 
to  cause  bloody  vomiting,  the  small  amount  of  blood  escaping  with  the 
food  into  the  bowel.  Moynihan  believes  that  all  ulcers  bleed  at  some  time 
in  their  existence.     (See  Diagnosis.) 

In  studying  the  question  of  perforation  of  gastric  ulcer  it  is  well  to 
recall  that  this  accident  may  or  may  not  be  preceded  by  symptoms  which 
will  serve  as  a  warning  to  the  physician  if  not  to  the  patient.  There  is,  in 
some  cases,  a  progressive  increase  in  discomfort  and  pain  after  eating,  a 
greater  degree  of  tenderness  or  pain  over  the  epigastrium,  and  more  fre- 
quent vomiting.  When  such  signs  are  present  the  patient  must  be  placed  at 
absolute  rest,  and  if  the  symptoms  do  not  speedily  become  modified  opera- 
tion must  be  considered.  On  the  other  hand,  the  literature  on  this  subject 
contains  cases  in  which  the  history  of  gastric  disorder  was  entirely  absent, 
and  the  patient  was  suddenly  seized  by  symptoms  of  perforation. 

When  perforation  does  develop,  it  is  usually  in  the  anterior  gastric  wall, 
and  from  what  has  been  said  of  the  various  ways  in  which  perforation  of  the 
stomach  occurs,  it  must  be  evident  that  the  symptoms  may  vary  over  a  wide 
range  of  severity.  When  no  inflammatory  adhesions  have  been  formed 
and  the  gastric  contents  escape  suddenly  into  the  general  peritoneal  cavity, 
the  onset  is,  of  course,  startling  in  its  acuteness  and  the  pain  is  exceedingly 
severe,  but  the  locality  of  the  pain  is  frequently  far  removed  from  the  area 
of  the  accident.  Vomiting  and  collapse  may  soon  develop,  and  general 
peritonitis  begins  if  operative  relief  is  not  promptly  given. 

If  the  perforation  is  more  gradual  the  symptoms  are  less  violent  and  the 
opening  may  at  first  be  so  small  that  only  a  little  of  the  gastric  contents 
escapes  into  the  peritoneal  cavity.  In  those  cases  in  which  adhesions  have 
formed  before  perforation  takes  place  a  subphrenic  abscess  may  result. 
In  such  instances  the  perforation  is  usually  on  the  posterior  wall  of  the 
stomach. 

Sometimes  perforation  of  the  stomach  may  take  place  without  the  sharp 
and  decisive  symptoms  just  described. 

While  the  pulse  usually  is  rapid  it  may  not  be  materially  increased  in 
rate. 

Again,  it  is  important  to  remember  that  after  perforation  of  the  stomach 
there  may  be  a  "period  of  repose,"  or  "fallacious  calm,"  during  which 
time  the  patient  feels  less  pain  and  distress,  and  the  pulse  approximates 
its  normal  speed. 

At  one  time,  it  will  be  recalled,  a  decrease  in  the  area  of  liver  dulness 
was  supposed  to  be  indicative  of  gastric  or  intestinal  perforation,  but  we 
now  know  that  the  absence  of  this  sign  does  not  negative  perforation.  Thus, 
Pearson  found  a  decrease  in  the  area  of  liver  dulness  in  33  per  cent,  of  140 


584  DISEASES  OF  THE  STOMACH 

cases  of  gastric  ulcer  at  some  period  during  their  stay  in  the  hospital,  yet 
perforation  took  place  in  none  of  them. 

Diagnosis. — Gastric  ulcer  in  some  instances  is  so  manifestly  present  that 
there  is  little  difficulty  in  determining  the  cause  of  the  illness.  Care  must 
be  taken  that  the  pain  of  appendicitis,  gallstone  colic,  renal  colic,  and  intense 
menstrual  colic  is  not  taken  for  that  due  to  perforation.  Moynihan  speaks 
of  3  cases  operated  upon  for  perforation  in  which  menstruation  was  the 
cause  of  the  pain,  and  states  that  of  49  cases  of  perforated  duodenal  ulcer 
appendicitis  was  thought  to  be  the  cause  of  illness  in  18.  In  the  gastralgic 
cases  ulcer  must  be  separated  from  ordinary  gastric  neuralgia  by  the  recol- 
lection of  the  fact  that  true  gastric  neuralgia  is  very  rare,  by  the  additional 
fact  that  the  pain  of  neuralgia  is  not  induced  by  taking  food  and  by  the 
fact  that  in  neuralgia  evidences  of  gastric  indigestion  are  not  constantly 
present,  as  they  are  in  most  cases  of  ulcer.  Severe  pains  in  the  stomach  due 
to  locomotor  ataxia  (gastric  crises)  can  usually  be  excluded  by  the  presence 
of  Argyll-Robertson  pupils,  absence  of  knee-jerks,  and  swaying  when  the 
patient  stands  with  the  eyes  shut. 

The  irritation  produced  by  gallstones  may  produce  symptoms  resembling 
gastric  ulcer,  but  in  these  cases  the  history  of  gallstone  colic  will  be  given 
and  the  taking  of  food  has  no  influence  upon  the  pain.  Then,  too,  the  pain 
in  the  back  due  to  ulcer  is  to  the  left  of  the  middle  line  near  the  twelfth 
dorsal  vertebra,  whereas  that  due  to  gallstone  is  on  the,  right  of  the  median 
line  and  a  little  lower  down.  So,  too,  palpation  of  the  neighborhood  of  the 
gall-bladder  may  reveal  an  enlargement  of  this  viscus,  and  jaundice  points 
to  cholelithiasis  rather  than  to  ulcer. 

Cases  of  chronic  ulcer  of  the  stomach  with  much  cicatricial  tissue  around 
the  ulcer,  or  at  the  seat  of  an  ulcer  which  has  healed,  may  present  symp- 
toms almost  identical  with  those  of  gastric  cancer.  Pain  and  obstruction 
to  the  passage  of  food  through  the  pylorus,  gastric  dilatation  due  to  this 
latter  cause,  and  emaciation  from  all  these  causes  may  combine  to  present 
a  clinical  picture  of  gastric  cancer,  particularly  if  the  physician  finds,  on 
palpation,  that  he  can  feel  a  mass  or  masses  in  the  gastric  wall.  The  com- 
parative youth  of  the  patient  in  cases  of  ulcer,  the  absence  of  cachexia  even 
if  anaemia  is  marked,  and  a  remembrance  that  ulcer  of  the  stomach  is  most 
common  in  the  female  sex  helps  to  make  the  diagnosis  possible.  Again,  in 
ulcer  the  gastric  contents  show  an  excess  of  hydrochloric  acid  after  a  test 
meal,  whereas  in  cancer  this  acid  is  usually  absent  or  less  than  normal. 
(For  the  tests  of  the  stomach  contents  see  article  on  Gastric  Cancer.) 

Finally  it  must  be  recalled  that  duodenal  ulcer  may  cause  symptoms  so 
closely  resembling  gastric  ulcer  that  a  differentiation  may  be  impossible. 
If  hemorrhage  occurs,  and  blood  is  passed  in  the  stools  in  considerable 
quantity,  the  lesion  is  probably  duodenal.     (See  Duodenal  Ulcer.) 

Boas  considers  the  demonstration  of  minute  quantities  of  blood  in  the 
feces  to  be  of  great  value  in  the  diagnosis  of  gastric  ulcer,  and  especially  in 
determining  whether  obscure  cases  of  gastric  disease  are  pure  gastralgia 
or  conditions  in  which  the  symptoms  are  produced  by  ulcerative  lesions  of 
the  gastric  mucosa.  It  has  been  proven  experimentally  that  the  ingestion 
of  so  small  a  quantity  as  3  c.c.  of  blood  gives  a  positive  reaction  for  blood 


GASTRIC  ULCER  .  585 

in  the  feces,  and  this  fact  shows  that  even  minute  hemorrhages  may  give 
rise  to  similar  positive  reactions. 

Before  performing  the  test  all  other  sources  of  hemorrhage,  such  as  the 
swallowing  of  blood  from  wounds  in  the  mouth  or  from  lesions  in  the  re- 
spiratory tract  must  be  guarded  against,  and  the  absence  of  hematuria,  and 
in  women  metrorrhagia  and  menstrual  blood,  must  also  be  assured.  No 
rare  meat,  fish,  or  sausages  are  allowed  for  two  days  before  the  test  is  made. 

Boas  prefers  the  aloin  test  as  recently  recommended  by  Klunge  and 
Schaer  to  the  older  guaiacum  test.  It  is  performed  as  follow^s:  5  to  10 
grams  of  feces,  which,  if  hard,  are  to  be  softened  by  the  addition  of  a 
small  quantity  of  water,  are  mixed  with  20  c.c.  of  ether,  3  to  5  c.c.  of 
glacial  acetic  acid,  and  the  mixture  is  well  shaken  in  a  reagent  glass.  Then 
more  ether  is  added,  and  also  20  or  30  drops  of  an  old  oil  of  turpentine.  If 
to  this  mixture  there  now  be  added  10  or  15  drops  of  a  solution  made  by 
dissolving  in  3  to  5  c.c.  of  70  per  cent,  alcohol  as  much  aloin  as  can  be 
taken  up  on  the  tip  of  a  small  spatula,  a  light-red  color  is  soon  produced 
if  blood  is  present.  This  light-red  gradually  assumes  a  cherry-red  hue  if 
the  mixture  is  allowed  to  stand.  If  no  blood  is  present  the  mixture  remains 
of  a  yellow  color  for  from  one  to  two  hours,  when  it  changes  to  rose  red. 

The  possibility  of  parenchjonatous  gastric  hemorrhage,  and  of  hemor- 
rhage from  varicose  or  atheromatous  bloodvessels  in  the  oesophagus  or 
stomach,  must  of  course  be  taken  into  consideration  before  a  diagnosis  of 
doubtful  cases  is  made. 

In  several  cases  Boas  has  found  blood  present  in  the  feces  shortly  after 
patients  had  experienced  an  attack  of  pain  in  the  epigastrium.  After 
several  days  of  mild  diet  it  was  often  found  that  no  blood  could  be  detected 
in  the  feces. 

Prognosis. — The  prognosis  of  cases  of  gastric  ulcer  must,  of  course,  vary 
greatly  with  the  severity  of  the  lesion,  and  the  time  during  which  it  has 
lasted.  In  those  cases  in  wdiich  superficial  erosions  are  present,  the  patient 
probably  recovers  in  the  great  majority  of  instances.  When  actual  ulcera- 
tion is  present,  the  proposition  is,  of  course,  a  different  one.  The  most 
divergent  views  exist  as  to  the  prognosis  in  this  type  of  case.  Brinton,  in 
his  now  somewhat  ancient  statistics,  states  that  50  per  cent,  recover  under 
medical  treatment.  Tricomi  places  the  percentage  at  25,  as  do  also  De- 
bove  and  Ramond.  Leube  states  that  25  per  cent,  die  as  a  direct  effect  of 
the  disease.  Whatever  may  be  the  percentage  as  to  recovery,  it  cannot  be 
doubted  that  in  many  instances  it  is  once  an  ulcer  always  an  ulcer,  in  the 
sense  that  relapses  take  place  soon  after  the  ulcer  seems  well.  In  a  collection 
of  500  cases  at  the  London  Hospital,  made  by  Bulstrode,  211  had  had  ulcer 
before,  18  per  cent,  died,  and  42  per  cent,  were  not  cured  on  discharge. 

Ulcers  near  the  pylorus  heal  more  slowly  than  those  which  occur  else- 
where. Some  gastric  ulcers  probably  become  cancerous  in  later  life. 
Graham  has  found  a  history  of  ulcer  in  60  per  cent,  of  125  cases  of  cancer 
of  the  stomach — a  fact  of  some  prognostic  importance. 

The  mortalitv  in  cases  which  suffer  from  hemorrhage  is  not  high. 
The  direct  mortality  from  this  cause  is  only  2.1  per  cent.,  according  to 
Russell.     So  far  as  recovery  from  the  ulcer  is  concerned  when  it  is  severe 


586  DISEASES  OF   THE  STOMACH 

enough  to  cause  hcemorrhage  the  outlook  is  not  good — 44.7  per  cent,  con- 
tinued in  ill  health  and  42.6  per  cent,  recovered  (Russell) . 

Treatment. — The  treatment  of  gastric  ulcer  consists  in  restricting  the 
diet,  in  the  administration  of  medicines  qualified  to  improve  the  state  of 
the  gastric  mucous  membrane,  and  in  the  institution  of  rest  for  the  general 
system  as  well  as  for  the  stomach.  Foods  which  are  very  hot  or  very  cold, 
particularly  those  which  are  very  hot,  should  be  carefully  avoided,  and 
hyperacidity  is  to  be  counteracted  by  the  use  of  calcined  magnesia  or  bicar- 
bonate of  soda. 

li  . — Sodii  bicarbonatis, 
Magnesise  ponderosse, 

Calcii  carbonat ^^     oJ- 

01.  menth.  piperita? Tltx. 

Sig. — A  heaping  teaspoonful  in  half  a  glass  of  water  when  needed 

In  most  instances  it  is  wise  to  insist  that  the  patient  remain  in  bed  for 
a  period  of  three  or  four  weeks,  during  which  time  the  rest  cure  may 
be  instituted  in  a  modified  form,  since  with  the  improvement  in  general 
health  and  the  cure  of  anaemia  healing  of  the  ulcer  progresses  more  rapidly. 

The  diet  should  consist  of  milk  which  is  predigested  by  a  peptonizing  pow- 
der either  before  or  immediately  after  it  is  taken  into  the  stomach.  Under 
certain  circumstances  it  may  be  permissible  to  give  the  patient  very  soft 
milk-toast  in  small  quantities,  or  to  give  scalded  soda-biscuits  digested  by 
means  of  taka-diastase  or  pancreatin.  When  the  ingestion  of  food  increases 
gastric  pain  and  distress  it  may  be  necessary  to  give  the  patient  nothing  by 
the  stomach  for  a  period  varying  from  one  or  two  days  to  two  weeks,  and 
to  nourish  him  as  far  as  possible  during  this  period  by  nutritive  enemata, 
which  should  consist  of  four  ounces  of  peptonized  milk  and  one  egg,  injected 
three  times  in  the  twenty-four  hours,  the  bowels  being  carefully  washed  out 
with  normal  saline  solution  before  each  injection  in  order  that  the  residue 
from  the  previous  injection  may  be  removed. 

For  the  purpose  of  relieving  thirst,  it  is  often  advantageous,  when  the 
stomach  is  irritable,  to  give,  daily,  normal  saline  solution  by  hypodermoclysis. 
In  other  instances  a  pint  to  a  quart  of  normal  saline  solution  may  be  given 
high  up  into  the  colon. 

A  number  of  years  ago  the  late  J.  M.  Da  Costa  strongly  recommended 
ice-cream  as  a  diet  for  these  cases.  Care  should  be  taken  that  the  ice-cream 
does  not  contain  too  much  sugar,  as  this  will  cause  fermentation  and  dis- 
tress.   Frozen  milk  flavored  with  vanilla  is  better. 

The  patient  suffering  from  gastric  ulcer  should  receive,  in  the  way  of 
medicine,  ^  of  a  grain  of  nitrate  of  silver  with  ^  of  a  grain  of  extract  of 
hyoscyamus  in  pill  three  or  four  times  a  day  and  take  them  an  hour  before 
taking  food,  in  order  that  these  drugs  may  act  upon  the  stomach,  exercising 
a  healing  influence,  and  preventing  an  excessive  secretion  of  gastric  juice. 
If  pain  is  severe,  opium  may  be  substituted  for  hyoscyamus,  but  there  is 
some  evidence  that  opium  does  not  decrease,  and  may  sometimes  increase, 
the  flow  of  gastric  juice.  In  other  instances  chloretone  in  the  dose  of  from 
3  to  5  grains  may  be  given  three  or  four  times  a  day,  and  it  is  particularly 


GASTRIC   ULCER  587 

useful  if  pain  is  present.  In  other  cases  hyperacidity  and  pain  are  best 
controlled  by  10  to  20  grain  doses  of  bromide  of  strontium  or  of  sodium. 

The  administration  of  massive  doses  of  bismuth  subnitrate  has  been 
strongly  recommended,  chiefly  by  Fleiner.  He  gives  150  to  300  grains, 
stirred  in  5  or  6  ounces  of  warm  water,  after  the  stomach  has  been  care- 
fully cleansed  by  lavage.  Of  course  a  heavy  precipitation  of  bismuth  occurs 
upon  the  gastric  mucous  membrane.  This  plan  is  more  suitable  for  chronic 
cases  than  for  acute  ones. 

In  all  cases  of  gastric  ulcer  it  is  important  that  the  bowels  should  be  moved 
every  day  or  two  by  means  of  one  of  the  alkaline  purgative  waters,  of  which 
probably  Carlsbad  water  has  the  greatest  reputation.  The  Carlsbad  and 
Hathorn  spring-waters  at  Saratoga  do  almost,  if  not  quite  as  well,  as  the 
imported  water.  The  advantage  of  employing  these  waters  is  that  they 
not  only  unload  the  bowels,  but  tend  to  correct  acidity  and  relieve  chronic 
gastric  catarrh  by  their  favorable  influence  upon  the  gastrointestinal  mucous 
membrane. 

Should  hemorrhage  from  the  stomach  occur,  the  patient  should  be  put  to 
bed,  and  if  not  too  depressed  by  the  bleeding,  a  small  ice-bag  may  be  placed 
over  the  epigastrium,  and  2  teaspoonfuls  of  adrenalin  chloride  (1 :  1000) 
mixed  with  2  or  3  ounces  of  water  may  be  given  by  the  mouth,  with 
the  hope  that  the  adrenalin  chloride  will  contract  the  bloodvessels  and 
arrest  the  hemorrhage.  Where  adrenalin  chloride  cannot  be  obtained, 
from  5  to  30  drops  of  Monsel's  solution  may  be  given  in  2  ounces  of  water. 
The  use  of  ergot  hypodermically,  or  by  the  mouth,  in  this  condition  can 
scarcely  be  of  benefit,  as  it  will  raise  arterial  pressure  in  other  parts  of  the 
body  and  may  increase  the  hemorrhage.  The  general  treatment  in  these 
cases  is,  of  course,  identical  with  that  of  profuse  hemorrhage  occurring 
from  other  parts  of  the  body,  and  consists  in  the  use  of  |  of  a  grain  of 
morphine  hypodermically  to  allay  mental  distress,  and  hypodermoclysis  of 
normal  salt  solution.  Should  the  hemorrhage  be  sharp  and  very  profuse, 
the  question  of  operative  interference  arises. 

The  decision  as  to  whether  an  operation  should  be  performed  in  gastric 
ulcer  with  hemorrhage  is  a  most  difficult  one  to  reach.  We  are  rarely  tempted 
to  operate  in  such  cases  unless  the  hemorrhage  is  so  severe  as  to  be  alarming, 
and  yet  its  very  severity  renders  the  condition  of  the  patient  unfavorable 
to  operation. 

In  deciding  whether  an  operation  is  needful  in  a  case  which  has  had  an 
attack  of  gastric  hemorrhage,  consideration  must  be  given  to  the  character 
of  the  ulcer.  Even  those  surgeons  who  are  most  radical  in  advising  opera- 
tive measures  in  these  cases  state  that  in  cases  of  hemorrhage  from  acute 
ulcer  medicinal  measures  will  usually  control  that  particular  bleeding,  and 
as  an  immediate  second  hemorrhage  is  rare  operation  is  not  demanded. 
(See  Prognosis.)  When  the  hemorrhage  does  recur  and  particularly  if  it  be 
profuse  on  recurrence,  operation  is  to  be  considered  carefully,  whether  the 
ulcer  be  acute  or  chronic.  The  operation  of  election  is  gastroenterostomy, 
for  it  has  been  found  impossible  to  find  the  bleeding  spot  in  most  cases 
because  the  bleeding  often  comes  from  several  spots,  and  indeed  may  ooze 
from  a  multitude  of  eroded  spots.  Needless  to  say  that  the  gastroenterostomy 


588  DISEASES  OF   THE   STOMACH 

is  not  designed  to  stop  a  bleeding  already  in  active  progress,  but  is  to 
be  performed  as  soon  as  possible  to  prevent  further  bleedings. 

When  the  ulcer  is  very  chronic — that  is,  has  lasted  a  long  time — its  edges 
may  be  so  indurated  and  the  bloodvessels  in  its  cavity  so  eroded  that 
little  hope  of  cure  by  natural  processes  can  be  entertained,  an  operation  is 
wise.  It  is  not  necessary  to  excise  the  ulcer.  A  gastroenterostomy  gives 
the  stomach  rest  and  the  circulation  in  its  walls  becomes  modified.  Not 
only  does  such  an  operation  remove  the  danger  of  hemorrhage,  but  it  may 
change  the  patient  from  a  chronic  dyspeptic  to  a  well-nourished,  healthy 
individual.  If,  however,  the  ulcer  causes  suffering  or  chronic  gastric  dis- 
tress, surgical  interference  should  be  carefully  considered.  This  holds  true 
with  special  force,  if  the  existence  of  a  chronic  ulcer  near  the  pylorus  is 
causing  obstruction. 

Operation  for  the  removal  of  the  ulcer,  when  as  yet  it  has  neither  under- 
gone perforation  nor  produced  hemorrhage,  has  been  advised,  but  of  course 
has  not  been  very  popular,  as  few  patients  care  to  submit  to  it,  and  few 
physicians  have  considered  it  advisable  to  strongly  urge  operative  inter- 
ference. 

The  surgical  treatment  of  gastric  ulcer  with  perforation  is  now  a  well- 
recognized  procedure  in  modern  medicine.  When  perforation  occurs  opera- 
tion should  be  resorted  to  at  once,  unless  the  patient  is  profoundly  shocked, 
when  some  delay  is  advisable  in  order  that  she  may  rally. 

The  best  results  are  obtained  in  the  cases  which  are  operated  on  during 
the  first  twelve  hours  after  the  occurrence  of  perforation.  An  analysis  of 
these  statistics  shows  that  the  mortality  under  operation  has  been  pro- 
gressively reduced: 

In  July,  1899,  Tinker  added  57  cases  to  Keen's  list  of  156,  and  in  1900 
he  collected  19  others,  which  made  the  total  number  232,  with  a  mortality 
of  48.81  per  cent.  Later,  in  the  year  1900  Finney  made  an  addition  of  36 
cases  to  Tinker's  last  list,  thus  bringing  the  number  up  to  268,  of  which  the 
mortality  was  48  per  cent.  Of  163  cases  collected  since  the  publication  of 
Finney's  paper  in  1900,  102  recovered  and  61  died — a  mortality  percentage 
of  37.04.     These  figures  bring  the  statistics  up  to  June,  1904. 


CANCER  OF  THE  STOMACH. 

Gastric  carcinoma  is  one  of  the  most  common  forms  of  malignant  growth. 
Many  years  ago  Welch  showed  that  in  31,482  cases  of  cancer  the  disease 
affected  the  stomach  in  21.4  per  cent.  Startling  statistics  as  to  the  increasing 
frequency  of  cancer  have  been  published  within  the  last  four  years  by  several 
writers,  of  which  one  of  the  leaders  has  been  Roswell  Park,  of  Buffalo.  In 
the  United  States  census  for  1890,  the  deaths  from  gastric  cancer  were  placed 
at  2014  as  against  304  for  cancer  of  the  rectum,  and  876  from  cancer  of  the 
liver;  whereas,  in  the  census  for  1900,  there  were  4220  deaths  from  cancer 
of  the  stomach,  574  from  cancer  of  the  rectum,  and  1784  from  cancer  of  the 
liver.  As  a  large  proportion  of  cases  of  cancer  of  the  liver  are  secondary  to 
growths  elsewhere,  particularly  in  the  stomach,  these  facts  are  of  great 


CANCER   OF   THE   STOMACH  589 

interest.  In  the  city  of  Washington  the  deaths  from  cancer  of  the  stomach 
in  the  decade  from  1881  to  1890  were  191,  and  in  the  decade  from  1891 
to  1900,  339,  which  shows  an  increase  greater  in  proportion  than  the  growth 
of  the  city  population.  So,  too,  Templeton,  of  Dundee,  found  that  from 
1877  to  1902  the  death  rate  from  gastric  and  oesophageal  cancer  increased 
12.66  per  10,000. 

Etiology. — Gastric  cancer  is  far  more  common  in  males  than  in  females. 
Welch  states  the  proportion  to  be  5  to  4,  but  in  Osier's  cases  the  proportion 
was  5  to  1.  The  fact  that  gastric  ulcer  may  in  some  cases  seem  to  be  the  site 
for  the  development  of  gastric  cancer  has  little  real  bearing  upon  the  etiology 
of  this  disease.  While  some  patients  state  that  they  have  been  subject  to 
gastric  disorders  for  years  before  the  final  illness  develops,  it  has  been  my 
experience  that  a  very  large  proportion  of  patients  state  that  hitherto  they 
have  had  perfect  digestion,  and  have  never  known  what  it  was  to  have  gastric 
distress  in  previous  years.  In  other  words,  given  a  man  who  complains  of 
grave  gastric  symptoms  and  loss  of  weight,  who  has  not  cirrhosis  of  the 
liver,  or. dilatation  of  the  stomach,  who  has  not  used  alcohol  to  excess, 
and  who  boasts  of  his  good  stomach  during  the  first  forty  years  of  life, 
that  man  will  often  be  found  to  have  gastric  cancer.  We  have  no  knowl- 
edge of  the  etiology  of  gastric  cancer  beyond  the  facts  already  named. 

Morbid  Anatomy. — Gastric  cancer  is  usually  primary,  but  it  may  be  second- 
ary. The  most  common  form  is  the  medullary  carcinoma,  a  form  of  the 
spheroidal-cell  cancer;  the  adenocarcinoma,  the  malignant  adenoma  of 
German  writers,  or  cylindrical-cell  cancer,  is  second  in  point  of  frequency. 
The  scirrhus  type  is  the  third  in  frequency.  Gelatiniform  degeneration 
occurs  in  the  first  and  second,  and  when  present  such  tumors  are  called 
colloid  cancers. 

The  medullary,  or  spheroidal-cell  type,  is  the  most  rapid  in  its  growth, 
usually  tends  to  ulcerate  early,  and  is  followed  by  metastasis  and  direct 
extension  to  contiguous  organs  sooner  than  the  other  types. 

The  scirrhus  is  a  denser  growth,  infiltrating  and  indurating  the  sub- 
mucosa  often  to  some  distance,  or  even  all  of  the  organ ;  under  such  circum- 
stances, the  thick,  dense,  gastric  wall  has  led  to  the  condition  being  called 
"India-rubber  bottle  stomach,"  or  "  leathery  stomach." 

The  colloid  growths  form  tumors  of  greater  size,  often  extending  by  con- 
tiguity and  matting  adjacent  organs  into  a  solid  mass.  On  section  the  clear 
or  grayish  gelatiniform  trembling  matrix  is  found  to  be  enclosed  in  alveoli, 
often  of  macroscopic  dimensions. 

The  pylorus  is  the  part  of  the  stomach  usually  affected;  next  to  it  in  fre- 
quency is  the  lesser  curvature,  but  out  of  Welch's  1300  cases  the  pylorus  was 
affected  791  times  and  the  lesser  curvature  but  148. 

Mr,  Moynihan,  of  I^eeds,  has  investigated  the  subject  of  how  malignant 
growths  spread  in  the  gastric  wall,  and  has  concluded: 

1 .  That  malignant  disease  of  the  stomach  begins  in  the  majority  of  instances 
near  the  pylorus,  just  below  the  lesser  curvature. 

2.  That  from  this  point  it  spreads  most  rapidly  and  most  widely  in  the 
submucosa. 

3.  That  the  rate  of  growth  toward  the  cardiac  orifice  is  rapid,  toward 


590 


DISEASES  OF   THE  STOMACH 


the  duodenal  side  extremely  slow.  The  duodenal  extremity  of  the  viscus 
is  rarely  affected  extensively. 

4.  That  the  tendency  of  the  growth  is  to  drift  toward  the  curvatures. 

He  found  that  the  lymphatic  system  of  the  stomach  was  comparatively 
simple.    There  are  three  chief  lymphatic  areas  of  the  stomach  (Fig.  80). 

1.  An  area  along  the  lesser  curvature  (a)  from  which  the  lymphatic  vessels 
pass  upward  and  to  the  left  into  the  coronary  glands.  The  coronary  glands 
lie  along  the  artery  of  the  same  name.  At  the  coeliac  axis  they  become  con- 
tinuous with  the  glands  along  the  upper  border  of  the  pancreas. 

2.  An  area  (b)  along  the  greater  curvature  from  which  the  lymphatic  vessels 
pass  downward  and  to  the  right  into  the  glands  lying  along  the  greater  curva- 
ture. These  glands  are  more  numerous  near  the  pylorus,  and  from  here  pass 
to  the  head  of  the  pancreas  and  become  continuous  with  the  hepatic  group 
of  glands  which  lie  along  the  hepatic  artery,  and  in  part  along  the  pyloric 
artery. 


Fig.  80 


The  lymphatic  vessels  and  glands  of  the  stomach:   a  is  the  most  frequently  affected  area,  6  is  next, 
and  c  is  the  "  isolated  area."    (Moynihan.) 


3.  In  addition  to  these  two  areas  is  a  third  (c),  for  which  I  (Moynihan) 
suggested  the  name  "isolated  area."  This  area  comprises  the  greater 
tuberosity  of  the  stomach,  the  lower  end  of  the  oesophagus,  and  an  area 
along  the  greater  curvature  as  far,  approximately,  as  the  limit  of  supply 
of  the  left  gastroepiploic  artery.  Its  lymphatic  vessels  pass  downward  to 
the  hilum  of  the  spleen.  The  term  "isolated  area"  seems  singularly 
appropriate  for  this  region,  for  it  is  very  rarely  affected  by  growth  spread- 
ing upward  from  the  pylorus. 

If  a  cancer  of  the  stomach  arising  independently  of  ulcer  is  examined  in 
its  early  stages  it  will  usually  be  found  covered  with  mucous  membrane, 
which  later  ulcerates.  The  entire  wall  of  the  viscus  may  soon  be  involved, 
but  in  the  colloid  form  the  mucous  membrane  may  not  be  destroyed. 

The  effects  of  cancer  of  the  stomach  upon  the  shape  of  this  viscus  depend 
largely  upon  the  character  of  the  growth,  and  chiefly  upon  its  situation.  The 
general  tendency  is  for  the  stomach  to  be  decreased  in  size,  but  if  the  growth 


CANCER  OF   THE  STOMACH 


591 


obstructs  the  pylorus  the  stomach  may  be  greatly  dilated.  When  the  tumor 
is  widely  diffused  the  gastric  walls  are  much  thickened,  and  if  it  be  of  large 
size  it  may  displace  the  pylorus  very  greatly  by  its  weight. 

Perforation  of  the  stomach  through  the  cancerous  mass  may  occur,  but 
this  is  not  a  frequent  complication. 

Symptoms. — The  symptoms  of  gastric  cancer  may  not  manifest  themselves 
for  a  long  period  after  the  growth  has  begun,  and  even  when  the  general 
nutrition  is  impaired  the  patient  may  not  complain  of  gastric  disorder.  It  is 
a  mistake  to  suppose  that  gastric  cancer  is  usually  very  painful. 


Fig.  81 


Stomach.  Large,  ulcerating,  fungoid,  cylindrical-cell  carcinoma,  situated  on  the  posterior  wall  near 
the  pylorus,  which  was  slightly  obstructed  by  the  projecting  growth.  A  glass  rod  is  passed  through  a 
perforation  near  the  centre  of  the  floor  of  the  ulcer.  The  cardiac  end  of  the  organ  is  moderately  dilated 
There  was  secondary  enlargement  of  the  lymph  nodes  behind  the  stomach,  and  metastatic  nodules  in 
the  liver. 


When  symptoms  are  present  they  may  be  divided  into  the  objective  and 
the  subiectwe.  The  objective  symptoms  are  pallor,  which  becomes  well 
marked;  a  loss  of  weight,  which  is  often  extraordinary,  amounting  to  a  loss  of 
from  fifty  to  seventy  pounds  in  a  few  months,  and  with  this  there  is  usually  a 
rapid  loss  of  strength.  The  ancemia  is  chiefly  the  result  of  a  marked  decrease 
of  haemoglobin,  although  marked  reduction  and  morphological  alteration  in 
the  erythrocytes  may  yield  a  blood  picture  resembling  pernicious  anaemia. 
Sooner  or  later  leukocytosis  occurs. 


592  DISEASES  OF  THE   STOMACH 

The  S}Tiiptoms  presented  by  the  patient,  in  the  sense  that  they  are  com- 
plained of  by  him,  are  loss  of  strength,  gastric  distress  and  "dyspepsia,"  loss 
of  appetite,  nausea,  and  not  rarely  vomiting.  Vomiting  is  a  far  more  con- 
stant symptom  when  the  pylorus  is  obstructed  than  when  it  is  free,  and  the 
matters  vomited  may  indicate  a  feeble  digestive  power  and  be  colored  like 
coffee  grounds  due  to  exuded  and  altered  blood  arising  from  the  ulcerated 
growth.  Sometimes  a  free  hceviateinesis  develops.  Care  should  be  taken  that 
the  presence  of  altered  bile  in  the  vomit  is  not  taken  for  altered  blood. 

Not  rarely  the  patient  complains  of  constant  gnawing  pain  in  the  stomach, 
which  may  or  may  not  be  increased  by  the  taking  of  food.  The  pain  is 
usually  more  severe  when  the  disease  is  in  the  region  of  the  pylorus.  If  the 
sldn  over  the  epigastrium  is  lightly  touched,  it  may  be  very  sensitive. 
There  may  be  moderate  fever,  constipation,  and  oedema  of  the  ankles. 

Robson  states  that  pain  is  present  in  86  per  cent,  of  cases,  vomiting  in 
85.3  per  cent.,  and  a  tumor  is  palpable  in  76.6  per  cent.  These  figures  refer 
to  the  entire  history  of  the  cases  recorded,  and,  as  pointed  out  elsewhere, 
none  of  these  symptoms  may  be  present  during  the  early  stage  of  the  dis- 
ease, when  it  is  most  amenable  to  surgical  treatment.  Such  percentages 
are,  therefore,  of  greater  value  from  a  statistical  than  from  a  diagnostic 
standpoint. 

Diagnosis. — The  pallid,  cachectic  hue  of  the  patient,  combined  with  a  his- 
tory of  loss  of  weight,  and  with  the  fact  that  the  patient  is  usually  beyond 
the  fortieth  year,  should  make  the  physician  suspect  at  least  the  presence 
of  a  malio-nant  growth,  and  this  suspicion  becomes  stronger  as  he  is  able 
to  exclude  other  causes  of  ansemia  and  emaciation,  such  as,  for  example, 
diabetes,  Bright's  disease,  and  pernicious  anaemia.  The  presence  of  cough 
will  usually  be  a  guide  to  the  examination  of  the  lungs  for  pulmonary  tuber- 
culosis. It  must  not  be  forgotten  that  abdominal  tuberculosis  produces,  as 
a  rule,  a  dry,  harsh  skin,  instead  of  the  peculiar  waxy  or  greasy  skin  of  malig- 
nant growth  and  pernicious  ansemia. 

In  the  diagnosis  of  malignant  growth  the  blood  may  give  considerable 
information  and  aid  us  in  separating  this  condition  from  pernicious  ansemia, 
which  resembles  it  very  closely  in  some  of  its  objective  symptoms.  Malig- 
nant growth  is  characterized  by  a  marked  decrease  in  the  amount  of  haemo- 
globin and  in  the  haemoglobin  index,  a  condition  the  reverse  of  that  in  per- 
nicious anaemia.  When  the  case  is  far  advanced  there  is  usually  a  dimi- 
nution in  the  number  of  red  cells,  but  this  diminution  is  only  moderate  in 
early  cases.  Leukoc}i:osis  is  usually  present  in  moderate  degree,  averaging, 
perhaps,  20,000  to  25,000,  and  it  is  much  more  marked  if  metastasis, 
hemorrhage,  ulceration,  or  septic  infection  occur.  The  increase  in  white 
cells  is  chiefly  in  the  polymorphonuclear  neutrophiles.  It  is  a  noteT\'orthy 
point  that  these  cells  may  be  relatively  increased  without  a  distinct  leuko- 
cytosis being  present.  Normoblasts  and  myeloc}ies  are  sometimes  found  in 
limited  numbers  when  the  disease  is  far  advanced. 

While  it  is  true  that  in  a  few  cases  of  pernicious  anaemia  there  is  a  marked 
diminution  in  the  quantity  of  hydrochloric  acid,  it  is  rarely  if  ever  so  per- 
sistently absent  as  it  is  in  gastric  carcinoma. 

Another  condition  which  may  give  rise  to  much  difficulty  in  diagnosis  is 


CANCER  OF   THE   STOMACH  593 

ulcer  of  the  stomach,  with  thickening  and  induration  around  it.  This  condi- 
tion is  particularly  prone  to  appear  in  the  neighborhood  of  the  pylorus,  and 
it  may  be  impossible  by  palpation  to  differentiate  ulcer  and  induration  from 
scirrhous  cancer.  In  other  words,  every  case  in  which  a  mass  can  be  felt  in 
the  stomach  is  not  one  of  cancer.  In  such  a  case  the  excess  of  hydrochloric 
acid  in  ulcer  and  its  absence  in  cancer  are  valuable  factors  in  diagnosis. 
Then,  too,  ulcer  is  much  more  frequently  present  in  persons  under  forty, 
but  cancer  is  more  common  in  persons  over  forty. 

Inspection  of  the  epigastrium  very  often  gives  most  valuable  information, 
because  it  may  reveal  a  bulging  and  undue  pulsation  due  to  impulse  from  the 
aorta  transmitted  by  the  growth,  or  the  presence  of  a  nodule.  A  deep  breath 
taken  during  inspection  may  reveal  distinct  movements  of  the  mass.  If 
a  Seidlitz  powder  is  taken  in  two  parts,  so  that  the  contents  of  one  paper 
follow  the  other,  the  tumor  can  sometimes  be  seen  to  be  projected  against 
the  abdominal  wall  by  the  distended  viscus.  Palpation  may  reveal  a  mass 
which  usually  presents  an  uneven  suTface,  and  this  may  be  distinctly  nodular. 

The  position  of  the  mass  may  be  varied  by  the  pressure  of  food  in  the 
stomach.  If  a  mass  cannot  be  felt,  immersing  the  patient  in  a  hot  bath 
may  relax  the  tense  belly  wall  so  that  the  tumor  may  be  demonstrable. 
Percussion,  if  it  is  carefully  and  gently  performed,  over  the  mass  may  give 
an  impaired  note. 

Additional  signs  on  palpation  consist  of  a  hardening  of  the  gastric  walls 
due  to  contraction  of  their  muscular  fibres,  and  if  the  patient  is  thin  the  mass 
may  be  so  movable  that  it  may  be  pushed  high  up  under  the  ribs  or  far 
down  toward  the  pelvis.  The  mobility  is  of  great  diagnostic  value,  for  if 
the  mass  be  due  to  induration  about  an  ulcer  the  gastric  wall  will  nearly 
always  be  glued  to  adjacent  tissues,  and  therefore  be  made  fast.  As  a  rule, 
tumor  at  the  pylorus  is  more  readily  palpated  than  one  at  the  middle  of  the 
stomach,  and  a  growth  at  the  cardia  is  rarely  to  be  felt. 

Auscultation  may  reveal  constant,  direct,  or  reversed  peristalsis  if  the 
growth  obstructs  the  pylorus,  and  all  the  symptoms  of  gastric  dilatation  may 
be  present  if  the  growth  be  so  situated.     (See  Gastric  Dilatation.) 

A  very  useful  and  reliable  method  for  the  purpose  of  determining  the 
presence  of  gastric  cancer  is  the  determination  of  the  character  of  the 
stomach  contents. 

If  the  stomach  contents  are  examined  after  a  test  meal,  there  will  be  an 
almost  complete  or  total  absence  of  hydrochloric  acid  and  an  abnormal 
amount  of  lactic  acid  present.  To  determine  these  facts,  we  resort  to  the 
use  of  a  test  meal  and  certain  chemical  tests,  as  follows: 

Boas'  test  meal  consists  in  the  use  of  an  ordinary  breakfast  roll  weighing 
about  1  ounce,  with  10  ounces  of  water,  or  of  weak  tea,  which  should  contain 
no  milk  or  sugar.  This  is  allowed  to  remain  in  the  stomach  for  one  hour, 
and  then  is  removed  by  the  stomach  tube.  The  quantity  of  fluid  obtained 
should  equal  from  three-quarters  of  an  ounce  to  an  ounce  and  a  half.  It  is 
best  to  examine  this  fluid  microscopically,  and  then,  after  filtering  it,  to 
apply  the  tests  for  hydrochloric  acid  and  the  organic  acids.  The  two  common 
tests  for  free  hydrochloric  acid  are  Giinzburg's  phloroglucin-vanillin  and 
Boas'  resorcin  test.  Giinzburg's  reagent  is  composed  of; 
38 


594  DISEASES  OF  THE  STOMACH 

Phloroglucin gr.  xXx  (2  grams) 

Vanillin gr.  xv  (1  gram) 

Alcohol  (absolute)         .         .         .         .         .         •     ^j  (30  c.c.) 

This  solution  should  be  carefully  protected  from  the  light  by  being  kept 
in  a  dark  bottle  and  should  be  frequently  prepared,  as  stale  solutions  are 
uncertain.  One  or  two  drops  of  this  reagent  are  placed  in  a  porcelain  dish  or 
capsule,  with  an  equal  quantity  of  the  filtrate  obtained  from  the  gastric  con- 
tents. The  dish  is  then  gently  heated  over  an  alcohol  lamp  or  Bunsen  burner 
to  such  a  degree  that  slow  evaporation  takes  place.  If  free  hydrochloric  acid 
is  present,  a  typical  rose-red  hue  develops  at  the  edge  of  the  mixture  where  it 
is  drying  on  the  dish,  or  it  may  be  less  of  a  pink  and  more  of  a  bright  red. 
This  test  is  exceedingly  delicate  and  very  certain. 

Boas'  reagent  depends  upon  the  fact  that  resorcin  produces  a  somewhat 
similar  reaction  with  free  hydrochloric  acid.    This  reagent  is  composed  of: 

Resublimed  resorcin     ......     gr.  Ixxv  (5  grams) 

Cane-sugar  ........     gr.  xlv  (3  grams) 

Alcohol  (94  per  cent.)  ......     ^iijss  (100  c.c.) 

A  few  drops  of  this  reagent  are  placed  in  a  porcelain  dish  and  an  equal 
quantity  of  the  stomach  filtrate  added  to  them.  Heat  is  applied  as  in  the 
previous  test,  and  if  the  acid  is  present  a  very  perceptible  red  color  appears 
at  the  edge  of  the  evaporating  mixture. 

Still  another  point  of  diagnostic  importance  is  the  examination  of  the 
stomach  contents  by  the  microscope,  which  may  reveal  blood  cells  and 
portions  of  malignant  growth.  While  it  is  true  that  the  presence  of  blood 
may  be  due  to  ulcer,  the  associated  pie9es  of  growth  are,  of  course,  diag- 
nostic. 

Rommelaere  asserts  that  if  a  patient  over  forty  years  of  age  with  chronic 
gastric  disease  eliminates  less  than  180  grains  of  urea  a  day,  he  has  cancer. 
This  is  probably  too  dogmatic.  A  better  way  of  putting  it  is  to  say  that  when 
a  patient  with  these  symptoms  eliminates  450  grains  a  day  he  has  not 
gastric  cancer. 

It  is  important  to  note  that  a  bacillus  called  the  Oppler-Boas  bacillus  is 
present  in  the  stomach  contents  of  cases  of  gastric  cancer  with  great  con- 
stancy. Indeed,  it  is  present  ninety-nine  times  in  a  hundred.  This  bacillus 
is  a  very  long,  non-motile  organism,  which  has  the  power  of  converting  sugar 
into  lactic  acid,  and  lactic  acid  is  present  in  large  amount  in  this  disease. 

Prognosis. — The  prognosis  is  only  hopeful  in  inverse  ratio  with  the  size  of 
the  growth,  the  ability  of  the  surgeon  to  remove  it,  and  the  general  state  of 
the  patient.  Even  surgery  can  offer  only  temporary  relief,  for  in  the  majority 
of  cases  recidivity  takes  place.  Fen  wick  asserts  that  if  the  potassium  sulpho- 
cyanide  disappears  from  the  saliva,  the  patient  dies  within  a  month. 

Duration. — This  varies  greatly.  In  some  instances  death  comes  in  a  few 
weeks  after  the  disease  is  recognized.  In  others  it  is  deferred  for  months, 
particularly  if  the  growth  be  scirrhous  and  involves  the  pylorus,  when  a 
gastroenterostomy,  by  relieving  obstruction  and  permitting  nourishment, 
may  prolong  life  for  a  long  period.  My  colleague.  Dr.  Keen,  performed 
gastroenterostomy  in  a  case  under  my  care  in  which  the  growth  was  so  great 


HYPERTROPHIC  STENOSIS  OF   THE  PYLORUS  595 

that  excision  was  impossible.  The  patient  was  greatly  emaciated  and  more 
than  sixty  years  of  age,  yet  he  gained  nearly  thirty  pounds  in  six  months,  and 
lived  in  comfort  for  two  years  and  a  half  after  the  operation. 

Treatment. — The  medicinal  treatment  of  gastric  cancer  consists  first  in  the 
administration  of  anodynes  if  there  is  much  pain.  These  anodynes  may  consist 
of  small  doses  of  morphine  or  codeine  or  cannabis  indica.  Much  of  the  dis- 
tress due  to  so-called  dyspepsia  can  be  relieved  by  the  use  of  5  to  10  drops 
of  dilute  hydrochloric  acid,  with  1  or  2  drachms  of  the  fluid  extract  of  con- 
durango,  given  immediately  after  or  with  each  meal.  If  starchy  foods  are 
taken,  taka-diastase  may  be  used. 

The  use  of  a  stomach  tube  for  washing  out  the  stomach  is  usually 
inadvisable,  as  it  may  produce  a  perforation  if  the  growth  is  soft  or  the 
ulceration  deep. 

Should  vomiting  occur  and  blood  be  in  the  vomit,  the  directions  for  the 
treatment  of  hsematemesis  in  the  article  on  Gastric  Ulcer  should  be  followed. 
Many  patients  with  gastric  cancer  can  be  much  improved  and  their  lives 
prolonged  by  operation,  but  it  is  essential  that  the  growth  shall  be  limited 
to  the  stomach  and  that  it  does  not  involve  neighboring  parts.  For  this 
reason  it  is  of  vital  importance  that  the  diagnosis  of  the  disease  shall  be 
made  at  the  earliest  possible  moment.  Indeed,  it  may  be  said  that  every 
patient  who  develops  persistent  gastric  symptoms  after  the  age  of  forty 
should  be  regarded  as  a  possible  case  of  gastric  cancer  until  repeated  studies 
of  the  gastric  contents  have  excluded  this  disease.  In  the  opinion  of  the 
writer,  every  case  of  gastric  cancer  in  its  early  stages  should  at  least  be 
subjected  to  exploratory  operation,  since  by  this  means  it  may  be  dis- 
covered that  the  diseased  area  may  be  excised.  The  danger  of  exploratory 
operation,  as  compared  to  the  certainty  of  death  if  the  growth  is  not 
interfered  with,  is  not  to   be  considered. 

Kronlein  has  shown  that  the  average  duration  of  life  after  patients  come 
under  observation  is  about  nine  months.  If  they  submit  to  operation  it  is 
more  than  twelve  months.  The  duration  of  life  was  greater  in  those  treated 
by  gastrectomy  than  in  those  treated  by  gastroenterostomy. 


HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 

Definition. — This  condition,  as  its  name  implies,  is  one  in  which  there  is 
thickening  and  overgrowth  of  the  muscular  fibres  in  the  pyloric  portion  of 
the  stomach,  with  spasm  and  consequent  obstruction  to  the  free  passage  of 
its  contents  into  the  bowel. 

Overgrowth  of  the  tissues  about  the  pylorus  may  be  divided  into  three 
types.  In  one  the  gastric  walls  become  thickened  by  an  overgrowth  of  con- 
nective tissue,  which  not  only  results  in  an  increased  diameter  of  the  part,  but 
also  in  a  diminution  of  the  size  of  the  entire  stomach.  A  second  form  has 
been  described  by  French  authors,  which  is  associated  with  sclerotic  hyper- 
trophic changes  in  the  other  abdominal  viscera,  such  as  the  liver,  pancreas, 
and  kidneys.  The  third  form  is  that  which  is  known  as  congenital  hyper- 
trophic stenosis,  which  has  no  etiological  relationship  to  the  two  forms  just 


596  DISEASES  OF  THE  STOMACH 

described.    All  three  of  these   forms  are  quite  rare,  the   last  being  most 
frequent. 

Etiology. — We  have  little  knowledge  of  the  causes  of  hypertrophic  stenosis 
of  the  pylorus.  In  some  instances  it  has  been  thought  that  the  overgrowth 
is  the  result  of  some  congenital  defect,  or,  in  other  words,  that  it  is  a  primary 
condition,  but  in  others  it  has  seemed  to  be  certainly  secondary.  It  is 
probable  that  in  the  hypertrophic  stenosis  of  adults  the  underlying  cause  is 
chronic  gastritis.  When  it  occurs  in  adults  hypertrophic  stenosis  is  usually 
a  disease  of  middle  life. 

Morbid  Anatomy. — In  that  form  of  this  disease  which  arises  in  middle  life 
and  which  develops  as  a  result  of  chronic  gastritis,  notwithstanding  the  non- 
existence of  the  obstruction  at  the  pyloric  opening,  dilatation  of  the  stomach 
as  a  secondary  condition  seems  to  be  rare,  but  this  depends  somewhat  upon 
how  diffuse  the  overgrowth  of  connective  tissue  happens  to  be.  When  it  is 
limited  strictly  to  the  pyloric  region,  dilatation  ensues  because  of  the  obstruc- 
tion. When  it  is  more  diffuse,  the  stomach  may  be  diminished  in  size.  Very 
rarely  does  the  overgrowth  of  connective  tissue  develop  to  such  an  extent  as 
to  make  it  possible  to  discover  any  mass  by  careful  palpation. 

When  the  condition  is  due  to  some  congenital  defect,  the  pathological  con- 
dition is  somewhat  different.  It  is  found  that  the  organ  is  larger  than  normal 
and  that  its  walls  are  thickened  by  overgrowth  of  its  muscular  fibres.  At  the 
pylorus  these  muscular  fibres  have  undergone  great  hypertrophy,  so  that 
this  part  of  the  stomach  feels  like  a  solid  mass  between  the  fingers,  and  on 
section  it  is  found  to  be  dense  and  firm,  the  mucous  membrane  lining  the 
part  being  thrown  into  folds  which  lie  in  the  direction  of  the  long  axis  of  the 
organ.  Sometimes  one  of  these  folds  is  so  much  larger  than  others  that  it 
aids  in  producing  obstruction  and  seems  to  form  a  large  part  of  the  over- 
growth. Moynihan  has  well  said  that  such  a  stomach  may  appear  and  feel 
much  like  the  bladder  and  prostate  when  they  have  been  removed  by  dissec- 
tion. If  the  duodenum  is  opened,  the  pyloric  orifice  may  resemble  that  of 
the  cervix  uteri  when  it  is  seen  through  the  vagina.  The  thickening  of  the 
muscular  fibre  is  not  always  limited  to  the  pyloric  area,  but  sometimes 
extends  into  the  duodenum.  The  longitudinal  muscular  layers  are  not 
greatly  increased  in  size,  and,  although  there  is  a  general  hypertrophy  of  the 
muscular  element  throughout  the  entire  organ,  it  is  often  so  slight  at  the 
cardiac  end  of  the  stomach  that  it  is  scarcely  noticeable. 

Symptoms. — ^The  symptoms  of  stenosis  of  the  pylorus  in  adults  consist  in  a 
sensation  of  fulness,  'pressure,  and  pain  in  the  stomach.  There  are  also  evi- 
dences of  motor  insufficiency,  and  when  the  obstruction  to  the  pylorus 
becomes  marked,  vomiting  may  come  on  to  relieve  the  stomach  of  materials 
which  cannot  escape  into  the  intestine.  So,  too,  the  patient  may  lose  flesh 
as  the  result  of  interference  with  the  digestion  and  with  the  retention  of 
proper  quantities  of  food.  The  hydrochloric  acid  of  the  gastric  contents  is 
usually  diminished,  probably  because  of  the  chronic  gastritis  which  precedes 
the  disease. 

Diagnosis. — It  may  be  exceedingly  difficult  to  differentiate  hypertrophic 
stenosis  of  the  pylorus  in  an  adult  from  gastric  cancer  occurring  in  this  por- 
tion of  the  stomach.    In  the  article  on  Gastric  Cancer  it  was  pointed  out  that 


HYPERTROPHIC  STENOSIS  OF   THE  PYLORUS  597 

many  of  these  patients  give  a  history  of  perfect  digestion  and  no  gastric  dis- 
tress until  the  cancer  develops;  but  in  hypertrophic  stenosis  there  is  usually  a 
history  of  many  years  of  discomfort,  with  a  constant  endeavor  to  find  food 
which  would  not  cause  indigestion.  The  absence  of  cachexia,  although  the 
patient  may  be  anaemic,  also  points  toward  hypertrophic  stenosis.  On  the 
other  hand,  if  the  liver  or  gall-bladder  seems  to  be  affected,  the  condition  is 
almost  certainly  carcinomatous.  In  some  instances  it  is  impossible  to  make 
a  differential  diagnosis  without  operation,  and  even  then  it  may  require  a 
microscopic  examination  to  determine  that  the  thickening  is  not  malignant. 
So  far  as  probabilities  are  concerned,  it  may  be  stated  that  the  presence  of 
obstruction  at  the  pylorus  in  a  person  at  or  past  middle  life  is  very  much 
more  likely  to  be  carcinoma  than  hypertrophic  stenosis,  since  the  former 
condition  is  quite  common  and  the  latter  condition  is  very  rare. 

Difficulty  may  also  be  experienced  in  differentiating  hypertrophic  stenosis 
from  cicatricial  contraction  due  to  the  remains  of  an  old  gastric  ulcer.  The 
physical  signs  and  symptoms  present  at  the  moment  of  examination  may 
give  us  no  information,  but  the  past  history  of  the  case  may  aid  us  materially. 
Thus,  when  gastric  ulcer  has  been  present,  there  may  be  a  history  of  hemor- 
rhage and  severe  pain,  which  is  absent  in  cases  of  stenosis. 

Congenital  Pyloric  Stenosis. — As  already  stated,  the  condition  of 
pyloric  stenosis,  when  not  due  to  ulcer  or  cancer,  is  met  with  in  the  majority 
of  cases  in  very  young  children,  and  in  such  is  undoubtedly  congenital.  In 
such  instances  the  child  is  born  apparently  healthy,  and  after  two  or  three 
days,  or  several  weeks,  of  life  is  seized  with  sudden  and  persistent  vomiting, 
for  which  no  errors  in  diet  can  be  held  responsible.  The  vomiting  is  often 
forcible  and  gives  the  child  relief  for  the  time  being  until  more  food  is  taken, 
when  it  recurs.  The  time  during  which  the  food  is  retained  varies  from  a 
few  minutes  to  several  hours,  and  in  some  instances  the  mere  act  of  swal- 
lowing seems  to  reflexly  produce  the  motions  of  vomiting.  In  some 
instances  the  vomiting  is  sufficiently  prolonged  to  empty  the  stomach  thor- 
oughly; in  others  a  considerable  quantity  of  food  may  be  retained.  It  is  a 
noteworthy  fact  that  even  if  the  vomiting  is  severe,  bile  is  never  present  in 
the  ejected  material,  because  the  closed  pylorus  prevents  it  from  being  drawn 
from  the  duodenum.  The  result  of  the  ejection  of  the  food  almost  as  soon 
as  it  is  swallowed,  combined  with  the  deficient  digestive  function  of  the 
stomach  which  is  nearly  always  present,  is  rapid  emaciation,  exhaustion,  and 
death.  Sometimes  a  period  of  semi-consciousness  ensues,  and  occasionally 
the  child  is  seized  with  a  convulsive  attack. 

The  duration  of  life  varies  from  four  to  five  weeks  to  six  months. 

As  the  disease  progresses  and  emaciation  becomes  marked,  it  may  be 
possible  to  see  the  outline  of  the  stomach  in  its  forcible  contractions  if  the 
abdomen  is  carefully  examined  in  a  good  light.  If  deep  palpation  can  be 
practised,  the  thickened  pyloric  portion  of  the  stomach  can  be  felt  forming 
a  distinct  contrast  to  the  empty  and  collapsed  intestines,  which  are  pre- 
vented from  containing  their  usual  food  and  liquid  by  the  obstruction  at  the 
pylorus.     (See  Fig.  82.) 

The  points  which  are  strongly  in  favor  of  hypertrophic  stenosis  of  the 
pylorus  in  infancy  are  the  causeless  and  persistent  vomiting,  the  absence  of 


598 


DISEASES  OF  THE  STOMACH 


bile  from  the  vomit,  the  constipation,  the  presence  of  a  tumor  in  the  pyloric 
area,  the  collapsed  intestines  and  distended  stomach,  and  the  fact  that  gas- 
tric digestion  is  almost  completely  arrested,  and,  finally,  that  these  symp- 
toms are  present  in  a  young  child. 

Prognosis. — ^The  prognosis  in  hypertrophic  stenosis  is  unfavorable  as  to 
recovery,  and  it  may  be  unfavorable  as  to  life  if  the  obstruction  is  very  great. 
A  very  few  cases  are  on  record  in  which  recovery  without  operation  has 
occurred. 

Treatment. — The  treatment  consists  in  the  use  of  lavage  and  in  feeding 
through  a  rubber  tube,  so  that  the  movements  of  swallowing  are  not  neces- 
sary. In  some  cases  it  may  be  possible  to  prevent  the  vomiting  by  gently 
washing  out  the  stomach  before  each  feeding.  When  this  measure  fails, 
or  if  the  symptoms  are  exceedingly  severe,  operative  procedure  must  be 


Fig.  82 


Showing  the  gastric  peristalsis.     Note  constriction  of  stomach  by  passing  wave. 

(Ibrahim.) 

resorted  to  before  the  child  is  sufficiently  exhausted  to  contraindicate  the 
operation.  The  operation  should  either  be  pyloroplasty  or  gastroenteros- 
tomy. Moynihan  states  that  anterior  gastroenterostomy  has  been  performed 
9  times,  with  5  recoveries  and  4  deaths,  but  1  of  these  deaths  was  due 
to  acute  obstruction  caused  by  a  Murphy  button.  Loreta's  operation  of 
pylorodiosis  has  been  performed  9  times,  with  7  recoveries. 


HOUR-GLASS  STOMACH. 


or 


Definition. — ^Hour-glass  stomach,  sometimes  called  "bilocular  stomach, 
"  Sanduhrmagen,"  is  a  condition  in  which  the  stomach  is  divided  into  two 
parts  by  a  contraction  which  may  exist  anywhere  between  the  cardiac  and 
pyloric  orifices.    Very  rarely,  indeed,  a  trilocular  condition  may  be  present, 
and,  still  more  rarely,  a  quadrilocular  state  may  exist. 


HOUR-GLASS  STOMACH  599 

Etiology. — Hour-glass  stomach  may  be  congenital  or  acquired.  There  is 
some  difference  of  opinion  as  to  the  relative  frequency  of  these  two  forms  of 
the  condition.  Some  authors  have  maintained  that  all  cases  are  acquired, 
while  others  assert  that  the  congenital  cases  are  more  common.  Fenwick 
says  that  about  45  per  cent,  of  the  cases  which  have  been  so  far  recorded 
showed  no  sign  of  either  ulcer  or  scar  in  the  stomach,  or  if  an  ulcer  or  scar 
were  present  it  was  manifest  that  it  was  more  recent  than  the  stricture  itself; 
and  again  he  states  that  only  1  case  of  the  acquired  type  has  been  found  in 
the  London  Hospital  in  forty  years,  whereas  several  instances  of  the  con- 
genital type  were  met  with  during  the  same  period  of  time.  To  those  who 
believe  in  the  congenital  origin  of  these  cases,  Moynihan  is  strongly  opposed. 
He  states  that  he  has  examined  a  number  of  specimens  and  searched  the 
literature  carefully,  and  can  find  no  instance  in  which  there  is  good  ground 
for  considering  the  contraction  as  congenital.  He  therefore  contradicts 
those  who  think  that  the  ulcer  is  secondary  to  the  contraction. 

According  to  Moynihan,  there  are  three  causes  of  hour-glass  contraction: 
first,  perigastric  adhesion;  second,  chronic  ulcer;  and  third,  malignant  dis- 
ease. The  perigastric  adhesions  are  most  commonly  due  to  ulcer  of  the 
stomach  or  to  a  nearby  inflammatory  process  set  up  by  the  presence  of  gall- 
stone. Chronic  ulcer  not  only  produces  perigastric  adhesions,  but  it  may, 
in  healing,  cause  much  contraction  and  thickening  of  the  stomach,  so  that  its 
wall  becomes  puckered  and  its  calibre  decreased.  Associated  with  this 
contraction,  due  to  the  formation  of  scar  tissue,  there  is  also  a  certain  amount 
of  muscular  spasm,  the  circular  muscular  fibres  contracting  in  such  a  way  as 
to  resemble  a  sphincter  muscle.  This  spasmodic  contraction  accounts  for  the 
paroxysms  of  discomfort  from  which  the  patient  occasionally  suffers. 

Pathology  and  Morbid  Anatomy. — On  examining  a  stomach  for  the  seat  of 
hour-glass  contraction,  two  sets  of  thickened  muscular  fibres,  which  cross  one 
another,  may  sometimes  be  seen.  These  bundles  are  usually  one-half  inch 
or  more  in  width,  and  cross  one  another  at  the  point  of  contraction,  and  it  is 
the  shortening  of  these  muscular  fibres  which  produces  the  deformity.  That 
this  is  not  the  cause  in  most  instances,  however,  is  shown  by  the  fact  that 
these  muscular  fibres  are  frequently  absent,  or,  at  least,  are  not  abnormally 
developed.  When  the  constriction  is  due  to  the  formation  of  a  cicatrix 
the  narrowed  band  forming  the  dividing  septum  between  the  two  pouches 
is  composed  of  fibrous  tissue;  this  may  be  puckered,  indicating  that  it  has 
followed  an  ulcer. 

Symptoms. — The  S3niiptoms  of  hour-glass  contractions  of  the  stomach  are 
by  no  means  definite.  There  are,  however,  certain  physical  signs  which  can 
be  elicited  in  some  cases  which  are  of  great  importance.  These  methods  are 
well  described  by  Moynihan  in  the  following  words: 

"1.  If  the  stomach  tube  be  passed  and  the  stomach  washed  out  with  a 
known  quantity  of  fluid,  the  loss  of  a  certain  quantity  will  be  observed  when 
the  return  fluid  is  measured.  Thus,  if  30  ounces  be  used,  only  24  ounces  can 
be  made  to  return.  Woelfler,  who  called  attention  to  this  sign,  said  that  some 
fluid  seemed  to  disappear  '  as  though  it  had  flowed  through  a  large  hole ' — as, 
indeed,  it  has,  in  passing  from  the  cardiac  to  the  pyloric  pouch  (Woelfler's 
'first  sign'). 


000  DISEASES  OF   THE  STOMACH 

"2.  If  the  stomach  be  washed  out  until  the  fluid  returns  clear,  a  sudden  rush 
of  foul,  evil-smelling  fluid  may  occur;  or  if  the  stomach  be  washed  clean,  the 
tube  withdrawn  and  passed  again  in  a  few  minutes,  several  ounces  of  dirty, 
offensive  fluid  may  escape.  The  fluid  has  regurgitated  through  the  connect- 
ing channel  between  the  pyloric  and  cardiac  pouches  (Woelfler's  'second 

sign'). 

"3.  Paradoxical  dilatation.  If  the  stomach  be  palpated  and  a  succussion 
splash  obtained,  the  stomach  tube  passed,  and  the  stomach  apparently 
emptied,  palpation  will  still  elicit  a  distinct  splashing  sound.  This  is  due  to 
the  fact  that  only  the  cardiac  pouch  is  drained;  the  contents  of  the  pyloric 
pouch  remain  undisturbed  and  cause  the  splashing  sound  on  palpation.  For 
this  phenomenon  Jaworskihas  suggested  the  appropriate  name  of '  paradoxical 
dilatation.'  Jaboulay  has  pointed  out  that  if  the  cardiac  loculus  be  filled  with 
water,  a  splashing  sound  can  still  be  obtained  by  palpation  over  the  pyloric 
pouch.  The  sign  of  paradoxical  dilatation  is  best  elicited  after  washing  out 
the  stomach  in  the  ordinary  manner.  When  the  abdomen  is  examined  at  the 
completion  of  the  washing,  and  when  the  stomach  has  been  apparently 
drained  quite  dry,  a  splashing  sound  is  readily  obtained,  for  some  of  the 
fluid  used  has  escaped  into  the  pyloric  pouch  through  the  connecting  channel. 

"4.  Von  Eiselsberg  observed  in  one  of  his  cases  that  on  distending  the 
stomach  a  bulging  of  the  left  side  of  the  epigastrium  was  produced;  after  a 
few  moments  this  gradually  subsided,  and  concomitantly  there  was  a  gradual 
filling  up  and  bulging  of  the  right  side. 

"5.  Von  Eiselsberg  also  called  attention  to  the  bubbling,  forcing,  'sizzling' 
sound  which  can  be  heard  when  the  stethoscope  is  applied  over  the  stomach 
after  distention  with  CO2.  If  the  two  halves  of  a  Seidlitz  powder  are  sepa- 
rately given  and  the  stomach  be  normal  or  dilated,  no  loud  sound  is  heard 
anywhere  except  at  the  pylorus;  if  a  constriction  is  present  in  the  stomach, 
a  loud,  forcible,  gushing  sound  can  be  easily  distinguished  at  a  point  two 
inches  or  three  inches  to  the  left  of  the  middle  line. 

"6.  I  (Moynihan)  first  called  attention,  two  years  ago,  to  a  sign  which  I 
have  since  found  of  great  service  in  establishing  a  diagnosis  of  hour-glass 
stomach.  The  abdomen  is  carefully  examined  and  the  stomach  resonance  is 
percussed.  A  Seidlitz  powder,  in  two  halves,  is  then  administered.  On 
percussing,  after  about  twenty  or  thirty  seconds,  an  enormous  increase  in  the 
resonance  of  the  upper  part  of  the  stomach  can  be  found,  while  the  lower 
part  remains  unaltered.  If  the  pyloric  pouch  can  be  felt,  or  is  seen  to  be 
clearly  demarcated,  the  diagnosis  is  inevitable,  for  the  increase  in  resonance 
must  be  in  a  distended  cardiac  segment.  If  the  abdomen  be  watched  for  a 
few  minutes  the  pyloric  pouch  may  sometimes  be  seen  gradually  to  fill  and 
become  prominent. 

"7.  Schmidt-Monard  and  Eichhorst  have  both  seen  a  distinct  sulcus 
between  the  two  pouches  inflated  with  COg.  In  one  case  the  two 
pouches,  with  a  hard — as  I  thought  malignant — mass  between  them,  could 
readily  be  seen.  When  both  pouches  were  distended  with  CO2,  alternate 
pressure  upon  them  showed  unmistakably  that  they  communicated  through 
a  very  narrow  orifice,  for  the  one  could  be  emptied  slowly  into  the  other,  and 
the  fluid  could  be  felt  to  ripple  gently  through.    The  diagnosis  in  such  a  case 


GASTRIC  NEUROSES  601 

is  simplicity  itself.  In  another  case  a  distinct  notch  was  seen  at  the  lower 
border  of  the  inflated  stomach. 

"8.  Ewald  has  called  attention  to  two  signs  which  he  considers  of  value  in 
establishing  a  diagnosis.  When  the  stomach  is  filled  with  water  and  exam- 
ined by  gastrodiaphany,  the  transillumination  is  seen  only  in  the  cardiac 
pouch;  the  pyloric  pouch  remains  dark. 

"9.  The  deglutable  India-rubber  bag  of  Tiirck  and  Hemmeter  is  passed 
and  distended.  The  bulging  caused  thereby  is  limited  to  the  cardiac  pouch, 
which  lies  to  the  left  of  the  middle  line. 

"The  two  aids  to  diagnosis  of  greatest  value  are,  it  will  be  seen,  the  wash- 
ing out  of  the  stomach  and  its  inflation  with  gas  by  the  administration  of  a 
Seidlitz  powder  in  two  portions.  The  fluid  used  for  the  washing  must  be 
carefully  measured  before  being  used;  the  tube  is  then  passed  and  the 
stomach  emptied,  the  contents  set  aside  in  a  separate  dish,  and  the  wash- 
ing commenced.  All  the  fluid  now  returning  is  collected  in  a  separate 
vessel  and  carefully  measured.  The  two  signs  of  Ewald  are  of  little 
importance;  a  correct  diagnosis  can  always  be  made  without  them." 

Treatment. — The  only  treatment  for  hour-glass  contraction  which  can 
afford  any  relief  is  operative.  Thus,  a  gastroenterostomy  may  be  done 
from  both  pouches,  or  gastroplasty  or  pyloroplasty  may  be  necessary.  For 
these  operations  the  reader  is  referred  to  books  on  surgery. 


GASTRIC  NEUROSES. 

At  the  present  time  several  states  of  the  stomach  are  known  to  exist  which 
depend  upon  an  altered  or  perverted  nerve  supply,  and  are  not  connected 
with  any  pathological  lesion  which  our  methods  of  examination  can  detect. 
Gastric  neuroses  are  not  commonly  met  with  as  conditions  independent  of 
true  lesions,  and  the  physician  must  not  rest  satisfied  with  a  diagnosis  of 
gastric  neurosis  until  he  has  exhausted  every  possible  means  of  discovering 
an  actual  morbid  change.  In  some  instances  the  nervous  affection  of  the 
stomach  is  a  manifestation  of  disease  of  the  central  nervous  system ;  in  others 
it  is  a  sign  of  perverted  nervous  function  due  to  neurasthenia  or  nervous  ex- 
haustion, and  in  still  other  cases  it  may  be  dependent  upon  growths  which, 
being  situated  in  adjacent  tissues,  press  upon  the  gastric  nerves  and  so  cause 
pain  or  spasm.  Finally,  it  is  to  be  remembered  that  even  if  the  physician  can 
discover  no  sign  of  gastric  lesion,  this  does  not  justify  a  diagnosis  of  gastric 
neurosis,  because  it  not  rarely  happens  that  disease  elsewhere  causes  pain 
which  is  incorrectly  referred  by  the  patient  to  the  region  of  the  stomach. 
Thus,  a  child  with  pericarditis  or  appendicitis  may  complain  bitterly  of 
epigastric  pain. 

True  gastric  neuroses  may  be  divided  for  study  into  three  classes,  viz., 
disorders  of  mobility,  disorders  of  sensation,  and  disorders  of  secretion,  and 
these  in  turn  are  divisible  into  states  of  excitation  and  depression. 

Cardiospasm,  or  cramp  of  the  muscular  fibres  in  the  cardiac  end  of  the 
stomach,  is  a  result,  as  a  rule,  of  irritation  of  the  gastric  mucous  mem- 
brane by  superacid  secretion.    Occasionally  it  may  develop  as  the  result 


602  DISEASES  OF  THE  STOMACH 

of  distention  of  the  stomach  by  gas,  and  in  some  instances  no  direct  cause 
for  its  existence  can  be  discovered  save  that  a  state  of  nervous  unrest  and 
instabiUty  is  present.  Cramp  of  the  cardia  appears  in  an  acute  and  fleeting 
form,  and  as  a  chronic  condition  which  causes  great  distress  and  may  be 
serious,  in  that  it  exhausts  the  patient.  In  the  former  cases  pain  and  spasm 
seize  the  patient  and  then  pass  away.  In  the  latter  it  often  happens  that  the 
patient  has  difficulty  in  swallowing  and  expresses  the  feeling  that  the  food 
cannot  enter  the  stomach,  but  remains  in  the  oesophagus.  If  the  taking  of 
food  is  persisted  in,  it  speedily  accumulates  in  the  oesophagus,  and  when 
this  tube  is  distended  the  patient  regurgitates  the  food  undigested  and 
devoid  of  gastric  juice,  for  it  has  never  entered  the  stomach.  The  emaciation 
which  follows  this  inability  to  take  food  may  lead  to  the  belief  that  a  gastric 
carcinoma  is  present,  particularly  if  the  patient  is  advanced  in  years.  When 
chronic  cardiospasm  lasts  for  a  long  time,  dilatation  of  the  oesophagus  may 
develop,  and  even  a  diverticulum  may  be  formed. 

Treatment. — ^The  treatment  consists  in  the  use  of  remedies  designed  to 
prevent  and  counteract  excessive  gastric  acidity,  the  avoidance  of  all  irritat- 
ing or  stimulating  forms  of  food  and  drink,  the  use  of  lavage  if  there  is  any 
evidence  of  chronic  gastric  catarrh  or  of  fermentation  in  the  stomach,  and  in 
feeding  through  a  stomach  tube  if  there  is  any  difficulty  in  giving  the  patient 
a  proper  amount  of  nourishment.  Boas  states  that  in  some  cases  solids  are 
taken  more  readily  than  liquids.  Sedatives,  such  as  chloretone,  the  bromides 
and  chloral,  may  be  used.  Sometimes  galvanic  electricity  gives  relief,  using 
for  its  application  an  intragastric  electrode.  In  some  instances  the  daily 
passage  of  a  large-sized  gastric  or  oesophageal  bougie  produces  a  cure. 

Pylorospasm. — Pylorospasm  is  nearly  always  secondary  to  lesions  else- 
where, although  a  primary  spasm  may  occur.  In  pylorospasm  a  contraction 
wave  may  be  seen  in  a  thin  patient  endeavoring  to  urge  the  gastric  contents 
through  the  closed  pyloric  orifice,  and  if  the  spasm  is  persistent  the  stomach 
contents  will  not  only  be  retained,  as  in  gastric  dilatation,  but  they  may 
undergo  fermentative  changes  as  well,  so  that  symptoms  of  chronic  gastric 
catarrh  or  dilatation  may  be  present.  In  other  cases  a  reversed  peristalsis 
is  set  up  and  vomiting  comes  on,  so  that  symptoms  like  those  of  hypertrophic 
pyloric  stenosis  ensue.    The  treatment  is  identical  with  that  of  cardiospasm. 

Gastric  Hyperperistalsis,  called  by  Kussmaul  "peristaltic  unrest,"  is  a 
condition  in  which  the  stomach  almost  incessantly  continues  to  maintain 
peristaltic  movement.  As  a  rule,  it  is  most  active  after  meals,  but  it  may  be 
present  when  the  stomach  is  empty,  and  even  persist  at  night  during  absolute 
rest.  Although  marked  pain  is  usually  not  present,  the  incessant  movement  of 
the  stomach  causes  restlessness  and  gastric  discomfort.  Often  the  wave-like 
movements  of  the  stomach  can  be  felt  through  the  abdominal  wall,  and  their 
progress  is  from  left  to  right.  These  undulatory  movements  are  not  demon- 
strable, as  a  rule,  unless  some  gastric  dilatation  is  present  and  the  belly  wall 
fairly  thin.  Three  causes  are  recognized,  viz.,  excessive  acidity  producing 
irritation,  great  reflex  excitability,  and,  most  important  of  all,  stenosis  of  the 
pylorus,  which  obstructs  the  flow  from  the  stomach. 

Treatment. — ^The  treatment  consists  in  the  use  of  sedatives,  such  as  the 
bromides,  chloral,  codeine,  and  hyoscyamus,  and  in  the  use  of  counter- 


GASTRIC  NEUROSES  603 

irritation  over  the  epigastrium.  Not  rarely  an  absolute  rest  cure,  with  rectal 
feeding  for  a  week,  may  be  needful  to  cause  gastric  quiet.  Causes  which 
produce  nervous  exhaustion  and  undigestible  foods  are  to  be  forbidden  and 
hydrotherapeutic  measures  should  be  instituted. 

Merycismus. — Merycismus  is  a  neurotic  condition  in  which  the  patient 
has  the  ability  at  will  to  regurgitate  the  food  from  the  stomach  into  the  mouth 
for  the  purpose  of  rechewing  it,  as  is  done  by  ruminants.  It  is  usually  met 
with  in  neurotic  degenerates. 

Nervous  Eructation. — Nervous  eructation  is  not  a  very  rare  affection.  The 
patient  is  usually  very  nervous  and  will  often  sit  for  hours  "rifting  up"  gas, 
which,  in  many  cases,  is  really  swallowed  air.  In  other  cases  the  movements 
of  eructation  are  performed  without  any  gas  being  brought  up.  This  condi- 
tion is  commonly  seen  in  hysteria.  It  is  best  treated  by  the  rest-cure  and 
the  administration  of  tonics  or  nervous  sedatives,  such  as  the  bromides, 
spirit  of  chloroform,  asafoetida,  or  chloretone. 

Closely  related  to  nervous  eructation  is  nervous  vomiting. 

HjTperaesthesia. — Among  the  sensory  disorders  of  the  stomach  is  hyper- 
cesthesia,  in  which  the  taking  of  food  causes  great  gastric  distress,  so  that  the 
patient  refuses  to  eat  enough  to  maintain  nutrition.  In  hysterical  cases  the 
patient  may  be  able  to  eat  what  she  wishes,  yet  has  pain  when  other 
articles  of  food  are  given  to  her. 

This  condition  is  to  be  separated  from  the  hyperresthesia  due  to  gastric 
ulcer,  since  it  sometimes  develops  when  this  lesion  is  not  present.  Some- 
times it  seems  to  arise  from  the  abuse  of  alcohol,  coffee,  ice,  or  certain  drugs, 
such  as  quinine  and  the  salicylates,  or  tobacco.  In  other  instances  it  arises 
from  nervous  exhaustion  due  to  sexual  excess,  great  mental  strain,  pro- 
longed lactation,  or  menorrhagia.  So,  too,  it  may  develop  in  the  course  of 
chlorosis,  and  while  in  the  majority  of  instances  this  condition  in  chlorosis 
points  to  ulcer,  the  possibility  of  no  ulcer  being  present  must  be  considered, 
in  view  of  our  knowledge  of  the  existence  of  this  state. 

Symptoms. — The  symptoms  consist  in  a  sense  of  fulness  and  distention  of 
the  stomach,  particularly  in  the  neighborhood  of  the  cardia,  with  some  aching 
or  burning,  which  extends  upward  under  the  ribs.  Constipation  is  usually 
present.  As  the  condition  advances  the  disagreeable  sensations  in  the 
stomach  become  so  severe  as  to  amount  to  pain,  and  the  taking  of  food  usually 
greatly  increases  the  suffering.  When  fully  developed  the  patient  often 
suffers  from  vomiting,  which  may  occur  after  every  meal.  In  ulcer,  vomit- 
ing usually  gives  temporary  relief,  but  in  hypersesthesia  of  the  stomach  it 
does  not.  If  the  disease  persists,  there  is  emaciation  due  to  the  pain  and 
constant  vomiting.  The  skin  over  the  epigastrium  is  usually  hypersesthetic, 
and  the  tenderness  on  deep  palpation  is  diffuse  and  not  localized  as  in  ulcer. 
An  examination  of  the  gastric  contents  usually  reveals  a  normal  acidity,  but 
in  some  cases  the  acidity  may  be  above  or  below  the  normal. 

Gastralgia. — Gastralgia,  gastrodynia,  or  gastric  neuralgia,  may  be  a  cause 
of  much  severe  suffering,  for  the  patient  may  be  seized  by  a  paroxysm  of 
pain  which  seems  as  violent  as  a  renal  or  hepatic  colic.  This  pain  is  felt  not 
only  in  the  epigastrium,  but  along  the  edges  of  the  floating  ribs  to  the  spine, 
and  it  often  recurs  with  a  peculiar  periodicity.    It  is  not  rare  in  hysteria  and 


504  DISEASES  OF   THE  STOMACH 

neurasthenia.  The  gastric  crises  of  locomotor  ataxia,  the  pain  of  ulcer, 
and  that  caused  by  gas  must  be  carefully  excluded  before  a  diagnosis  of 
gastralgia  is  reached;  indeed,  a  diagnosis  of  simple  gastralgia  should  always 
be  looked  upon  with  suspicion,  because  gastric  pain  is  so  commonly  due  to 
some  organic  cause.  Unhke  the  pain  of  ulcer,  this  form  is  usually  relieved 
by  taking  food. 

Bulimia. — A  neurosis  of  the  stomach  characterized  by  excessive  hunger 
and  the  ingestion  of  great  quantities  of  food  to  alleviate  the  discomfort  is 
called  "Bulimia."  It  is  usually  met  wdth  in  cases  of  hysteria,  in  cases  of 
exophthalmic  goitre,  and  in  cerebral  tumor  and  epilepsy. 

Anorexia  Nervosa  is  a  form  of  neurosis  with  persistent  lack  of  appetite. 

Nervous  Disorders  of  Secretion. — A  form  of  nervous  disorder  of  secre- 
tion consists  in  hypersecretion  of  gastric  juice,  producing  the  ordinary 
symptoms  due  to  acid  stomach.  It  is  often  met  with  in  chlorotic  girls,  and 
is  usually  associated  with  constipation.  The  excessive  secretion  may  occur 
in  paroxysms  or  be  continuous. 

The  antithesis  of  this  state  is  that  in  which  there  is  an  absence  of  secretion, 
sometimes  called  achylia-gastrica  nervosa.  This  state  of  absence  of  HCl  is, 
of  course,  common  in  gastric  cancer,  and  it  arises  also  from  atrophy  of  the 
gastric  tubules,  but  there  are  instances  in  which,  apparently  because  of  dis- 
ordered nerve  supply,  there  is  absence  of  secretion  for  weeks,  months,  or  even 
years,  yet  finally  it  is  perfectly  re-established. 

Treatment. — The  treatment  of  these  disorders  of  sensation  consists  in  the 
institution  of  a  rest  cure  for  the  rehabilitation  of  the  patient's  nervous  tone; 
in  the  use  of  hydrotherapeutic  measures  and  electricity  designed  to  bring 
about  the  same  result,  and  in  the  prescription  of  a  mode  of  life  which  will 
avoid  nervous  worry  and  strain,  provide  a  sufficient  number  of  hours  of  sleep 
and  out-door  exercise,  and  prevent  the  ingestion  of  articles  of  food  which  are 
diSicult  to  digest  or  irritating  to  the  stomach.  For  the  prevention  or  relief 
of  painful  or  disagreeable  sensations,  a  number  of  remedies  may  be  employed. 
Not  infrequently  a  dose  of  a  drachm  of  spirit  of  chloroform  and  a  drachm  of 
compound  spirit  of  lavender  in  a  little  water  will  dispel  gas  and  distention 
and  act  as  a  sedative  to  the  stomach.  In  other  instances  I  to  1  grain  of 
menthol  may  be  given  in  capsule  or  pill.  In  still  others  one  of  the  coal-tar 
products,  as  antipyrin,  acetanilid,  or  phenacetin,  may  be  used,  and  in  some 
instances  much  relief  wiW  be  obtained  by  the  use  of  chloretone  in  capsule  or 
tablet  in  3  to  5  grain  doses.  Where  there  is  a  distinct  hysterical  element 
and  it  is  considered  desirable  to  exercise  a  mental  influence,  the  stomach  tube 
may  be  passed  once  or  twice  a  day.  If  an  excessive  secretion  of  hydrochloric 
acid  is  present,  associated  with  much  nervousness,  the  bromides  may  be 
employed,  or  nitrate  of  silver  and  hyoscyamus  may  be  used. 


HEMORRHAGE  FROM  THE  STOMACH. 

Hemorrhage  into  the  stomach  is  called  gastrorrhagia,  and  when  the  blood 
is  vomited  the  condition  is  one  of  hoBmatemesis.  It  may  result  from  rupture 
of  dilated  gastric  and  oesophageal  veins,  from  ulcer  of  the  stomach,  from 


HEMORRHAGE  FROM   THE  STOMACH  605 

cancer  of  the  stomach,  and  from  dilatation  of  the  gastric  veins  in  chronic 
gastric  catarrh.  It  has  also  been  known  to  follow  severe  injuries  over  the 
epigastrium.  Occasionally  the  vomiting  of  blood  has  been  due  to  an  aneurysm 
which  has  perforated  the  oesophagus  and  then  drained  into  the  stomach. 
The  physician  must  also  remember  that  malingerers  sometimes  swallow 
blood  for  the  purpose  of  deceiving  their  attendants.  Sometimes  "  coffee- 
ground  vomit,"  due  to  the  presence  of  altered  blood,  is  met  with  in  cases  of 
gastric  cancer,  in  certain  forms  of  purpura,  in  haemophilia,  and  in  persons 
suffering  from  such  poisons  as  phosphorus  and  carbolic  acid.  Occasionally, 
too,  in  cases  of  exceedingly  severe  infectious  disease,  such  as  yellow  fever 
and  smallpox,  vomiting  of  coffee-ground  material  occurs.  By  far  the  most 
frequent  causes  of  bloody  vomiting,  however,  are  cirrhosis  of  the  liver,  ulcer, 
and  cancer  of  the  stomach.  When  due  to  cirrhosis  it  is  usually  met  with  in 
males,  and  when  due  to  ulcer  it  most  commonly  occurs  in  females. 

Preble  has  made  a  most  complete  statistical  study  of  gastrointestinal 
hemorrhage  in  hepatic  cirrhosis,  and  finds  that  the  great  majority  of  cases 
occur  in  the  atrophic  form,  although  occasionally  hemorrhage  takes  place 
in  hypertrophic  cirrhosis.  In  one-third  of  the  cases  the  first  hemorrhage 
is  fatal;  while  in  the  other  two-thirds  the  hemorrhage  occurs  at  intervals 
varying  from  a  few  years  to  several  years,  the  longest  duration  being  over  a 
period  of  eleven  years. 

In  some  instances  it  is  possible  to  make  the  diagnosis  of  hepatic  cirrhosis, 
but  in  other  instances  the  change  in  the  size  of  the  liver  is  so  slow  that  not 
for  months  after  the  hemorrhage  occurs  is  this  organ  found  to  be  smaller  than 
normal.  In  80  per  cent,  of  the  cases,  according  to  Preble,  there  are  varices  in 
the  oesophagus,  and  in  more  than  one-half  of  these  there  are  evidences  of 
their  rupture  (Fig.  83).  It  has  also  been  found  that  fatal  hemor- 
rhages may  occur  in  cases  which  do  not  suffer  from  oesophageal  varices. 
These  cases  are  probably  due  to  the  rupture  of  a  large  number  of  capillaries 
in  the  alimentary  mucous  membrane.  It  is  interesting  to  note  that  in  only 
6  per  cent,  of  the  cases  which  showed  oesophageal  varices  was  the  cirrhosis 
typical  in  the  sense  that  the  ordinary  symptoms  of  this  condition  were 
present.  Very  profound  hemorrhages  may  come  from  a  very  small  open- 
ing in  a  bloodvessel,  so  that  at  autopsy  it  may  be  almost  impossible  to 
discover  the  source  of  the  bleeding. 

Aside  from  the  actual  vomiting  of  blood,  the  symptoms  of  gastric  hemor- 
rhage are  those  of  ordinary  hemorrhage,  namely,  'pallor,  faintness,  or 
actual  syncope,  and  sometimes  death.  The  vomited  blood,  if  it  has  been 
poured  out  in  large  quantities,  is  somewhat  venous  in  color  and  filled  with 
clots,  and  if  it  remains  in  the  stomach  any  length  of  time  it  may  become 
brown  or  granular  in  appearance,  through  the  action  upon  it  of  the  digestive 
juices.  It  must  always  be  remembered  that  the  quantity  of  blood  vomited 
does  not  necessarily  indicate  the  quantity  of  blood  which  has  escaped  from 
a  bloodvessel,  as  a  very  large  amount  may  leak  into  the  stomach  before 
vomiting  occurs,  and  the  stomach  in  vomiting  may  not  completely  empty 
itself.  Care  must  be  taken  in  determining  that  the  blood  comes  from  the 
stomach,  and  that  the  red  color  is  really  due  to  blood.  Sometimes  a  bloody 
color  of  the  vomit  may  be  due  to  claret  or  the  juice  of  various  berries.    A 


606 


DISEASES  OF  THE  STOMACH 
Fig.  83 


Dilated  venules  in  lower  part  of  oesophagus  due  to  hepatic  cirrhosis.      CKast  and  Rumpler.) 


CYCLIC  VOMITING  607 

distinction  can  be  made  by  a  microscopic  examination,  by  the  history  of  the 
ingestion  of  certain  articles  of  food,  and,  if  need  be,  by  the  use  of  the  spectro- 
scope and  the  various  tests  which  are  employed  to  determine  the  presence 
of  blood.  It  must  also  be  borne  in  mind  that  persons  who  suffer  from  nose- 
bleed, in  which  the  leaking  vessel  is  far  back  in  the  nose,  may  swallow  con- 
siderable quantities  of  blood  and  then  vomit  it. 

Hemorrhage  from  the  lungs,  or  haemoptysis,  is  to  be  separated  from  hsema- 
temesis  by  the  fact  that  in  hemorrhage  from  the  lungs  the  blood  comes  up 
with  coughing,  and  in  hemorrhage  from  the  stomach  by  vomiting,  although 
at  times  both  of  these  symptoms  may  be  present  in  each  class  of  cases.  The 
characteristic  appearance  of  a  patient  well  advanced  in  tuberculosis  will  be 
of  great  diagnostic  aid  in  such  cases,  and  an  examination  of  the  chest  in  the 
case  of  haemoptysis  will  usually  reveal  some  lesion;  whereas,  the  lungs  will 
be  clear  in  haematemesis.  In  a  case  of  haematemesis  an  examination  of  the 
abdomen  may  reveal  an  atrophied  liver  and  an  enlarged  spleen,  or  some 
other  abdominal  state,  such  as  the  ca'put  medusce,  which  will  indicate  that 
there  is  venous  stasis  in  the  abdomen.  (See  Hepatic  Cirrhosis.)  In  haemop- 
tysis the  blood  is  pink  and  frothy.  In  hemorrhage  from  the  stomach  it  is 
dark,  has  little  air  mixed  with  it,  and  is  often  acid  in  reaction;  whereas,  that 
in  haemoptysis  is  usually  alkaline.  In  haemoptysis  no  dark,  tarry  stools  are 
present,  but  they  are  frequently  seen  after  an  attack  of  haematemesis.  A 
day  after  an  attack  of  haemoptysis  the  patient  may  cough  up  some  thick- 
ened, bloody  mucus,  but  there  is  no  difficulty  in  separating  this  from  the 
more  fluid,  dark  blood  from  the  stomach.  An  additional  aid  in  the  diagnosis 
of  haematemesis  is  Boas'  test  given  in  the  article  on  Gastric  Ulcer. 

Notwithstanding  the  profound  mental  shock  and  vital  depression  which 
often  follows  a  profuse  hemorrhage  from  the  stomach,  it  is  worthy  of  note 
that  death  very  rarely  occurs  as  the  immediate  result  of  this  loss  of  blood, 
unless  the  patient  is  already  devitalized  by  advanced  disease  or  repeated 
hemorrhages. 

For  the  treatment  of  bloody  vomiting  see  Treatment  of  Gastric  Ulcer. 


CYCLIC  VOMITING. 

Under  the  name  of  cyclic,  periodical,  or  recurrent  vomiting,  a  condition 
has  been  rarely  met  with  in  which,  at  certain  periods,  a  child  is  seized  by  an 
attack  of  'persistent  vomiting,  which  not  only  continues  while  the  stomach  is 
being  emptied  of  its  normal  contents,  but  persists  for  many  hours  afterward, 
and  in  some  instances  ends  fatally.  The  condition  in  all  probability  depends 
upon  a  form  of  autointoxication.  This  autointoxication  consists,  appar- 
ently, in  a  condition  of  acidiosis.  Marfan  believed  that  it  was  due  to  an 
acetonaemia.  Edsall,  on  the  other  hand,  who  has  studied  the  disease  most 
carefully,  and  who  has  done  much  work  upon  the  subject  of  acid  intoxication, 
reports  5  cases  in  which,  at  the  time  of  the  attacks,  this  condition  existed. 
The  urine  between  the  paroxysms  was  normal,  but  immediately  before  the 
attack  contained  diacetic  acid  and  acetone.  He  found  that  the  immediate 
administration  of  large  doses  of  bicarbonate  of  soda,  as  much  as  2  drachms. 


608  DISEASES  OF   THE  IXTESTIXES 

prevented  attacks  which  seemed  impending.  He  contradicts  the  theory  of 
Marfan  as  to  the  cause  of  acetoneemia,  and  does  not  think  that  acetone,  as 
such,  ever  appears  in  the  blood. 


DISEASES   OF   THE  INTESTINES. 

DIARRHCEA. 

Diarrhoea  is  not  a  disease,  but  a  s}Tiiptom,  just  as  headache  and  dropsy 
are  svmptoms.  It  occurs,  however,  from  so  many  different  causes  and  is  so 
often  present  without  the  presence  of  any  organic  change  in  the  intestinal 
walls  that  it  is  best  considered  as  a  malady,  at  least  in  several  of  its  forms. 
Diarrhoea  is  the  symptom  or  condition,  above  all  others,  in  some  cases,  but 
in  others  it  is  of  little  significance  as  compared  to  the  organic  lesion  which 
produces  it. 

Serous  Diarrhoea. — Serous  or  watery  diarrhoea  may  arise  from  the  inges- 
tion of  irritating  foodstuffs,  which  cause  the  intestinal  mucosa  to  become 
hypertemic  and  to  pour  into  the  calibre  of  the  bowel  the  serum  of  the  blood, 
to  dilute  the  poison,  and  to  wash  it  out  of  the  intestine.  In  many  instances 
the  attack  is  very  brief,  and  even  if  by  an  accident  an  autopsy  is  possible,  no 
lesion  may  be  found. 

In  still  other  cases  the  same  result  may  follow  sudden  exposm-e  to  cold  and 
dampness,  in  which  case,  if  the  visceral  congestion  is  severe,  a  secondary 
catarrh  of  the  intestinal  mucosa  may  develop  as  a  later  condition. 

In  some  instances  a  serous  diarrhoea  seizes  persons  who  are,  or  who  are 
about  to  be,  subjected  to  a  severe  nervous  strain,  as  actors  at  their  first 
appearance,  or  medical  students  about  to  go  before  a  severe  examiner,  upon 
whose  verdict  much  depends.  Such  a  nervous  diarrhoea  is  not  rarely  met 
with  in  hysterical  persons. 

Finally,  in  chronic  renal  disease,  patients  sometimes  are  seized  by  a  pro- 
fuse watery  purging  designed,  apparently,  to  eliminate  from  the  body  certain 
poisonous  materials  that  the  diseased  kidneys  permit  to  accumulate. 

All  of  these  forms  of  serous  diarrhoea  occur  without  being  accompanied 
by  much  pain  and  without  the  passage  of  much  flatus. 

Treatment. — The  treatment  depends  largely  upon  the  cause  of  the  dis- 
order. If  it  is  due  to  the  ingestion  of  bad  food,  the  patient  should  receive  a 
moderate  dose  of  castor  oil  (-^-  to  1  ounce),  and  with  it  a  dessertspoonful  of 
paregoric  to  prevent  griping.  By  this  means  the  offending  matter  is  swept 
out  and  a  secondary  constipating  influence  follows,  or  can  be  produced  by 
the  measures  about  to  be  referred  to. 

Aside  from  this  condition,  all  cases  of  serous  diarrhoea  are  to  be  treated  by 
rest,  counterirritation  in  the  form  of  a  capsicum  or  mustard  plaster  over  the 
abdomen,  the  appUcation  of  external  heat  if  the  temperature  falls,  and  the 


ILEOCOLITIS  OF  CHILDHOOD  609 

internal  use  of  a  grain  of  camphor  every  two  hours  for  three  doses,  or  of  a 
mixture  of  aromatic  sulphuric  acid  and  fluid  extract  of  hsematoxylon  in  syrup 
of  ginger  every  two  hours.  All  foods  should  be  forbidden  until  the  diarrhoea 
is  to  some  extent  controlled,  when  predigested  milk,  arrowroot,  and  broths 
may  be  allowed. 

When  the  purging  is  an  effort  at  elimination  in  Bright's  disease,  care  must 
be  taken  not  to  check  the  diarrhoea  suddenly,  lest  toxaemia  develop. 


CATARRHAL  ENTERITIS. 

Acute  and  chronic  catarrh  of  the  small  intestine  are  of  frequent  occur- 
rence, and  the  symptoms  produced  in  the  acute  form  may  be  very  like  those 
described  under  serous  diarrhoea,  save  that,  as  a  rule,  there  is  more  fain  and 
griping  in  the  bowels.  In  both  conditions  there  is  present  at  first  an  acute 
hyperemia  of  the  intestinal  mucosa,  followed  by  a  true  catarrhal  process,  in 
which  the  glandular  epithelium  becomes  swollen  and  the  submucous  tissues 
infiltrated  with  exudate.  A  careful  examination  of  the  mucous  membrane 
reveals  slight,  if  any  distinct  reddening,  except  at  the  edges  of  the  valvules 
conniventes.  If  the  process  has  been  subacute  or  chronic  the  intestinal 
mucosa  is  boggy  and  swollen,  but  not  reddened,  and  the  lymph  follicles,  as 
well  as  the  mucous  glands,  are  enlarged.  After  some  days,  rarely  earlier, 
and  not  in  all  cases,  the  swollen  solitary  follicles  may  be  the  seat  of  superficial 
necroses,  shown  by  yellowish,  grayish,  or  grayish-yellow  erosions  surmount- 
ing each  follicular  eminence;  such  ulcers  are  rarely  of  any  size.  When  the 
process  has  lasted  many  days  the  mucosa  may  be  thickened.  It  is  to  be 
remembered  that  in  all  of  these  cases  the  changes  are  not  confined  to  the 
small  bowel,  but  are  also  present  in  the  large  intestine  as  well. 

Symptoms. — Aside  from  the  diarrhoea  and  griping  pain  already  referred  to, 
the  patient  suffers  from  rumbling  in  the  bowels  due  to  hyperperistalsis,  from 
loss  of  appetite,  and  weakness  due  to  the  abdominal  discomfort  and  the 
serous  purging.  The  stools  may  be  light  yellow  and  very  fluid,  and  in  the 
water  which  is  discharged  will  be  found  particles  of  undigested  food,  cast-off 
epithelium,  flakes  of  bile-stained  mucus,  and  myriads  of  micro-organisms. 
The  pulse  is  usually  quick,  and  there  may  be  fever  of  moderate  degree. 

Treatment. — ^The  treatment  is  rest  in  bed,  counterirritation  to  the  abdomen, 
and  full  doses  of  bismuth  after  the  bowel  has  been  swept  out  by  castor  oil. 

ILEOCOLITIS  OF  CHILDHOOD. 

Definition. — The  ileocolitis  of  childhood  is  a  state  in  which  symptoms  of 
gastrointestinal  disorder  develops,  as  manifested  by  purging,  vomiting,  and 
abdominal  distress.  It  cannot  be  distinctly  separated  from  the  catarrhal 
enteritis  of  adults,  either  from  the  standpoint  of  pathology  or  symptom- 
atology, yet  clinicians  have  universally  recognized  the  fact  that  such  a 
division  at  the  bedside  is  advisable. 

Etiology. — ^The  ileocolitis  of  infancy  depends  chiefly  for  its  existence  upon 
the  action  of  micro-organisms  and  their  poisons  on  the  intestinal  mucosa. 
39 


610  DISEASES  OF   THE  INTESTINES 

This  infection  may  be  produced  by  a  large  number  of  organisms,  some  of 
which  are  not  pathogenic  when  the  child  is  in  perfect  health,  and  which  only 
become  competent  to  cause  disorder  or  disease  when,  by  some  additional 
cause,  the  general  or  local  vitality  of  the  patient  is  reduced.  Thus,  it  not 
rarely  happens  that  the  stools  contain  myriads  of  streptococci,  staphylococci, 
the  Bacterium  lactis  aerogenes,  or  the  Bacillus  pyocyaneus,  the  pathogenic 
micro-organism  which  causes  green  stools,  and  other  bacteria.  More  impor- 
tant than  all,  the  bacillus  of  dysentery  of  Shiga  and  Flexner  is  now  known 
to  be  a  cause  in  a  large  proportion  of  cases.  (See  Cholera  Infantum  and 
Dysentery.) 

The  relationship  of  specific  micro-organisms  to  the  summer  diarrhoea  of 
children  is  well  summed  up  by  Pease  and  Shaw  in  the  following  sentences: 

"We  think  it  can  be  fairly  concluded  that  there  exists  a  group  of  bacilli 
having,  in  general,  similar  characteristics  which  differentiate  them  from  the 
typhoid  bacillus  on  the  one  hand,  and  the  colon  bacillus  group  on  the  other, 
which  can  be  said  to  have  an  etiological  relation  to  most  cases  of  endemic 
and  epidemic  dysentery,  whether  the  same  occur  in  adults  or  children.  That 
there  probably  are  rare  epidemics  of  this  disease  in  which  the  clinical  course 
may  not  conform  exactly  to  the  usual  type,  in  which  bacteria  other  than  the 
group  of  dysentery  bacilli  are  the  etiological  factors.  An  example  of  this  kind 
is  the  epidemic  of  dysentery  due  to  the  Bacillus  pyocyaneus  infection  reported 
by  Lartigau. 

"Whether  the  cases  of  summer  diarrhoea  in  children  not  showing  symp- 
toms of  true  dysentery,  and  not  having  been  more  or  less  closely  associated 
with  true  cases  of  the  disease,  can  be  considered  as  uniformly  caused  by 
either  of  these  two  types  of  dysentery  bacillus  is  still  open  to  question." 

The  causes  that  usually  permit  these  organisms  to  develop  are  exposure 
to  cold  or  excessive  heat,  so  that  the  bowel  is  congested  and  its  circulation 
impaired,  and  the  use  of  foods  which  are  unsuitable  in  kind  or  have  become 
so  by  infection  or  chemical  change.  Winds  carrying  dust,  flies  carrying 
infection,  and  air  carrying  gases  may  all  aid  in  impairing  the  quality  of  food. 
At  times  the  condition  develops  as  a  result  of  an  attack  of  an  infectious 
disease,  such  as  measles.  Heat  and  humidity  not  only  reduce  the  resistance 
of  the  child,  but  greatly  increase  the  number  of  micro-organisms  in  raw  foods, 
especially  milk,  in  which  they  sometimes  number  as  many  as  100,000,000  per 
cubic  centimetre.    (Park  and  Holt.^) 

Pathology  and  Morbid  Anatomy. — The  ileocolitis  of  childhood  affects  par- 
ticularly the  lower  part  of  the  ileum  and  the  colon,  the  extent  depending 
upon  the  vital  resistance  of  the  child  and  the  virulence  of  the  infection.  Even 
in  those  cases  due  to  the  bacillus  of  Shiga,  the  most  varied  lesions  are  found. 
The  degree  of  pathological  change  varies  within  wide  limits.  In  some 
instances  there  is  only  a  superficial  catarrh,  with  some  infiltration  of  the 
mucous  membrane,  while  in  others  the  submucous  tissues  are  affected,  and 
in  still  others  areas  of  mucous  membrane  may  slough.  In  these  severe 
cases  the  mucous  membrane  of  the  entire  alimentary  canal  may  show  more 
or  less  catarrh. 

1  Those  interested  in  the  effect  of  temperature,  season,  and  milk  supply  upon  infant  mortality  should 
read  a  statistical  paper  by  Park  and  Holt  in  the  Medical  News,  December  5,  1903. 


ILEOCOLITIS  OF  CHILDHOOD  611 

^  If  the  mucous  membrane  of  the  small  intestine  is  examined  at  autopsy,  its 
villi  are  found  to  be  soft  and  swollen,  so  that  the  surface  of  the  bowel  presents 
a  velvety  aspect.  In  mild  cases  the  hyperaemia  is  not  intense.  A  universal 
congestion  is  present  in  severe  cases,  and  even  punctate  extravasations  of 
blood  may  be  seen.  The  solitary  follicles  are  swollen  and  protrude  above 
the  surface  in  both  the  small  and  large  bowel  and  at  the  summits  of  follicles 
beginning  ulceration,  which  rarely  is  extensive,  is  noticeable.  Peyer's 
patches  may  also  be  infiltrated,  but  they  are  rarely  ulcerated.  In ' 
severe  or  long-continued  cases  the  solitary  glands  may  ulcerate,  but  the 
agminated  glands  very  rarely.  An  appearance  which  at  first  glance  may 
be  thought  to  be  an  ulcerated  Peyer's  patch  will  be  found  to  be  due  to  the 
running  together  of  several  ulcers  of  solitary  follicles. 

In  severe  cases  a  condition  of  acute  membranous  enteritis  develops,  the 
lower  ileum  and  colon  being  covered  by  a  thin  false  membrane,  which  can 
be  seen  in  some  cases  only  with  difficulty.  This  membrane  may  be  of  a 
yellowish-green  hue  and  it  lies  over  a  part  of  the  bowel  which  is  greatly 
thickened  by  an  inflammatory  process  which  involves  its  deeper  coats. 
Curiously  enough,  ulceration  of  the  mucous  membrane  in  such  an  area  is 
unnsual. 

Symptoms. — ^The  symptoms  of  acute  ileocolitis  in  childhood  vary  greatly 
in  their  severity  and  duration.  In  the  mild  catarrhal  form  there  is  a  slight 
rise  of  temperature  of  from  1°  to  2°,  with  several  loose  movements  of  the 
bowel  each  day.  These  stools  have  a  little  mucus  in  each  of  them  and  perhaps 
a  few  small  flecks  of  undigested  food. 

If  the  conditio?!  is  more  severe  there  is  paiji  in  the  bowels,  with  vomiting, 
high  fever,  and  the  frequent  passage  of  yellow  or  greenish  stools  containing 
mucus  and  considerable  amounts  of  undigested  food,  and  if  the  condition 
persists  the  mucus  may  become  streaked  with  blood,  and  tenesmus  may  be 
severe.  There  is  little  flatus  and  little  odor  to  the  passages.  The  tongue  is 
coated  and  anorexia  is  marked. 

Because  of  the  fever,  vomiting,  and  diarrhoea,  the  patient  is  rapidly  pros- 
trated and  loses  flesh  with  remarkable  speed. 

If  the  course  of  the  colon  is  palpated  through  the  tumid  abdominal  wall, 
some  tenderness  is  usually  found.  As  recovery  begins  the  stools  become 
less  frequent,  have  a  more  normal  color,  the  quantity  of  mucus  decreases, 
and  the  fever  falls.  If,  on  the  other  hand,  at  the  end  of  a  week  or  two  there 
is  no  change  for  the  better,  the  more  severe  state,  in  which  ulceration  of  the 
intestinal  lining  takes  place,  is  probably  present,  and  death  may  ensue  from 
exhaustion  and  depression,  with  signs  of  toxaemia. 

If  recovery  takes  place  it  is  very  slow,  a  tendency  to  looseness  of  the 
bowels  persisting  for  weeks,  mucus  being  seen  in  almost  every  stool,  and  a 
relapse  being  threatened  at  each  change  in  weather  or  in  the  food. 

In  the  well-developed  ulcerated  form  the  systemic  disturbance  is  profound 
and  often  sudden  in  onset,  and  its  very  severity  may  serve  to  prevent  a  sharp 
febrile  reaction.  The  stools  are  often  much  fewer  per  day  than  in  the  catarrhal 
form,  but  they  contain  more  mucus  and  less  blood.  Unlike  the  stools  in  the 
mildertype,  these  passages  smell  badly.  The  belly  is  distended  and  the  general 
loss  of  flesh  is  very  severe.    The  mouth  and  tongue  are  dry  and  foul. 


612  DISEASES  OF   THE  INTESTINES 

In  the  membranous  form  the  stools  contain  mucus  and  blood  and  par- 
ticles of  false  membrane,  which  are  easily  discerned  if  the  stools  are  first 
mixed  with  water  and  then  strained  through  a  sieve.  The  degree  of  pros- 
tration and  evidence  of  toxaemia  in  these  cases  is  very  severe,  and  upon  the 
prolapsed  rectal  mucous  membrane  the  false  membrane  may  be  sometimes 
seen.  At  times  such  cases  present  at  onset,  or  late  in  the  disease,  severe 
cerebral  symptoms  which  may  mask  the  intestinal  state. 

Diagnosis. — Ileocolitis  must  be  separated  from  the  typhoid  fever  of  infancy. 
In  most  cases  this  is  not  difficult,  because  in  the  typhoid  fever  of  children 
constipation  is  often  present,  and  the  rose  spots  may  be  found.  The  chief 
diagnostic  points  which  separate  the  two  affections  are  that  enteric  fever  is 
rare  and  ileocolitis  common,  that  in  enteric  fever  the  onset  is  usually  gradual; 
in  ileocolitis  it  is  acute.  In  one  there  is  an  enlarged  spleen  and  the  Widal 
reaction;  in  the  other  neither  one  of  these  signs  is  present.  If  the  illness 
is  due  to  the  Bacillus  dysenterioe,  the  agglutination  test  may  reveal  that  fact. 
(See  Dysentery.) 

Prognosis. — ^The  prognosis  depends  upon  several  facts.  Young  children 
fare  worse  than  children  after  the  fourth  year.  City-bred  children  succumb 
more  rapidly  than  children  in  the  country,  particularly  if  the  weather  is  hot. 
Children  who  are  strong  and  hearty  at  the  onset  have  a  better  prospect  than 
poorly  nourished  weaklings.  High  fever,  many  stools,  much  vomiting,  much 
mucus,  marked  nervous  symptoms  and  signs  of  toxtemia  are  of  evil  omen. 

Treatment. — The  treatment  of  ileocolitis  consists  in  the  application  of 
mild,  continuous,  counterirritation  over  the  abdomen  by  means  of  a  spice 
poultice,  which  consists  of  equal  parts  of  powdered  nutmeg,  allspice,  cloves, 
and  cinnamon,  moistened  with  warm  brandy  or  vinegar.  If  this  cannot  be 
had  a  mustard  plaster,  composed  of  one-quarter  to  one-half  mustard  flour 
and  wheat  flour,  may  be  applied,  the  idea  being  to  produce  continuous,  but 
not  severe,  counterirritation. 

The  child's  diet  should  be  carefully  regulated.  If  it  is  passing  undigested 
food  in  its  stools,  those  articles  which  are  not  being  properly  dealt  with 
by  the  digestive  apparatus  should  be  withheld.  If  undigested  curds  of 
milk  are  present,  milk  should  be  stopped,  or  diluted  sufiiciently  to  make  its 
digestion  easy,  and  pepsin  and  hydrochloric  acid,  or  pancreatin  with  bicar- 
bonate of  soda,  should  be  used  to  aid  digestion.  Beef-juice,  or  beef-broth, 
and  chicken-broth  may  be  administered,  and  if  the  child  is  not  a  very  young 
infant  their  nutritional  value  may  be  greatly  increased  by  adding  to  them 
strained  barley  or  wheat  gruel.  The  digestion  of  these  vegetable  broths 
should  be  aided  by  the  use  of  liquid  pancreatin  or  liquid  taka-diastase.  If 
there  are  any  evidences  of  inactivity  of  the  liver,  minute  doses  of  calomel 
every  third  or  fourth  day  are  advantageous. 

If  mucus  is  present  in  considerable  quantity  in  the  stools  a  moderate  dose 
of  castor  oil,  varying  from  a  drachm  to  a  tablespoonful,  may  be  used  once 
or  twice.  Griping  may  be  prevented  by  the  addition  of  a  few  drops  of 
paregoric. 

In  some  instances  small  doses,  such  as  1  or  2  grains  of  chloride  of  ammo- 
nium dissolved  in  fluid  extract  of  licorice  and  water,  may  be  given  twice  or 
thrice  a  day. 


CHOLERA  INFANTUM  613 

If  the  illness  occurs  in  hot  weather,  it  may  be  impossible  to  produce  a 
cure  without  the  aid  of  a  change  in  climate.  If  the  child's  home  is  in  the 
city,  removal  to  the  seashore  may  be  absolutely  necessary;  w^hereas,  if  the 
condition  develop  while  at  the  seashore,  removal  to  a  moderate  altitude  of 
1000  or  2000  feet  is  advisable. 

Antidysenteric  serum  may  be  given  if  an  examination  of  the  stools  reveals 
the  presence  of  the  Bacillus  dysenterioe. 


CHOLERA  INFANTUM. 

Definition. — Cholera  infantum  is  an  acute  affection  of  infancy  charac- 
terized by  profuse  watery  purging,  rapid  emaciation,  and  profound  depres- 
sion. It  is  so  closely  related  to  that  form  of  diarrhoea  due  to  catarrhal 
enteritis  in  adults  and  to  that  met  with  in  the  ileocolitis  of  infancy  that  it 
scarcely  deserves  a  separate  consideration  from  the  standpoint  of  etiology 
and  pathology,  yet  its  symptom-complex  aids  us  to  some  extent  in  making 
it  a  distinct  entity  at  the  bedside.  The  malady  is  almost  always  met  with 
in  the  hot  months  of  the  year. 

Etiology. — The  causes  of  cholera  infantum  are  practically  identical  with 
those  of  enterocolitis,  and  in  a  considerable  number  of  cases  the  bacillus  of 
dysentery  (Shiga's  bacillus)  is  the  cause.  Thus,  in  a  series  of  cases  of  typical 
summer  diarrhoea  occurring  in  Baltimore,  Duval  and  Bassett  isolated  this 
bacillus  from  no  less  than  42  patients.  It  was  found  in  large  numbers  in  the 
stools  of  acute  cases  and  in  the  mucous  membrane  of  the  bowel.  They 
could  not  find  this  bacillus  in  the  stools  of  25  healthy  children,  nor  in  those 
of  patients  with  ordinary  diarrhoea. 

Pathology  and  Morbid  Anatomy. — When  a  case  of  cholera  infantum  comes  to 
autopsy  the  mucous  membrane  lining  the  bowel  presents  a  peculiar  pallor, 
which  is  most  marked  in  the  ileum.  The  colon  may  show  areas  of  conges- 
tion. The  tissues  of  the  body  are  shrunken  because  of  the  profuse  purging, 
the  body  is  wasted,  the  skin  wrinkled,  and  the  eyes  sunken.  The  belly  may 
be  distended  or  collapsed.  If  enterocolitis  has  been  present  before  the 
severe  choleraic  character  of  the  purging  is  developed,  the  lesions  described 
under  the  discussion  of  that  disease  may  be  found. 

Symptoms. — Cholera  infantum  receives  its  name  because  its  chief  symp- 
toms are  like  those  of  Asiatic  cholera,  in  that  profuse  watery  purging,  inces- 
sant vomiting,  and  collapse  soon  develop.  The  pulse  rapidly  becomes  weak 
and  feeble,  the  extremities  cold  and  the  face  pinched,  so  that  the  expression 
of  the  child  may  be  shrunken  like  that  of  a  very  aged  person.  This  anxious, 
pinched  look,  with  a  peculiar  drawing  down  of  the  mouth,  as  if  the  child 
were  about  to  cry,  is  very  characteristic.     The  fontanelles  are  depressed. 

At  first  the  child  may  be  exceedingly  restless  and  peevish,  but  if  the  attack 
is  severe  it  speedily  becomes  apathetic,  listless,  and  finally  comatose. 
Although  the  peripheral  temperature  is  low,  the  rectal  temperature  is  often 
very  high,  even  to  105°  or  106°.  There  is  often  a  mottling  of  the  skin,  due 
to  the  poor  capillary  circulation.  Thirst  is  excessive,  and  cannot  be  relieved 
because  of  constant  vomiting.   The  urine  is  scanty  or  suppressed.   As  the  end 


614  DISEASES  OF   THE  INTESTINES 

approaches,  the  patient  develops  irregular  respirations,  the  head  is  retracted, 
the  temperature  is  subnormal,  and  the  life  ends.  When  the  cerebral  symp- 
toms are  marked,  the  condition  is  called  one  of  "spurious  hydrocephalus," 
a  most  unfortunate  and  inaccurate  name. 

The  symptoms  are  not  only  those  of  exhaustion,  but  of  profound  toxaemia 
as  well. 

Prognosis. — Given  a  case  of  well-advanced  cholera  infantum,  the  prog- 
nosis is  very  grave.  It  depends  upon  the  vitality  of  the  child,  the  severity 
of  the  purging  and  vomiting,  the  degree  of  response  to  treatment,  and  the 
age  of  the  patient,  for  very  young  infants  seldom  recover  if  the  disease  is  once 
well  developed. 

Treatment. — The  treatment  of  cholera  infantum  consists  first  of  all  in  the 
absolute  prohibition  of  milk  for  twelve  or  twenty-four  hours  after  the  patient 
is  first  seen.  It  matters  not  whether  the  milk  be  from  the  breast  or  from  the 
bottle,  it  must  nevertheless  be  withheld  from  the  child.  Indeed,  it  may  be 
said  that  there  is  little  use  in  treating  these  cases  medicinally  if  milk  is  given. 
This  is  particularly  so  when  undigested  particles  of  milk  are  passed  in  the 
stools. 

During  the  period  in  which  milk  is  forbidden,  the  child  should  receive 
5  to  10  drops  of  Valentine's  beef-juice  in  1  or  2  tablespoonfuls  of  cool 
water  every  hour  or  two,  according  to  its  thirst  and  its  age.  In  other 
instances  a  rump  steak  may  be  heated  sufficiently  to  start  its  juices, 
then  squeezed  in  a  meat-press  or  lemon-squeezer,  and  this  juice,  pure  or 
diluted  with  cool  water,  may  be  given  to  the  child.  When  these  juices  cannot 
be  obtained,  or  where  for  some  reason  they  cannot  be  taken,  barley-water, 
rice-water,  or  a  water  made  by  boiling  and  straining  wheaten  grits  may  be 
used. 

Over  the  abdomen  of  the  child  should  be  applied  a  spice  plaster,  com- 
posed of  a  tablespoonful  each  of  powdered  allspice,  cloves,  nutmeg,  and 
cinnamon.  This  should  be  moistened  with  warm  brandy  or  vinegar,  and 
renewed  as  frequently  as  it  becomes  hard  or  dry. 

The  child  should  receive  internally  gig-  of  a  grain  of  podophyllin  dissolved 
in  a  few  drops  of  brandy,  and  mixed  with  a  little  water  just  before  it  is  taken, 
every  hour  until  three  or  four  doses  have  been  used;  or,  instead,  5-^^^  of  a 
grain  of  bichloride  of  mercury  may  be  given  in  the  same  manner.  If  the 
vomiting  is  incessant,  it  may  be  necessary  to  get  the  solution  of  bichloride  or 
podophyllin  into  the  stomach  by  dropping  the  medicine  into  the  mouth  of  the 
child  with  a  medicine-dropper,  and  only  introducing  a  few  drops  at  a  time. 
It  is  of  the  greatest  importance  that  the  liver  shall  secrete  and  expel  bile  into 
the  intestine.  The  appearance  of  a  little  bile  upon  the  diaper  of  the  child  in 
place  of  the  colorless  liquid  which  has  previously  been  expelled  is  a  most 
encouraging  sign,  and  its  absence  is  correspondingly  discouraging. 

If  there  is  much  distention  of  the  abdomen,  some  relief  to  the  tympany 
may  be  given  by  introducing  a  rectal  tube  through  which  the  gas  may  escape, 
and  if  the  stools  are  exceedingly  fetid  and  musty  it  is  often  advantageous  to 
irrigate  the  lower  bowel  with  Jiormal  salt  solution  once  or  twice  a  day,  insert- 
ing into  the  rectum  alongside  the  nozzle  of  the  fountain  syringe  a  soft-rubber 
catheter,  through  which  the  injected  material  may  readily  return.    The  tube 


APPENDICITIS  615 

attached  to  the  syringe  should,  however,  pass  up  into  the  bowel  for 
eight  inches  or  a  foot;  while  the  tube  of  exit  should  be  just  within  the 
sphincter. 

If  much  tenesmus  is  present,  with  a  tendency  to  eversion  of  the  bowel,  1 
or  2  tablespoonfuls  of  olive  oil  containing  2  grains  of  iodoform  may  be 
injected  once  or  twice  a  day,  or  even  oftener,  for  its  local  anaesthetic  effect 
upon  the  intestine,  and  after  this  injection  the  anus  should  be  supported  by 
the  nurse's  hand,  the  ball  of  her  thumb,  covered  by  a  napkin,  being  placed 
between  the  buttocks  to  aid  in  the  retention  of  the  fluid.  In  children,  older 
than  six  or  eight  months,  good  results  sometimes  follow  the  use  of  weak  sul- 
phuric acid  solutions.  Thus,  1  minim  of  aromatic  sulphuric  acid  may  be 
given  in  4  tablespoonfuls  of  cool  water  every  two  hours.  The  acid  not 
only  acts  as  an  astringent,  but  it  probably  also  aids  in  destroying  infecting 
micro-organisms . 

When  symptoms  of  collapse  ensue  the  patient  should  be  surrounded  by 
hot  bottles,  but  care  should  be  taken  that  a  peripheral  low  temperature  is 
not  considered  as  representing  the  temperature  of  the  central  portions  of 
the  body,  which  are  often  highly  febrile.  When  the  peripheral  temperature 
is  low,  the  central  temperature  high,  and  the  circulation  in  the  peripheral 
capillaries  is  impaired,  so  that  the  child  is  somewhat  livid  and  its  skin  mot- 
tled, excellent  results  will  often  be  obtained  by  immersing  it  several  times, 
for  a  fraction  of  a  minute,  in  quite  hot  water  for  the  purpose  of  producing 
a  certain  amount  of  reaction,  relieving  internal  congestion,  and  bringing  the 
blood  to  the  surface.  If  marked  fever  is  present  and  the  extremities  are  hot, 
equally  good  results  may  come  from  the  use  of  a  cold  bath  or  cold  sponging 
with  friction. 

Some  practitioners  have  been  in  the  habit  of  employing  minute  doses  of 
morphine,  hypodermically,  or  by  the  mouth.  In  some  instances  this  method 
of  treatment  may  be  advantageous,  but  too  often  it  seems  to  increase  the 
toxaemia  from  which  the  patient  is  suffering. 

A  very  valuable  method,  which  should  always  be  recollected  in  desperate 
cases,  is  the  use  of  normal  salt  solution  by  hypodermoclysis. 


APPENDICITIS. 

Definition. — Appendicitis  is  an  inflammation  involving  the  appendix  vermi- 
formis. 

History. — Although  inflammation  of  the  appendix  vermiformis  had  been 
described  by  a  number  of  physicians  many  years  before  Reginald  Fitz,  of 
Boston,  prepared  his  classical  paper  on  this  subject  in  1886,  the  importance 
and  frequency  of  this  condition  was  not  appreciated  until  he  called  attention 
to  it. 

Etiology. — The  causes  of  appendicitis  may  be  divided  into  two  classes, 
namely,  those  that  depend  upon  the  anatomical  structure  and  position  of  the 
appendix  and  those  that  arise  as  the  result  of  changes  in  its  walls. 

The  appendix  vermiformis  is  a  vestige  of  what  was  a  large  and  important 
portion  of  the  alimentary  canal  in  our  early  evolutionary  ancestry,  and,  like 


616  DISEASES  OF  THE  INTESTINES 

most  vestiges  of  this  character,  its  tissues  are  possessed  of  less  vital  resist- 
ance than  are  those  of  active  organs.  This  is  the  first  reason  why  severe  in- 
flammatory processes  so  often  arise  in  it.  Again,  it  is  a  sac  the  neck  of  which 
is  usually  narrower  than  the  rest  of  its  cavity,  and  as  a  consequence  it  happens 
that  infecting  micro-organisms  find  their  way  into  it,  and  when  imprisoned 
there  by  swelling  of  the  mucous  membrane  rapidly  attack  and  destroy  the 
epithelial  lining  of  the  appendix  and  migrate  into  its  walls.  As  is  well  known, 
nothing  is  more  favorable  for  the  growth  of  micro-organisms  than  the  pres- 
ence of  warmth,  moisture,  and  a  condition  in  which  drainage  is  impossible. 
Nothing  is  less  favorable  to  the  vital  resistance  of  a  part  than  swelling, 
with  pressure  upon  the  bloodvessels  and  lymphatic  channels.  Still  another 
anatomical  cause  of  disease  in  the  appendix  is  the  fact  that  the  mesoappen- 
dix  is  very  short,  and  this  results  in  the  appendix  being  curved  or  drawn  on 
one  side.  The  mesoappendix  carries  the  chief  bloodvessel  which  nourishes 
the  appendix,  and  if  from  swelling,  or  other  cause,  the  appendix  is  distorted 
or  twisted,  the  circulation  of  blood  in  the  nutrient  vessels  may  be  so  impaired 
that  the  vitality  of  the  part  is  greatly  decreased.  Again,  in  those  cases  in 
which  the  appendix  is  very  long  (for  it  varies  in  length  from  one  to  six  inches) 
the  free  end  may  become  attached  to  other  parts  and  become  greatly  dis- 
placed, the  appendix  itself  being  twisted.  Finally,  the  fact  that  the  appendix 
lies  near,  or  on,  the  ileopsoas  muscle  may  aid  in  provoking  appendicular 
irritation,  and  this  is  probably  one  of  the  reasons  why  appendicitis  so  often 
follows  violent  rowing,  golfing,  and  bicycling. 

Among  the  causes  which  exist  in  the  appendix  itself,  in  the  sense  that  they 
are  present  in  its  cavity,  is  the  presence  of  fecal  concretions  (20  per  cent.), 
and  rarely  foreign  bodies,  of  which  a  multitude  have  been  recovered,  such 
as  pins,  tacks,  seeds,  and  other  objects  accidentally  swallowed.  Occasionally 
intestinal  worms,  amoebre,  and  other  parasites  have  been  found.  Foreign 
bodies,  however,  are  comparatively  rarely  found  in  this  viscus  (less  than  4 
per  cent.).  Primary  tumor  of  the  appendix,  of  which  a  number,  mainly 
carcinoma,  have  been  reported,  appears  to  be  at  least  a  predisposing  cause 
in  some  instances. 

In  a  very  large  proportion  of  cases,  nearly  85  per  cent.,  the  micro-organism 
which  is  directly  responsible  for  the  inflammation  is  the  Bacillus  coli  com- 
munis, which  is  always  present  in  the  bowel,  and  is  benign  unless  the  condi- 
tions are  such  as  to  make  it  malignant,  as  when  it  is  confined  in  a  swollen 
and  closed  appendix.  In  some  instances  the  streptococcus  or  the  staphylo- 
coccus is  the  cause.  Any  micro-organism  capable  of  exciting  inflammation 
upon  gaining  access  to  the  appendix  may  be  the  cause.  Thus,  the  pneumo- 
coccus,  the  pyogenic  staphylococcus  and  streptococcus,  the  typhoid  bacillus, 
and  even  the  ray  fungus  may  act  in  this  way. 

Errors  in  diet  may  be  a  productive  factor,  for  in  a  certain  number  of  cases 
of  appendicitis  there  is  a  history  that  the  patient  has,  a  few  hours  before  the 
attack  or  immediately  before  it,  eaten  heartily  of  ordinary  or  indigestible  food. 

The  age  of  the  patient  is  undoubtedly  an  important  factor  in  the  develop- 
ment of  the  malady.  Although  it  is  met  with  in  young  children  and  in  old 
persons — that  is,  after  sixty  years  of  age— appendicitis  is  certainly  very  much 
more  rare  at  these  periods  of  life  than  in  the  interval.    For  this  there  is  no 


APPENDICITIS  617 

adequate  explanation.  The  period  of  greatest  frequency  is  from  the  fifteenth 
to  the  thirtieth  year,  and  Fitz  states  that  more  than  half  the  cases  occur 
before  the  twentieth  year. 

Another  predisposing  factor  is  sex.  About  six  times  as  many  men  as 
women  have  appendicitis.  This  is  in  part  due  not  only  to  greater  physical 
activity,  but  to  the  more  frequent  causes  of  intestinal  catarrh  in  males.  It 
also  depends  in  part  upon  the  fact  that  women  have  a  second  blood  supply 
to  the  appendix,  at  least  in  many  cases,  namely,  an  artery  which  passes  from 
the  right  ovary  to  the  appendix  by  means  of  a  fold  of  peritoneum,  which  has 
been  called  the  appendiculo-ovarian  ligament.  By  this  means  a  greater 
blood  supply  enables  the  part  to  combat  infection  when  the  mesenteric  vessel 
is  twisted.  Appendicitis  is  more  frequent  in  the  well-to-do  than  in  the 
poorer  classes,  although  it  might  be  supposed  that  the  greater  muscular 
exertion  in  the  latter  class  would  predispose  its  members  to  the  malady. 

Pathology  and  Morbid  Anatomy. — A  knowledge  of  the  pathology  of  appendi- 
citis makes  it  possible  to  understand  the  symptoms  which  will  be  described 
farther  on,  for  these  depend,  to  a  large  extent,  upon  the  severity  of  the 
changes  in  the  appendix,  and  upon  the  extent  to  which  adjacent  tissues  are 
diseased. 

Appendicitis  may  be  divided  for  pathological  study  into  the  catarrhal, 
ohliterative,  ulcerative,  gangrenous,  and  'perforative  types. 

In  the  catarrhal  type  hyperasmia  and  congestion  of  the  deeper  layers  of  the 
appendix  may  be  present,  but  the  chief  lesion  is  in  the  mucous  membrane 
lining  the  organ.  This  results  in  a  free  secretion  of  mucus  and  in  distention 
of  the  appendix,  the  cervix  of  which  is  occluded  by  the  swelling  of  its  lining 
membrane.  By  this  means  pain  is  produced  and  colic  ensues,  partly  as  a 
result  of  the  endeavor  of  the  appendix  to  expel  its  contents  into  the  colon 
and  partly  as  a  result  of  colic  in  the  large  bowel  produced  by  reflex  irritation. 
It  can  be  readily  seen  that  this  state  may  from  this  point  proceed  to  recovery 
by  a  decrease  in  the  constriction  of  the  neck  of  the  appendix  and  the  escape 
of  its  contents,  or  to  a  far  more  grave  condition  dependent  upon  a  continu- 
ance of  the  stoppage,  a  local  and  general  impairment  of  resistance,  and  the 
presence  of  a  virulent  micro-organism.  If  the  attack  has  been  preceded 
by  others,  so  that  the  vitality  of  the  part  is  already  greatly  impaired  and 
altered,  the  case  is  even  more  grave. 

Even  in  the  mild  catarrhal  form  just  described  there  is  usually  left 
behind  distinct  traces  of  the  presence  of  the  acute  attack,  and  this  predis- 
poses the  patient  to  another  seizure.  In  those  cases  in  which  the  catarrhal 
process  is  severe  and  in  which  the  submucous  tissues  are  much  affected,  it 
not  infrequently  happens  that  after  the  acute  process  passes  away  a  subacute 
or  low-grade  inflammatory  condition  ensues,  which  results  in  round-cell 
infiltration  and  in  thickening  of  the  mucous  membrane  and  submucous 
tissues.  The  epithelium  lining  the  appendix  is  desquamated  and  slight 
ulceration  may  occur,  with  the  result  that  the  calibre  of  the  appendix  may 
be  greatly  decreased  in  several  places,  or  even  entirely  closed  by  the  adhesion 
of  its  opposing  surfaces.    In  this  manner  appendicitis  obliterans  is  developed. 

If  considerable  quantities  of  pus,  or  mucus,  are  imprisoned  back  of 
the  constriction,   pain,  tenderness,  and  attacks  of  appendicular  colic,  or 


618  DISEASES  OF  THE  INTESTINES 

true  appendicitis,  are  prone  to  recur.  When  the  inflammatory  process  is 
severe  enough  to  affect  the  external  surface  of  the  appendix  the  free  end  or 
side  of  it  may  become  adherent  to  the  bowel  or  other  parts,  and  by  this  means 
the  appendix  may  not  only  be  distorted  and  held  fast,  but  the  infecting  germs 
may  pass  through  its  walls  and  affect  nearby  structures. 

When  the  ulcerative  type  is  present,  it  is  a  condition  but  one  degree 
removed  in  severity  from  that  just  spoken  of,  and  it  can  be  readily  seen  that 
no  sharp  dividing  line  can  be  drawn  except  that  there  is  greater  likelihood  of 
the  adjacent  tissues  being  infected,  owing  to  the  fact  that  the  unprotected 
submucosa,  with  its  lymphvessels  and  bloodvessels,  is  a  fair  field  for  infec- 
tion and  for  its  further  spread.  Ulceration  is  particularly  prone  to  occur  if 
a  fecal  concretion  or  other  foreign  body  is  present  which  may  damage  the 
mucosa.  Tuberculosis  or  typhoid  fever  may  cause  it.  Sometimes  a  foreign 
body  may  be  the  cause  of  such  deep  ulceration  that  perforation  occurs,  or  in 
other  cases  the  floor  of  the  ulcer  is  unable  to  stand  the  stress  of  accumulated 
pus  or  mucus,  and  the  same  accident  happens. 

The  gangrenous  type  of  appendicitis  is  the  most  important  of  all  lesions 
of  the  appendix,  not  because  it  is  the  most  frequent,  but  because  it  not  rarely 
changes  the  apparently  healthy  man  of  one  hour  into  a  corpse  within  a  few 
hours,  and  this  without,  it  may  be,  any  history  of  previous  attacks  which  would 
lead  to  the  belief  that  the  appendix  was  gravely  diseased  and  unable  to  resist 
infection.  When  this  state  is  present  in  its  most  severe  type,  the  appendix 
undergoes  rapid  necrosis,  its  tissues  become  gangrenous,  and  it  may  slough 
away  completely  in  so  short  a  time  as  forty  hours,  so  that  it  may  be  impos- 
sible to  find  it  in  the  pus  which  is  set  free  by  the  surgeon's  knife,  only  shreds 
of  tissue  being  present.  In  other  cases,  however,  the  process  is  not  so 
destructive,  but  nevertheless  the  organ  is  utterly  necrotic  and  decomposed. 
In  many  instances  the  gangrenous  process  may  not  involve  the  entire 
appendix,  but  occur  in  one  spot,  speedily  causing  perforation  and  so 
endangering  the  life  of  the  patient. 

Gangrene  of  the  appendix  arises  from  the  invasion  of  its  walls  by  virulent 
infecting  germs  when  its  vitality  is  impaired  by  some  unknown  cause,  or  it 
follows  from  thrombosis  or  capillary  stasis  in  its  nutrient  bloodvessels, 
whereby  the  same  destruction  ensues.  Gangrenous  appendicitis  may  be 
rapid,  widespread,  and  fatal,  or  the  vital  forces  of  the  patient  may  be  suffi- 
ciently vigorous  in  the  work  of  resistance  to  wall  off  the  infected  area  by 
lymph,  and  so  confine  the  morbid  process  to  the  immediate  neighborhood  of 
the  part  affected. 

The  secondary  effects  of  the  pathological  processes  just  described  are 
dependent  entirely  upon  their  severity  and  the  ability  of  the  patient  to  pro- 
tect himself  from  general  infection.  The  acute  catarrhal  form  rarely  leaves 
behind  it  anything  more  than  some  thickening  of  the  walls  of  the  appendix, 
with  an  associated  susceptibility  to  another  attack.  If  all  the  coats  have  been 
involved,  the  tissues  about  the  appendix  become  fihed  with  lymph,  and  the 
consequent  induration  may  be  extreme,  the  appendix  becoming  buried  in 
an  adherent  mass,  which  may  not  only  hide  it  from  view,  and  form  with 
the  adjacent  tissues  a  matrix,  but  prevent  the  surgeon  from  finding  the 
appendix  if  operation  is  attempted. 


APPENDICITIS  619 

When  the  inflammation  is  severe  enough  to  result  in  the  escape  of  infection 
into  the  adjacent  tissues,  we  not  only  have  pus  in  the  appendix,  but  in  the 
surrounding  parts  as  well,  a  perityphlitic  or  periappendicular  abscess,  and 
in  those  instances  in  which  the  appendix  is  perforated  either  an  abscess 
is  formed  and  walled  off  from  the  general  peritoneum  by  adhesions  or  a 
general  peritonitis  ensues. 

The  situation  of  the  abscess  varies  with  the  direction  in  which  the  infec- 
tion escapes  from  the  appendix.  If  the  infection  escapes  anteriorly  the 
site  of  the  abscess  is  often  between  the  navel  and  the  anterior  superior 
spine  of  the  ilium.  When  it  escapes  on  the  surface  of  the  iliac  fascia  or 
in  the  pelvis  behind  the  csecum,  it,  of  course,  lies  behind  the  peritoneum, 
not  in  the  serous  cavity,  and  retroperitoneal  suppuration  develops.  From 
here  the  pus  may  burrow  in  as  many  ways  as  only  pus  can  burrow,  upward 
to  the  region  of  the  kidney,  downward  along  the  psoas  muscle  into  the 
thigh,  or  it  may  discharge  into  the  bladder,  the  rectum,  or  even  into  the 
scrotum. 

On  the  other  hand,  it  must  not  be  forgotten  that  appendicular  abscess 
may  develop  with  very  little  systemic  disturbance  and  exist  for  a  long  time 
entirely  unsuspected,  being  found  by  accident,  it  may  be,  when  seeking  for 
some  cause  of  distress  and  discomfort  with  impaired  health.  At  other 
times  such  an  abscess,  after  having  developed  insidiously,  produces  signs  of 
septic  infection  the  source  of  which  at  first  cannot  be  traced. 

Finally,  attention  must  be  called  to  the  possibility  and  frequency  with 
which  infection  of  the  retroperitoneal  lymphatics  and  of  the  portal  vessels 
may  occur  from  disease  of  the  appendix.  Attention  has  been  called  to  this 
by  several  writers,  notably  by  A.  O.  J.  Kelly,  and  by  Munro  in  the  Thera- 
peutic  Gazette.  Not  only  may  retroperitoneal  abscess  be  due  to  perforation 
of  the  appendix  behind  the  peritoneum,  but  organisms  passing  along  the 
mesoappendix  produce  pus  when  they  reach  the  connective  tissues  in  the 
retroperitoneum.  Infection  of  the  portal  vessels  and  consequent  hepatic 
abscess  is  not  common,  but  several  cases  of  this  character  have  been 
reported. 

Symptoms. — It  must  be  manifest  from  the  description  just  given  of  the 
pathological  changes  that  appendicitis  is  a  malady  capable  of  producing 
very  different  symptoms  in  degree  and  kind.  It  is  not  possible,  for  this 
reason,  to  enumerate  a  set  of  symptoms  present  in  all  cases.  There  are, 
however,  certain  symptoms  which  are  fairly  constantly  present.  The  most 
constant  symptom  is  pain  in  the  abdomen.  This  may  be  diffuse,  or  at  least 
the  patient  may  not  be  able  to  localize  it.  Not  rarely,  if  the  physician 
repeatedly  asks  that  it  be  localized,  it  is  described  as  being  in  the  "pit"  of 
the  stomach  or  in  the  epigastrium.  If  the  epigastrium  is  pressed  upon  the 
pain  may  be  increased.  This  fictitious  localization  of  the  pain  in  the  early 
stages  of  appendicitis  may  be  most  misleading.  As  a  matter  of  fact,  how- 
ever, it  should  be  most  indicative,  and  every  person  seized  with  pain  of  this 
character  should  be  suspected  of  suffering  from  appendicitis.  In  some 
cases  the  pain  is  referred  to  the  left  iliac  region,  and  it  is  only  when  the 
physician  applies  pressure  to  the  right  iliac  area  that  the  patient  appreciates 
that  that  is  the  real  centre  of  his  suffering,  and  by  manifestations  of  an 


^20  DISEASES  OF  THE  INTESTINES 

unquestionable  character  shows  that  the  source  of  pain  has  been  discovered. 
There  is  one  spot  called  "McBurney's  point,"  situated  two  inches  from 
the  anterior  superior  spinous  process  of  the  ilium,  on  a  line  drawn  from 
this  point  to  the  navel,  in  which  pain  on  pressure  can  nearly  always  be 
elicited.  It  corresponds  rather  with  the  origin  than  with  the  tip  of  the 
appendix. 

The  pain  of  appendicitis  is  usually  severe  and  sharp,  and  in  some  cases 
agonizing.  It  is  usually  sudden,  in  onset,  and  for  this,  and  the  other  reasons 
just  given,  it  may  be  confused  at  first  with  renal  or  gallstone  colic.  I  have 
seen  more  than  one  case  in  which  the  diagnosis  of  acute  pleurisy  had  been 
made.  Occasionally  cases  are  met  with  in  which  the  pain  is  less  spasmodic 
and  more  dull  in  character,  but  they  are  the  exception. 

Perhaps  the  most  important  fact  that  can  be  impressed  upon  the  mind  of 
the  student  in  connection  with  the  symptom  of  pain  in  appendicitis  is  this, 
viz.,  that  the  sudden  cessation  of  pain  in  a  case  of  appendicitis  is  not  a  good 
sign,  but  an  exceedingly  bad  one  in  most  instances,  for  it  indicates  that 
the  distention  of  the  inflamed  appendix  has  been  relieved  by  perforation  or 
gangrene. 

When  the  pain  occurs  in  paroxysms,  it  is  thought  to  be  due  to  contractions 
of  the  appendix — appendicular  colic. 

Next  to  pain,  the  most  important  symptom  in  appendicitis  is  rigidity  or 
fixation  of  the  right  rectus  muscle.  Barring  voluntary  rigidity  of  this  muscle, 
which  can  usually  be  prevented  by  diverting  the  patient's  mind  from  his 
abdomen,  it  is  a  sign  of  great  reliability,  and  its  degree  often  measures  the 
severity  of  the  inflammatory  process. 

Vomiting  is  very  commonly  present  in  these  cases.  In  some  of  them  it 
occurs  so  early  as  to  seem  to  usher  in  the  attack.  This  is  particularly  apt 
to  be  the  case  if  the  stomach  has  been  overloaded  with  food  just  before  the 
attack.  If  the  stomach  is  empty  at  the  time  of  onset,  vomiting  is  often 
absent. 

The  febrile  movement  in  a  case  of  appendicitis  is  rarely  very  great.  The 
temperature  varies  from  99°  to  101°,  and  occasionally  reaches  102°  in 
adults.     In  children  it  may  be  higher. 

The  pulse  is  quick,  but  not  very  rapid,  unless  serious  abdominal  disturb- 
ance has  already  developed.  It  ranges  from  90  to  110  per  minute.  If  it 
goes  higher  than  this,  general  peritonitis  is  probably  present.  Distention  of 
the  belly  with  gas  is  usually  a  late  symptom,  and  if  well  marked  may  be  indic- 
ative of  general  peritonitis,  when  it  is,  of  course,  a  very  grave  symptom. 

After  the  malady  has  been  present  for  some  days  a  swelling  in  the  right 
iliac  region  may  appear  and  be  due  to  pus  or  to  a  large  protective  exudation 
of  lymph.  The  latter  formation  is,  however,  usually  met  with  in  relapsing 
cases  rather  than  in  primary  cases. 

Finally,  we  meet  with  cases,  usually  in  women,  but  sometimes  in  men,  in 
which  there  is  present  a  true  mucous  colitis  with,  it  may  be,  a  chronic  catarrh 
of  the  appendix.  In  these  persons  a  tiny  discharge  of  mucopus  may  daily 
infect  the  colon.  They  are  to  be  considered  as  cases  of  chronic  catarrhal 
appendicitis  and  operated  upon,  not  because  the  appendix  is  so  gravely  dis- 
eased as  because  it  causes  disorder  in  the  colon. 


APPENDICITIS  621 

Diagnosis. — When  the  question  arises  as  to  the  cause  of  severe  abdominal 
pain,  an  examination  of  the  blood  should  be  made.  If  a  distinct  leukocytosis 
is  present,  the  white  cells  of  the  polymorphonuclear  group  being  particularly 
increased,  it  is  indicative  of  an  acute  inflammatory  process  somewhere  in  the 
body,  and  probably  in  the  appendix,  if  the  symptoms  are  appendicular.  It 
is,  however,  a  great  mistake  to  allow  the  determination  to  do  an  operation 
to  rest  upon  this  sign,  for  it  has  at  times  proved  a  "hollow  reed."  At  best 
it  is  to  be  regarded  as  collateral  and  not  direct  evidence  of  appendicitis. 

One  of  the  most  important  differentiations  for  the  physician  and  surgeon 
is  that  between  appendicitis  and  early  typhoid  fever.  At  first  glance  this 
would  seem  to  be  easy,  but  those  of  experience  know  that  it  is  often 
difficult,  not  that  typhoid  fever  often  develops  suddenly,  but  that  appendi- 
citis may  develop  slowly  during  a  mild  influenzal  infection,  or  during  an 
attack  of  gastrointestinal  catarrh  that  has  been  obscure  in  its  nature.  Further 
than  this,  the  lymphoid  tissues  of  the  appendix  and  nearby  parts  are  usually 
involved  in  typhoid  fever,  and  may  cause  appendicular  symptoms.  (See 
Plate  I.)  These  localized  typhoid  lesions  may  cause  pain  and  tenderness 
in  the  right  iliac  area.  The  absence  of  very  severe  pain,  the  failure  to 
find  the  leukocytosis  of  acute  inflammation,  the  peculiarly  coated  tongue, 
the  presence  of  tympany,  and  the  later  development  of  rose  spots  and 
the  Widal  test  will  prove  the  case  to  be  one  of  typhoid  fever. 

Care  should  be  taken  that  pain  and  swelling  in  this  area  occurring  in  one 
who  has  tuberculosis  is  not  taken  for  appendicitis.  It  is  not  rare  to  find  these 
signs  in  consumptives  who  are  by  no  means  far  advanced  in  their  disease. 
The  condition  is  often  one  of  local  tuberculous  infection  of  a  chronic  type. 

Hepatic  colic  is  separated  from  appendicitis  by  the  presence  of  a  history  of 
previous  attacks,  by  the  absence  of  jaundice,  the  absence  of  tenderness  over 
the  gall-bladder,  and  by  the  fact  that  in  gallstone  colic  the  pain  is  referred  to 
the  chest  between  the  right  shoulder-blade  and  the  spine;  whereas,  in  appen- 
dicitis it  is  not  so  referred. 

Renal  colic  is  differentiated  from  appendicitis  by  the  pain  being  referred 
to  the  testicle,  pelvis,  or  the  inside  of  the  thigh;  by  the  fact  that  the  urine 
contains  blood,  if  not  macroscopically,  at  least  microscopically;  there  is  no 
excess  of  pain  on  pressure  over  "McBurney's  point,"  and  there  may  be  a 
previous  history  of  renal  stone.  Irritability  of  the  bladder  is  of  no  value  as  a 
differential  symptom,  as  it  is  often  present  in  both  renal  colic  and  appen- 
dicitis.    In  neither  form  of  colic  is  leukocytosis  marked. 

Ovarian  or  tubal  inflammation  may  simulate  appendicitis,  but  a  pelvic 
examination  will  usually  reveal  these  states. 

In  some  cases  of  intestinal  obstruction  the  pain  may  resemble  that  of 
appendicitis,  but  the  presence  of  obstinate  constipation,  the  development  of 
fecal  vomiting,  and  the  discovery  of  a  mass  in  the  belly  elsewhere  than  at  the 
appendix  may  enable  the  physician  to  make  a  differential  diagnosis. 

The  possibility  of  acute  hemorrhagic  pancreatitis  being  present  is  to  a  large 
extent  excluded  by  the  fact  that  it  is  a  very  rare  condition,  by  the  site  of 
the  pain  and  the  onset  of  early  collapse  in  this  disease. 

Osier  has  pointed  out  that  in  persons  subject  to  the  erythematous  erup- 
tions, severe  attacks  of  abdominal  pain  may  develop  which  give  rise  to  a 


522  DISEASES  OF  THE  INTESTINES 

diagnosis  of  appendicitis,  which  may  be  excluded  only  after  a  careful  study 
of  the  case  with  reference  to  this  state  and  urticaria. 

Prognosis. — The  prognosis  of  appendicitis  depends  largely  upon  the 
severity  of  the  condition.  Statistics  which  show  that  a  certain  percent- 
age of  all  cases  get  well  are  of  interest,  but  they  do  not  help  the  physician 
in  an  individual  case,  because  definite  statements  as  to  the  character  of  the 
statistics  are  not  given.  A  series  of  mild  catarrhal  cases  will  give  a  recovery 
percentage  of  100;  whereas,  a  series  of  severe  gangrenous  cases  will  give  a 
mortalitv  of  100  per  cent.  That  recovery  frequently  takes  place  is  shown  by 
the  fact  that  about  one-third  of  all  postmortems  show  signs  of  the  existence 
of  appendicular  disease  at  some  time  in  life,  yet  there  may  be  no  history  of 
such  an  illness. 

The  substance  of  our  present  knowledge  is  that  the  prognosis  in  an  ordinary 
attack  of  appendicitis  is  good  for  recovery  from  that  attack,  but  that  recur- 
rences are  likely.  In  the  perforative  or  gangrenous  type  the  prognosis  is 
always  grave  and  often  fatal.  Much  depends  upon  prompt  surgical  inter- 
ference. If  this  is  delayed,  death  is  the  result  in  the  majority  of  cases  of 
this  type. 

If,  however,  all  cases  of  appendicitis  of  whatever  type  are  considered 
statistically,  it  is  found  that  the  percentage  of  mortahty  is  only  about  15 
per  cent,  under  medical  treatment.     (See  Treatment.) 

Treatment. — There  is  perhaps  no  more  difficult  point  for  decision  in  med- 
ical practice  than  that  as  to  the  treatment  for  appendicitis.  It  is  impossible 
to  discuss  the  vast  array  of  arguments  for  and  against  early  operative  inter- 
ference in  this  brief  space. 

Given  a  case  of  appendicitis  of  the  acute  type,  the  first  thing  for  the 
physician  to  do  is  to  call  in  a  surgeon  as  a  consultant,  not  as  an  operator, 
provided  a  surgeon  qualified  to  do  good  abdominal  surgery,  if  it  is  required, 
is  obtainable.  If  none  such  can  be  had,  the  patient  is  far  better  off  without 
than  with  operation.  If  by  medical  treatment  the  case  can  be  controlled  and 
carried  through  the  acute  attack,  the  surgeon  should  not  interfere,  for  the 
mortality  of  operation  in  the  acute  stage  is  far  greater  than  it  is  when  the 
operation  is  performed  in  the  interval  between  the  attacks. 

Fourteen  years  ago  Fitz  showed  that  40  per  cent,  die  after  surgical  meas- 
ures, and  11  after  medical  treatment;  but  this  does  not  prove  that  the 
latter  is  better  than  the  former,  but  rather  that  the  surgical  cases  did  not 
get  to  the  surgeon  unless  desperately  ill.  At  present  the  percentage 
of  deaths  in  surgical  cases  is  far  less,  chiefly  because  they  are  seen 
early  enough  or  operation  is  performed  at  the  time  of  election;  but 
even  at  a  much  later  date  than  that  of  Fitz's  paper  we  find  Caley  (1899) 
recording  98  medical  cases  with  3  deaths,  and  102  surgical  cases  with  22 
deaths.  When  we  consider  Sprengel's  statistics  of  516  cases,  232  of  which 
were  operated  on  in  the  interval  with  2  deaths,  and  284  during  the  attack 
with  57  deaths  and  Sahli's  7000  cases  treated  medically  with  90  per  cent, 
recoveries,  the  value  of  delay,  in  mild  cases,  is  evident. 

The  plan  of  treatment  in  mild  cases  is  as  follows:  The  patient  is  required 
to  take  absolute  rest  in  bed.  An  ice-bag  is  placed  over  the  appendix.  No 
purgatives  are  given  nor  pain-relieving  drugs  are  to  be  used  unless  the  pain 


INTESTINAL  OBSTRUCTION  623 

is  excessive,  when  enough  morphine  may  be  used  hypodermically  to  take 
the  edge  off  of  the  agony,  but  never  enough  to  make  the  patient  comfortable 
or  to  make  him  sleep,  for  such  an  effect  masks  the  symptoms.  No  food  is  to 
be  given  by  the  mouth  and  no  drink  is  to  be  taken.  If  need  be,  liquid  can  be 
given  by  hypodermoclysis  or  by  rectal  injection.  If  the  bowels  move,  a  bed- 
pan must  be  used.  If  the  pulse  is  excitable  it  may  be  quieted  with  a  little 
aconite.  Under  this  treatment  the  acute  inflammatory  process  may  be 
arrested,  and  the  operation  can  be  performed,  if  need  be,  after  it  has  sub- 
sided. If  by  the  end  of  twelve  or  twenty-four  hours  the  symptoms  are  not 
rapidly  subsiding,  it  is  necessary  to  operate  at  once.  Fowler  has  shown 
that  when  operation  is  done  within  forty-eight  hours  83  per  cent,  recover. 
When  the  cases  are  left  to  the  fourth  day  60  per  cent,  recover;  to  the  fifth 
and  sixth  days,  58  per  cent.;  to  the  seventh  and  eighth  days,  50  per  cent.; 
and  to  the  ninth  and  tenth  days,  only  33  per  cent. 

The  signs,  however,  which  will  force  the  surgeon  to  immediate  operation 
when  the  patient  is  first  seen,  or  if  he  does  not  improve  under  treatment,  are: 
great  rigidity  of  the  rectus  muscle,  persistent  vomiting,  a  rapid  pulse  (above 
110),  an  anxious  facies,  and,  perhaps,  as  an  indication  of  some  importance, 
a  very  high  leukocytosis.  In  such  cases  the  only  salvation  of  the  patient  lies 
in  immediate  surgical  interference,  and  each  hour  of  delay  diminishes  the 
chance  of  recovery.  The  whole  question  is  one  of  severity  of  infection.  If 
there  is  reason  to  believe  that  the  tissues  are  becoming  infected  and  that  the 
local  tissues  cannot  resist  the  spread  of  the  inflammation,  then  we  must 
operate. 

This  question  of  deferring  operation  to  the  interval  between  the  attacks  is 
still  under  debate.  There  are  some  radicals  who  insist  that  operation  should 
be  resorted  to  without  waiting,  and,  indeed,  before  the  appendicitis  is  severe. 
There  are  others  who  are  content  to  wait  till  the  storm  is  past,  and  still  others 
who  believe  that,  given  a  patient  who  has  had  but  one  attack  of  moderate 
severity,  he  may  go  free  until  another,  or  a  third  attack,  makes  it  evident  that 
a  recurrence  is  likely  to  take  place  at  any  time,  when  he  should  be  operated 
upon  in  the  interval.  As  Dennis  well  says:  "The  plan  of  allowing  the  simple 
catarrhal  cases  which  are  doing  well  after  thirty-six  hours  to  recover  without 
immediate  operation,  and  relegating  them  subsequently  to  the  group  known 
as  interval  cases,  and  the  prompt  operation  after  thirty-six  hours  when  the 
cases  are  not  doing  well,  seems  to  hold  out  the  best  prospects  of  recovery. 
The  pendulum  has  swung  too  far  toward  indiscriminate  operation.  But 
now  the  introduction  of  the  interval  operation  has  brought  the  pendulum 
back  to  swing  within  the  proper  limits."     (See  Peritonitis.) 

It  must  not  be  thought  that  patients  who  have  had  recurrent  appendicitis 
can  be  promised  perfect  comfort  by  operation,  for  not  rarely,  while  they 
recover  from  the  operation,  they  continue  to  have  tenderness  and  pain  in 
the  right  groin  for  years. 

INTESTINAL  OBSTRUCTION. 

Definition. — Intestinal  obstruction  is  a  term  applied  to  a  condition  of  the 
bowel  in  which,  by  reason  of  some  mechanical  impediment  or  intestinal 


624  DISEASES  OF   THE  INTESTINES 

paralysis,  the  normal  movement  of  its  walls  and  contents  cannot  take  place. 
In  its  acute  form  it  occurs  as  the  result  of  no  less  than  six  causes:  first,  con- 
genital malj  or  motion;  second,  invagination,  or  telescoping  of  one  portion  of 
the  bowel  within  the  other,  or  so-called  intussusception;  third,  strangulation 
by  bands,  diverticula,  membranous  adhesions,  or  by  attachment  to  other 
organs,  and  by  the  slipping  of  a  coil  of  intestine  through  an  aperture;  fourth, 
as  a  result  of  twisting  of  the  bowel,  called  volvulus;  fifth,  from  lodgement  of 
foreign  bodies,  as  gallstones,  etc.;  and  sixth,  from  intestinal  "paralysis  and 
distention. 

Chronic  intestinal  obstruction  arises  from  stricture,  from  tumors  in  the 
bowel,  from  tumors  external  to  the  bowel,  and  from  the  impaction  of  fecal 
masses. 

Congenital  Malformation. — Congenital  malformations  usually  consist  in 
closure  of  the  intestinal  tube  by  reason  of  improper  development.  Such  a 
closure  may  exist  at  any  part  of  the  alimentary  canal  from  the  oesophagus 
to  the  anus.  Rarely  the  bowel  becomes  strangulated  or  incarcerated  or 
twisted  because  of  some  congenital  defect.  A  common  congenital  defect  is 
imperforate  anus  and  rectum.  Less  frequently  there  is  atresia  at  the  pylorus. 
Not  rarely  children  born  with  this  condition  have  other  congenital  defects 
in  the  alimentary  canal.  In  the  statistics  collected  by  Martin  and  myself, 
28  per  cent,  of  such  cases  showed  more  than  one  point  of  obliteration.  In 
cases  in  which  the  atresia  does  not  exist  in  the  anus  or  rectum,  it  is  most 
commonly  found  near  the  ileocsecal  valve,  in  the  duodenum,  or  in  the 
sigmoid  flexure. 

Symptoms. — The  symptoms  of  intestinal  obstruction  due  to  congenital 
causes  usually  appear  after  food  is  first  taken.  There  is  no  passage  of 
meconium  from  the  anus,  and  the  vomited  materials  are  often  fecal  in  odor 
and  in  appearance.  Not  rarely  violent  peristaltic  waves  can  be  seen  through 
the  abdominal  wall.    There  is  also  pain  and  efforts  at  defecation. 

Diagnosis. — An  examination  of  the  anus  or  rectum  will  usually  reveal  the 
cause  of  the  trouble.  If  the  finger  cannot  reach  the  obstruction,  a  bougie 
may  discover  it.  In  other  cases,  water  from  a  fountain  syringe,  hung,  not 
over  two  feet,  above  the  patient's  buttocks,  may  be  allowed  to  flow  into  the 
bowel  to  determine  its  capacity. 

Prognosis  and  Treatment. — The  prognosis  is,  of  course,  exceedingly 
unfavorable,  but  if  the  closure  is  near  the  anus  a  surgical  operation  may  give 
relief,  and,  as  all  die  without  operation,  the  knife  should  always  be  resorted  to. 
Death  ensues  from  inanition  or  exhaustion. 

Intussusception. — The  invagination  in  this  condition  is  composed  of  three 
layers  of  bowel.  The  intussusceptum  is  composed  of  the  entering  and 
returning  layers,  while  the  receiving  sheath  constitutes  the  intussuscipiens. 
To  the  point  where  the  entering  layer  is  turned  sharply  upon  itself  to  form 
the  returning  layer,  the  name  "apex"  is  applied.  The  word  "neck"  is 
applied  to  the  ring  which  results  from  the  flexure  formed  by  the  returning 
layer  as  it  merges  into  the  sheath. 

Intussusception  may  be  separated  into  divisions,  according  to  the 
severity  of  the  condition,  or  according  to  the  part  of  the  intestine  which 
is    involved.      Rafinesque    makes    three    divisions,  namely,  those   which 


INTESTINAL  OBSTRUCTION  625 

are  ultra-acute,  death  taking  place  within  the  first  twenty-four  hours; 
those  which  are  acute,  death  occurring  in  the  first  week ;  those  which  are 
subacute,  lasting  a  month  and  upward.  From  an  anatomical  stand- 
point, intussusception  may  be  divided  into  the  enteric,  in  which  the  small 
intestine  is  alone  involved;  the  ileocsecal,  in  which  the  ileum  and  caecum, 
together  with  the  ileocsecal  valve,  are  turned  into  the  colon;  and  the  ileo- 
colic, in  which  the  ileum  is  prolapsed  through  the  ileocfecal  valve,  the  latter 
retaining  its  proper  position,  at  least  for  a  time.  When  the  condition  is 
called  "colic,"  it  involves  the  colon  only.  In  still  other  cases,  the  rectum  is 
solely  affected,  forming  the  rectal  type  of  the  malady.  In  the  great  majority 
of  cases  the  upper  segment  of  the  gut  is  received  into  the  lower,  but  occa- 
sionally the  reverse  condition  occurs,  and  when  this  happens  the  term 
'"retrograde  intussusception"  is  apphed.  Double  and  triple  intussusception 
has  occasionally  been  noted. 

Etiology. — The  causes  of  intussusception  are  not  clearly  understood,  but 
probably  depend  upon  irregular  innervation  of  the  intestine,  whereby  a 
sudden,  spasmodic  contraction  of  one  portion  of  the  bowel  occurs,  the 
adjacent  portion  being  relaxed.  Intussusceptions  of  this  character  are  not 
infrequently  met  with  at  the  postmortem  table,  having  occurred  at  the 
time  of  dissolution.  Polyps  of  the  intestine  may  be  forced  along  the  lumen 
of  the  canal,  thereby  dragging  the  wall  at  the  point  of  attachment  and 
causing  intussusception. 

Frequency. — In  1652  cases  of  intestinal  obstruction,  excluding  hernia,  col- 
lected by  Leichtenstern  and  Bryant,  657  cases,  or,  approximately,  40  per 
cent.,  were  due  to  intussusception.  It  is  evident,  therefore,  that  this  form  of 
obstruction  is  not  rare.  Intussusception  occurs  most  frequently  during 
the  first  twelve  months  of  life.  After  the  fifth  year  it  becomes  compara- 
tively rare  until  the  fortieth  or  fiftieth  year,  when  it  again  increases  in  fre- 
quency. The  ileocsecal  region  is  the  favorite  site  of  invagination  at  all  ages, 
but  ileum  invagination  is  exceedingly  rare.  If  the  colic  form  occur,  it  is 
usually  at  the  sigmoid  flexure. 

Pathology. — The  pathological  changes  resulting  from  intussusception  con- 
sist in  an  extravasation  of  the  blood  into  the  mucous  membrane  and  mesen- 
tery of  the  part  affected,  and  in  an  acute  inflammatory  process  in  the  walls 
of  the  intestine,  which  particularly  affects  the  serous  surfaces  of  the  entering 
and  returning  layers,  so  that  they  become  glued  to  one  another.  Not  infre- 
quently, however,  this  condition  does  not  arise,  and  adhesions  do  not  form. 
As  a  result  of  the  strangulation  of  the  invaginated  bowel,  it  sometimes  hap- 
pens that  this  portion  of  the  intestine  sloughs  away,  and  if  sufficiently 
strong  adhesions  have  formed  between  the  neck  and  the  upper  portion  of 
the  intussusceptum,  the  coming  away  of  this  slough  may  result  in  the 
recovery  of  the  patient.  Very  large  portions  of  bowel  have  been  known  to 
be  passed  in  this  manner.  Pampier  has  recorded  one  instance  in  which 
124  cm.,  Bottcher  another  in  which  112  cm.  were  passed.  In  other 
instances,  however,  if  gangrene  of  the  bowel  develops,  perforation  and 
general  peritonitis  ensue. 

Symptoms. — These  depend  upon  the  degree  of  constriction  at  the  neck  of 
the  intussusceptum.  Usually  the  first  symptom  is  sudden  and  violent  pain. 
40 


626  DISEASES  OF  THE  INTESTINES 

This  pain  sometimes  ceases  as  suddenly  as  it  begins,  the  patient  being  in 
comparative  comfort.  After  an  interval  the  pain  returns,  and  the  paroxysms 
become  violent  and  prolonged,  v^ith  shorter  intervals  of  ease.  Pressure  does 
not  always  elicit  tenderness;  indeed,  at  times  it  seems  to  relieve  the  pain. 
Vomiting  is  an  even  more  constant  symptom  than  pain,  and  usually  begins 
early  in  the  attack,  but  in  adults  it  may  be  absent.  Of  all  forms  of  intussus- 
ception the  ileum  invagination  is  the  one  which  is  most  frequently  accom- 
panied by  early  vomiting,  chiefly  because  it  produces  the  most  complete 
obstruction.  In  children  a  very  constant  symptom  is  the  passage  of  bloody 
mucus.  Out  of  108  cases,  analyzed  by  Martin  and  myself,  occurring  in  the 
first  year  of  life,  this  symptom  was  absent  in  only  4. 

Tenesmus  and  bearing  down  is  also  commonly  met  with.  In  about  one- 
half  the  cases  the  tumor  can  be  felt  through  the  abdominal  wall,  and  under 
the  pliable  abdominal  wall  of  children  it  should  always  be  most  carefully 
sought  for.  Such  a  tumor  is  most  commonly  found  when  the  ileocsecal  type 
is  present.  Occasionally  in  the  colic  type  the  invaginated  bowel  can  be  felt 
in  the  rectum.  The  movement  of  the  bowel  may  distinctly  change  the 
position  of  the  tumor. 

Prognosis. — The  prognosis  in  intussusception  is  not  very  good.  Treated 
by  the  expectant  method,  the  mortality  is  70  per  cent.,  according  to  Leichten- 
stern.  The  statistics  of  Martin  and  myself  give  a  mortality  of  90  per  cent. 
The  mortality  is  greater  in  infants  than  it  is  in  older  persons.  The  sloughing 
and  discharge  of  the  intussusceptum  is  always  to  be  considered  distinctly 
favorable,  and  Martin  and  myself  found  that  in  408  children  in  whom  slough- 
ing had  not  taken  place  85  per  cent,  died,  while  of  149  who  passed  a  portion 
of  the  intestine  41  per  cent,  recovered.  Sloughing  rarely  occurs  before  the 
second  or  third  week  of  the  disease. 

Treatment. — The  treatment  consists  in  the  use  of  a  fountain  syringe  filled 
with  normal  salt  solution,  at  the  temperature  of  105°,  and  this  fluid  is  to  be 
injected  slowly  at  the  rate  of  4  ounces  to  the  minute.  The  pressure  in  the 
hydrostatic  syringe  should  not  be  over  two  pounds.  This  method  is  available 
only  when  the  intussusception  occurs  in  the  lower  portion  of  the  bowel.  If 
it  is  in  the  ileum  it  is  valueless.  If,  after  pressure  has  been  continued  for  the 
period  of  a  half-hour,  the  tumor  does  not  disappear  under  gentle  manipula- 
tion, abdominal  section  must  be  resorted  to  at  once.  The  older  statistics  in 
regard  to  this  operation  were  not  very  favorable,  most  of  them  being  gathered 
in  preantiseptic  days.  At  the  present  time  operation  gives  much  more 
favorable  results. 

Internal  Strangulation. — Internal  strangulation  by  bands  is  the  next 
most  frequent  form  of  intestinal  obstruction,  forming  about  36  per  cent,  of 
the  classified  cases.  The  condition  occurs  most  frequently  in  males  between 
the  twentieth  and  fortieth  years,  and  seems  to  arise  in  the  majority  of  cases 
from  a  former  peritonitis;  although  occasionally  the  bowel  is  strangulated  by 
slipping  through  the  foramen  of  Winslow  or  through  a  slit  in  the  diaphragm. 
Numerous  cases  of  obstruction  due  to  a  Meckel's  diverticulum  have  been 
reported.  The  diverticulum  may  become  twisted  or  by  adhesions  to  neigh- 
boring structures  form  a  constricting  band. 

Out  of  151  reported  cases  the  small  intestine  was  involved  in  133. 


INTESTINAL  OBSTRUCTION  627 

Symptoms. — The  symptoms  consist  in  sudden  agonizing  pain  which  is  con- 
stant, although  it  has  paroxysmal  increments.  The  pulse  becomes  rapid  and 
weak;  the  temperature  is  abnormal;  the  vomiting  is  persistent,  and  becomes 
jecal,  but  this  condition  of  the  vomit  rarely  develops  before  the  beginning 
of  the  third  day.  Constipation  is  present,  but  fecal  matter  may  be  passed 
from  the  lower  part  of  the  bowel  once  or  twice.  If  a  large  coil  of  gut  is 
involved,  a  distinct  area  of  distended  intestine  may  perhaps  be  found. 
While  the  presence  of  this  train  of  symptoms  in  a  young  child  would  be 
indicative  of  intussusception,  in  an  adult  it  is  indicative  of  strangulation  by 
a  band,  for  intussusception  is  rare  in  adults. 

The  only  method  of  treatment  which  is  satisfactory  is  operative. 

Volvulus. — According  to  Brinton,  this  condition  occurs  in  8  per  cent,  of 
fatal  cases  of  intestinal  obstruction;  according  to  Treves,  in  2.5  per  cent., 
and  according  to  Martin  and  the  writer's  statistics,  in  4  per  cent.  Some- 
times the  intestine  is  twisted  for  three  or  four  complete  turns.  The  condition 
occurs  most  frequently  after  middle  life,  and  occurs  more  frequently  in  men 
than  in  women.  In  18  cases  collected  by  Haven,  16  were  men.  In  Martin's 
and  my  own  table  of  100  cases,  64  were  men.  The  twist  is  usually  about  the 
mesentery  as  an  axis  and  involves  the  small  intestine.  Occasionally  it  may 
appear  in  the  colon;  rarely  the  stomach  may  be  affected.  The  twisting 
of  the  intestine  interferes  with  its  circulation,  and  this,  combined  with  the 
decomposition  of  the  intestinal  contents  and  the  resulting  distention,  soon 
produces  peritonitis,  and  even  perforation.  The  abdomen  is  prone  to 
become  immensely  distended. 

Symptoms, ^The  symptoms  consist  in  absolute  constipation,  vomiting,  and 
abdominal  distention.  Meteorism  is  constant.  The  points  in  favor  of  a 
diagnosis  of  volvulus  are  the  advanced  age  of  the  patient,  the  fact  that  the 
disease  usually  occurs  in  a  male,  that  the  pain  is  not  as  agonizing  as  in 
other  forms  of  obstruction,  and  that  the  obstructed  bowel  is  greatly  dis- 
tended. 

Prognosis. — The  prognosis  is  much  more  favorable  than  in  other  forms  of 
intestinal  obstruction.  When  intestinal  obstruction  is  due  to  paralysis,  the 
cause  is  most  frequently  some  injury  or  an  operation  upon  the  abdominal 
contents.  The  bowel  is  simply  dilated  or  kinked,  and  the  failure  in  peri- 
stalsis is  due  to  paralysis  of  its  muscular  fibres.  This  is  the  type  of  obstruc- 
tion which  all  abdominal  surgeons  greatly  fear  as  a  sequence  of  operation 
upon  the  peritoneal  contents. 

Treatment. — When  the  volvulus  is  due  to  paralysis  after  operation  it  is  to 
be  treated  by  the  administration  of  concentrated  salines  repeated  until  the 
bowels  are  moved.  When  distention  has  reached  a  very  great  degree  and 
vomiting  is  present,  salines  are  no  longer  useful.  The  rectal  tube  should  be 
passed  in  the  hope  of  exciting  peristalsis  and  drawing  off  gas.  The  patient 
should  be  freely  stimulated  and  the  rapidly  interrupted  faradic  current 
should  be  applied  to  the  abdominal  wall,  or  one  pole  may  be  placed  in  the 
rectum  and  the  other  passed  to  and  fro  over  the  abdomen. 

If  the  condition  is  not  due  to  paralysis  after  operation  purgatives  are 
absolutely  contraindicated,  and  enemata  can  be  of  no  value.  Such  cases 
should  be  subjected  to  operation. 


(528  DISEASES   OF   THE  INTESTINES 

Obstruction  from  Foreign  Bodies  arises  from  such  articles  as  coins, 
pebbles,  knives,  and  scissors,  gallstones  and  enteroliths.  While  gallstones  are 
usually  small,  they  at  times  may  be  very  large,  and  are  often  greatly  added 
to  by  concretions.  Thus,  Leichtenstern  states  that  one  such  stone  was  five 
inches  in  circumference,  and  he  describes  an  enterolith  nine  inches  in  circum- 
ference. Such  a  stone  is  usually  formed  by  concretions  about  a  foreign  body, 
as  a  cherry-stone.  Cases  of  intestinal  obstruction  of  this  character  are,  how- 
ever, very  rare,  about  0.2  of  1  per  cent,  of  all  cases.  The  obstruction  is 
usually  found  in  the  small  intestine,  sometimes  at  the  ileocsecal  valve,  and 
occurs  more  frequently  in  females  than  in  males. 


DUODENAL  ULCER. 

Ulcer  of  the  duodenum  is  probably  a  more  frequent  condition  than  is  gen- 
erally supposed,  and  in  some  cases  is  associated  with  ulcer  of  the  stomach. 
The  proportion  given  by  Burwinkel  of  gastric  and  duodenal  ulcer  is  12 
to  1.  On  the  other  hand,  von  Wyl  found  only  3  duodenal  ulcers  in  nearly 
13,000  postmortem  examinations,  and  Kinnicutt,  in  an  analysis  of  30,000 
postmortems,  places  its  frequency  at  0.4  of  1  per  cent.  The  condition  may 
arise  at  any  period  of  life,  but  is  most  frequent  between  the  tenth  and  fortieth 
years.  Hahn  has  recorded  a  case  in  a  child  only  a  day  and  a  half  old.  Such 
an  ulcer  must  have  been  antenatal. 

Unlike  gastric  ulcer,  the  great  majority  of  duodenal  ulcers  are  found  in 
men.  Murphy,  of  Chicago,  quotes  Laspeyres  as  stating  that  men  are 
affected  two  or  three  times  oftener  than  women.  Thus,  Krauss,  in  64 
cases,  found  the  ratio  to  be  10  to  1;  Lebert,  in  39  cases,  4  to  1;  Trier,  in 
54  cases,  5  to  1;  and  out  of  176  cases  collected  by  Weir,  144  were  in  men. 

Etiology. — Among  the  causes  of  duodenal  ulcer  may  be  mentioned 
burns,  which  in  some  unknown  way  produce  ulceration  in  this  portion  of 
the  bowel.  Renal  disease,  which  occasionally  results  in  the  ulceration  of 
the  large  bowel,  may  also  cause  this  lesion  in  the  duodenum.  Pulmonary 
tuberculosis,  which  produces  its  lesion  by  infection  of  a  solitary  follicle, 
and  diseases  of  the  heart  and  liver,  which  result  in  impairment  of  vitality 
in  the  intestinal  wall,   so   that   localized  infections  may  occur,  are   also 

causes. 

As  with  gastric  ulcer,  so  with  duodenal  ulcer,  a  large  number  of  theories 
have  been  advanced  as  to  its  direct  causation.  Most  authorities  at  the 
present  time  believe  that  it  is  due  to  erosion  produced  by  the  gastric  juice, 
the  vital  resistance  of  the  part  having  been  diminished  by  inflammation  or 
circulatory  changes.  That  acidity  of  the  gastric  contents  may  so  result  seems 
likely,  from  the  fact  that  ulcer  most  frequently  occurs  in  the  duodenum  near 
the  pylorus,  at  a  point  where  the  acidity  of  the  gastric  juice  may  be  but  little 
modified  by  the  alkaline  secretion  which  it  would  meet  a  few  inches  farther 
on  in  the  bowel. 

It  would  seem  probable,  however,  that  a  number  of  factors  may  produce 
this  form  of  ulcer,  acting  in  some  cases  together  and  in  other  cases  singly. 
These  factors  are  well  summed  up  by  Murphy  and  made  into  four  divisions: 


DUODENAL  ULCER  629 

hyperchlorhydria,  local  infection,  embolism  with  thrombosis,  and  foreign 
bodies.  To  these  four  divisions  Murphy  would  add  a  fifth,  namely,  disorders 
of  the  organs  of  elimination,  as  in  burns  of  the  skin  or  other  serious 
lesions  in  this  part  of  the  body,  as  pemphigus  and  erysipelas,  and  in  other 
cases  renal  disease. 

Pathology  and  Morbid  Anatomy. — Duodenal  ulcers  are  usually  single,  but 
they  may  be  multiple.  Out  of  233  cases  collected  by  Colhns,  195  were  single. 

Ulcer  usually  occurs  in  the  first  part  of  the  duodenum.  Out  of  149  cases 
collected  by  Perry  and  Shaw,  the  first  portion  of  the  duodenum  was  involved 
123  times,  the  second  portion  16  times,  and  the  third  and  fourth  portions 
twice.  These  statistics  agree  with  those  which  have  been  collected  concerning 
the  area  and  greatest  frequency  of  perforation  complicating  ulcer  of  the 
duodenum. 

When  perforation  occurs,  it  takes  place  nearly  twice  as  often  in  the 
anterior  as  in  the  posterior  wall,  still  more  rarely  in  the  superior  wall,  and 
almost  never  in  the  inferior  wall.  Perforation  occurs  much  more  frequently 
in  ulcer  of  the  duodenum  than  in  ulcer  of  the  stomach,  if  we  can  rely  upon 
the  statistics  which  have  so  far  been  collected.  Thus,  in  404  cases  mentioned 
by  Chvostek,  Collins,  and  Oppenheimer,  perforation  took  place  in  246.  On 
the  other  hand,  it  must  be  remembered  that  a  very  large  number  of  cases  of 
duodenal  ulcer  are  not  recognized  unless  perforation  does  occur,  and  it  is 
highly  probable  that  this  accident  is  far  less  frequent  in  duodenal  ulceration 
than  these  statistics  would  indicate,  because  it  is  a  well-known  fact  that 
duodenal  ulcer  is  a  condition  most  difficult  to  recognize  unless  it  is  found  in 
the  course  of  an  abdominal  section,  and,  further,  it  is  well  known  that  these 
ulcers  frequently  heal.  Thus,  Perry  and  Shaw  found  evidence  of  repair  in 
half  of  their  cases,  and  Krug,  in  1220  autopsies,  met  with  30  cases  of  healing 
of  duodenal  ulcer. 

As  in  perforations  of  the  stomach,  so  in  perforation  of  the  duodenum, 
a  general  peritonitis  ensues,  or  a  localized  peritonitis  may  develop, 
the  extravasated  materials  being  walled  off  from  the  rest  of  the  peri- 
toneal cavity  by  an  inflammatory  exudate.  As  with  gastric  ulcer,  so 
again  with  duodenal  ulceration,  adhesions  may  take  place  in  neighboring 
organs,  and  perforation  may  take  place  into  them.  Thus,  it  has  occurred 
that  the  duodenum  has  been  perforated,  and  so  permitted  its  contents  to 
enter  the  gall-bladder,  the  abdominal  aorta,  the  vena  cava,  the  portal  vein, 
the  superior  mesenteric  vein,  and  the  hepatic  artery;  but  Murphy  asserts  that 
a  gastroduodenal  fistula  has  never  been  found  as  a  result  of  perforation  of  a 
duodenal  ulcer.  In  some  instances  perforation  of  the  duodenum  has  resulted 
in  subphrenic  abscess. 

Symptoms. — The  symptoms  of  duodenal  ulcer,  unless  the  ulceration  pro- 
ceeds to  hemorrhage  or  perforation,  are  too  indefinite  to  make  a  positive 
diagnosis  possible  in  most  cases.  Indeed,  in  fully  half  the  cases  in  which 
duodenal  ulcers  are  found  at  autopsy,  there  have  been  no  symptoms  during 
life  which  have  raised  suspicion  of  its  existence. 

When  the  symptoms  do  occur,  they  so  closely  resemble  those  of  gastric 
ulcer  that  a  differentiation  may  be  impossible.  There  is  'pain  and  vomiting, 
and  if  a  bloodvessel  is  ulcerated  there  may  be  hoematemesis  or  bloody  stools. 


630  DISEASES  OF   THE  INTESTINES 

The  pain  is  usually  much  less  severe  than  in  ulcer  of  the  stomach,  but  at 
times  it  may  be  agonizing.  There  seems  to  be  a  general  consensus  of 
opinion  that  it  rarely  radiates  toward  the  back,  as  does  the  pain  of  gastric 
ulcer,  but  cases  have  been  reported  in  which  pain  in  the  neighborhood 
of  the  shoulder-blade  has  been  a  pronounced  symptom.  It  differs  from 
gastric  ulcer  in  that  the  taking  of  food  is  not  immediately  followed  by 
pain,  the  pain  being  delayed  for  several  hours  after  a  meal,  then  develop- 
ing when  the  food  enters  the  duodenum  from  the  stomach.  Moynihan 
says  that  the  nearer  the  ulcer  is  to  the  stomach,  the  sooner  is  the  pain 
developed. 

The  hemorrhage,  when  it  takes  place,  may  be  sufficiently  profuse  to 
cause  death,  or  it  may  be  small  in  amount  and  be  frequently  repeated,  in 
which  case  death  may  ultimately  occur  from  exhaustion.  Vomiting  rarely 
occurs  except  when  the  stomach  is  overloaded,  or  when  blood  enters  it  from 
the  duodenum. 

Perforation  of  a  duodenal  ulcer  may  be  the  first  manifestation  of  any 
lesion  in  this  portion  of  the  bowel.  According  to  Schwartz,  patients  suffer- 
ing from  perforation  of  the  duodenum  were  healthy  in  20  out  of  25  instances 
prior  to  the  accident,  and  in  Weir's  51  cases  -they  were  without  gastric  or 
duodenal  symptoms  in  25  out  of  34.  So,  too,  in  Perry  and  Shaw's  151 
cases,  91  per  cent,  presented  no  evidences  of  disease  until  perforation  or 
hemorrhage  developed. 

While  cases  of  ulcer  may  recover,  the  tendency  is  to  a  progression  of 
the  disease.  On  the  other  hand,  progress  does  not  necessarily  mean  early 
death,  for  Chvostek  has  reported  a  case  in  which  there  had  been  present 
symptoms  of  duodenal  ulcer  occasionally  for  thirty-nine  years. 

Symptoms  of  perforation  of  duodenal  ulcer  are  severe  epigastric  or  right 
hypochondriac  pain,  followed  it  may  be  by  collapse;  the  symptoms  resemble, 
perhaps,  acute  hemorrhagic  pancreatitis,  and  death  occurs  sometimes  as 
early  as  twenty-one  hours  after  the  accident.  The  symptoms  of  general 
peritonitis  soon  develop,  or,  if  the  lesion  is  localized  by  adhesions,  localized 
peritonitis  is  found,  as  already  stated.    Leukocytosis  is  usually  marked. 

Diagnosis. — The  tests  for  minute  traces  of  blood  in  the  stools,  which  are 
described  in  the  article  on  gastric  ulcer,  may  be  used  in  these  cases. 

Duodenal  ulcer  must  be  separated  from  gastric  ulcer,  if  possible.  In 
the  majority  of  instances  this,  perhaps,  cannot  be  done  unless  there  are 
bloody  stools,  the  character  of  the  blood  being  dark  and  tarry,  owing  to 
its  alteration  by  the  intestinal  juices.  If  it  is  bright  in  character,  it  probably 
comes  from  ulceration  of  a  lower  portion  of  the  bowel.  Another  important 
point  in  the  diagnosis  is  the  period  at  which  pain  develops  after  food  is  taken, 
for,  as  already  pointed  out,  the  development  of  pain  is  delayed  in  cases  of 
ulceration  of  the  duodenum,  and  is  immediate,  as  a  rule,  in  gastric  ulcer. 
While  von  Wyl  admits  that  it  is  impossible  to  make  a  differential  diagnosis 
in  90  per  cent,  of  the  cases,  he  gives  us  the  following  points  which  are  of  value 
in  differentiation: 


DUODENAL   ULCER  631 

Gastric  Ulcer.  Duodenal  Ulcer. 

1.  Usually  in  w6men  twenty  to  thirty -five         1.  Most  frequent  in  men. 

years  of  age. 

2.  Pain  comes  on  soon  after  eating.  2.  Pain  two  to  four  hours   after   eating, 

and  located  in  right  hypochondrium. 

3.  Pain  lessened  by  vomiting.  3.  Vomiting  does  not  relieve  pain. 

4.  Vomitus   contains    mucus,    food    rem-         4.  Vomiting  more  rare  than  in  gastric  ulcer, 

nants,  and  often  blood.  and  does  not  often  contain  blood. 

5.  Severe    dyspeptic    symptoms    usually         5.  Dyspeptic  symptoms  slight. 

present. 

6.  Meleena  rare.  6.  Melsena  comparatively  frequent. 

Gallstone  colic  is  to  be  separated  from  duodenal  ulcer  by  the  fact  that 
hemorrhage  does  not  occur  in  gallstone  colic,  and  by  a  previous  history  of 
gallstones ;  but  it  is  to  be  remembered  that  the  absence  of  a  history  of  jaundice 
is  of  little  value,  for  jaundice  is  not  a  constant  symptom  in  cholelithiasis.  As 
Murphy  well  points  out,  jaundice  was  present  only  16  times  in  400  cases 
of  cholelithiasis  operated  on  by  him. 

Acute  fat-necrosis  often  can  not  be  differentiated  from  duodenal  ulcer  with 
perforation.  As  a  rule,  the  vomiting  in  fat-necrosis  is  more  persistent,  and 
the  depression  or  collapse  is  more  prompt  and  severe.  A  high-pitched  per- 
cussion note  is  found  in  the  right  hypochondrium  in  fat-necrosis,  but  this 
area  is  usually  flat  in  perforation  of  the  duodenum,  unless  peritonitis  has 
already  progressed  to  the  stage  of  general  tympanitic  distention.  In  fat- 
necrosis  there  is  an  absence  of  leukocytosis;  in  perforation  there  is  a  marked 
leukocytosis.  In  fat-necrosis  there  is  usually  no  rise  in  temperature;  in  per- 
foration there  is  not  infrequently  a  primary  rise. 

Intestinal  obstruction  may  closely  resemble  perforated  duodenal  ulcer. 
The  pain  in  ulcer  is  constant;  in  obstruction  colicky;  there  is  hyperperistalsis 
in  obstruction ;  there  is  an  absence  of  peristalsis  in  perforation ;  there  is  absence 
of  leukocytosis  in  obstruction;  there  is  marked  leukocytosis  in  perforation. 
In  both  there  is  usually  a  history  of  constipation. 

As  illustrative  of  how  difficult  it  is  to  make  a  correct  diagnosis,  even  when 
perforation  occurs,  Moynihan  tells  us  that  in  only  12  out  of  51  cases  of 
duodenal  ulcer  was  a  correct  diagnosis  made  before  operation,  and  that  in 
49  cases  of  perforated  duodenal  ulcer  18  were  operated  upon  for  appendicitis. 

Prognosis. — The  prognosis,  like  that  of  gastric  ulcer,  is  not  good  for  recov- 
ery. In  perforative  cases,  if  operation  is  not  performed,  the  outlook  depends 
entirely  upon  whether  the  infective  material  is  walled  off  by  adhesions.  If 
this  is  the  case,  and  a  subphrenic  abscess  is  formed,  much  depends  upon 
the  point  at  which  this  abscess  ruptures.  If  the  extra vasated  material  is  not 
confined  by  adhesions,  death  occurs  from  general  peritonitis. 

When  the  condition  is  recognized  and  operation  is  performed,  the  prog- 
nosis is  much  more  favorable.  The  difficulty  is  that  in  many  cases  the 
diagnosis  is  so  obscure  that  operation  is  not  performed  until  so  many  hours 
have  passed  that  recovery  is  impossible.  Thus,  out  of  51  cases  operated 
upon  in  Moynihan's  collection  there  were  only  8  recoveries,  and  in  20  cases 
collected  by  Darras  only  3  recovered.  In  79  cases  collected  by  Weir  and 
Foote  the  mortality  after  operation  was  71  per  cent. 


632  DISEASES  OF  THE  INTESTINES 

Treatment. — The  treatment  of  these  cases  consists  in  absolute  rest  in 
bed.  Aside  from  these  measures  it  is  purely  surgical.  If  perforation  has 
taken  place  and  surgery  cannot  be  resorted  to,  then  there  is  nothing  left 
for  the  physician  but  to  relieve  pain  by  the  use  of  opium  and  to  hope  that 
the  inflammatory  process  may  be  localized.^ 


ENTEROPTOSIS. 

Definition. — Enteroptosis  is  a  condition  in  which  the  intestines  fall  to  a 
lower  level  than  that  which  they  normally  occupy.  Not  only  the  intestines, 
but  the  stomach,  liver,  spleen,  and  kidneys  may  be  displaced  downward,  the 
displacement  being  due  to  stretching  or  relaxation  of  the  mesenteric  and 
peritoneal  ligaments  and  to  laxity  of  the  abdominal  wall,  so  that  it  fails  to 
support  the  contents  of  the  belly  cavity.  Of  the  various  names  which  have 
been  applied  to  this  state,  other  than  enteroptosis,  may  be  mentioned  splanch- 
noptosis, visceroptosis,  and  "Glenard's  disease."  When  the  stomach  is  chiefly 
afi^ected  it  is  called  gastroptosis.    Enteroptosis  is  a  condition,  not  a  disease. 

Etiology. — Glenard  thinks  that  overloading  the  transverse  colon  with  feces 
may  cause  so  great  a  strain  upon  that  portion  of  the  mesocolon  which  sup- 
ports the  large  transverse  bowel,  particularly  at  its  right  flexure,  that  this 
part  may  sag  and  so  predispose  the  rest  of  the  colon  to  drop  downward, 
drawing  with  it  other  parts.  The  objection  to  this  argument  is  that  the  right 
flexure  of  the  colon  is  practically  never  loaded  heavily  with  feces,  or,  at  least, 
the  instances  in  which  it  is  so  loaded  are  far  more  rare  than  is  enteroptosis. 
Further  than  this,  the  ligaments  concerned  in  the  support  of  the  abdominal 
contents  are  not  the  chief  source  of  support.  Schwerdt  states  that  they  do  not 
bear  more  than  one-eighth  of  the  weight.  The  upper  organs  are  buoyed  up 
by  the  lower  ones,  provided  these  are  retained  in  a  normal  position.  Although 
constipation  may  be  a  minor  factor  in  producing  this  state,  the  chief  factors 
are  relaxation  of  the  abdominal  wall  and  the  loss  of  fat  produced  by  an  acute 
illness  or  some  chronic  disease,  and  occasionally  by  old  age.  This  affection 
is  not  uncommon  in  the  insane,  particularly  when  chronic  constipation, 
inactivity,  and  wasting  are  associated.  The  relaxation  of  the  abdominal 
wall  may  also  be  due  to  loss  of  fat  and  to  repeated  pregnancies,  particularly 
if  the  woman  has,  by  wearing  corsets,  weakened  her  abdominal  muscles  and 
then  had  them  subjected  to  prolonged  distention  in  pregnancy.  Occasionally 
the  rectus  muscles  not  only  atrophy,  but  separate.  I  have  in  my  ward  as  I 
write  a  woman  who  has  this  very  condition.  (Figs.  84  and  85.)  Cases 
occasionally  arise  in  which  enteroptosis  follows  the  removal  of  a  large 
ovarian  cyst  or  of  ascites. 

To  appreciate  the  failure  on  the  part  of  the  abdominal  muscles  in  a 
well-developed  case  of  enteroptosis,  it  is  only  necessary  to  stand  behind  the 
patient  and  place  the  palms  of  the  hands  upon  the  lower  zone  of  the  abdomen, 
pressing  upward  and  inward,  when  the  entire  weight  of  the  abdominal  con- 

1  The  literature  of  this  subject,  which  is  of  increasing  importance,  can  best  be  obtained  by  consults 
ing  the  valuable  papers  of  Weir  in  the  Transactions  of  the  American  Surgical  Association,  and  of 
Murphy  in  the  American  Journal  of  Obstetrics  for  Decenaber,  1902.  From  these  contributions  much  of 
the  information  in  this  article  ■was  obtained. 


ENTEROPTOSIS 

Fig.  84 


633 


Enteroptosis  due  to  relaxation  of  the  abdominal  wall.     Hornets'-nest  belly. 


534  DISEASES  OF  THE  INTESTINES 

tents  may  be  felt  resting  upon  the  hands.  The  complete  inability  of  the 
abdominal  wall  to  give  support  is  then  appreciated. 

Enteroptosis  is  far  more  frequent  in  women  than  in  men.  Gl^nard  found 
it  in  women  in  306  out  of  404  cases. 

Symptoms. — ^The  symptoms  in  many  cases  are  by  no  means  definite.  The 
patient  is  often  regarded  as  a  chronic  dyspeptic,  as,  indeed,  she  is.  There  is 
more  or  less  constant  discomfort  in  the  abdomen,  and  the  intestines  may  be  in 
a  state  of  peristaltic  unrest,  so  that  borborygmi  and  rumbling  are  annoying. 
At  times  the  bowels  seem  hyperaesthetic,  and  the  patient  complains,  not  of 
pain,  but  of  a  sense  of  movem.ents  which  in  health  are  never  felt.  Some 
patients  describe  the  sensation  as  if  their  abdominal  contents  were  "falling 
out"  of  them.  Some  have  a  distaste  for  food;  others  crave  it,  with  the  hope 
that  it  will  relieve  the  sense  of  emptiness,  and  then  regret  taking  it  because 
its  presence  in  the  displaced  stomach  increases  the  distress.  Constipation  is 
usually  persistent,  and  the  use  of  purgatives  may  serve  to  cause  a  great 
increase  in  rumbling  without  causing  a  satisfactory  evacuation.  The  reason 
for  this  is  evident,  for  the  fallen  bowel  presents  sacculations  or  depressions 
that  act  like  a  plumber's  trap  and  prevent  free  progress  of  the  contents  of 
the  intestinal  tube. 

Associated  with  these  symptoms  there  is  often  a  good  deal  of  nervous 
unrest  and  mental  depression,  and  not  rarely  some  vertigo  on  changing  the 
posture  of  the  body.  There  may  also  be  cardiac  palpitation  and  breath- 
lessness. 

An  examination  of  such  a  patient  will  reveal  on  inspection,  provided 
a  certain  degree  of  leanness  or  emaciation  is  present,  that  the  abdominal 
wall  is  thinner  than  normal,  that  it  is  relaxed,  and  that  when  the  patient 
stands  erect  its  muscles  are  soft  and  without  tone.  In  health  palpation  of 
the  abdominal  wall  reveals  some  resistance,  whereas  in  this  state  it  yields 
readily  to  pressure  like  the  side  of  a  partly  filled  water-bag.  Inspection  not 
rarely  reveals  the  fact  that  the  zone  of  the  abdomen  between  the  ensiform 
cartilage  and  the  navel  is  empty,  and  that  below  the  navel  the  abdomen 
is  unduly  prominent  and  sags. 

The  appearance  of  such  a  patient  is  often  noteworthy,  for  emaciation  may 
be  so  marked  as  to  raise  the  suspicion  of  malignant  disease,  a  suspicion  which 
is  increased  by  the  anaemia  which  is  present.  Rarely  the  patient  suffering 
from  enteroptosis  may  develop  jaundice  because  adhesions  constrict  the 
bile-ducts. 

If  the  patient  with  enteroptosis  be  placed  upon  the  back  in  a  good  light, 
and  the  abdominal  wall  observed  at  a  distance,  peristaltic  waves  may  often 
be  seen  traversing  it.  Tapping  the  knuckles  of  intestine  through  the 
abdominal  wall  with  the  finger-tip  will  increase  or  arrest  these  movements 
for  a  moment. 

Deep  palpation  may  reveal  the  liver  much  lower  than  normal.  That  this 
is  not  due  to  an  enlargement  of  this  organ  may  be  proved  by  the  discovery 
that  as  its  lower  border  passes  down  into  the  abdomen  its  upper  border 
also  becomes  lower,  the  actual  area  of  liver  dulness  on  percussion  being 
the  same  as  in  health.  The  liver  is,  however,  rarely  out  of  place,  except  in 
extreme  cases. 


ENTEROPTOSIS  635 

Distention  of  the  stomach  with  gas  from  a  Seidlitz  powder,  or  by 
pumping  air  into  it  with  an  atomizer  bulb  attached  to  a  tube,  will  reveal 
its  abnormal  position,  and  if  it  is  carefully  outlined  it  may  be  found  that 
this  viscus  occupies  a  more  vertical  position  than  in  health,  the  pylorus 
being  greatly  displaced,  while  the  cardiac  portion  is  in  a  relatively  normal 
posture  because  it  is  more  firmly  suspended.  The  cardia  is  very  rarely  greatly 
displaced,  but  Steele  has  reported  five  such  cases  in  a  comparatively  short 
time  of  observation.  The  gastrodiaphane  of  Einhorn  may  be  used  for  the 
purpose  of  defining  the  site  of  the  stomach.  Ptosis  of  the  stomach  is  not 
rarely  associated  with  dilatation  and  with  motor  insuflRciency,  (For  the 
measures  by  which  the  presence  of  gastroptosis  can  be  determined  see 
article  on  Gastric  Dilatation.) 

The  spleen  is  very  commonly  displaced.  It  may  be  well  forward  in  the 
median  line,  or  it  may  fall  more  directly  downward  and  be  found  as  low  as 
the  pelvic  organs 

Nephroptosis  is  described  in  the  section  devoted  to  Diseases  of  the 
Kidneys. 

During  the  performance  of  deep  palpation  there  can  sometimes  be  felt  a 
moderately  firm  mass  lying  transversely  in  the  abdomen  in  the  epigastric  area. 
This  is  said  by  Glenard  to  be  the  colon,  but  if  this  be  the  case  the  colon  is 
not  much  displaced,  and  is  certainly  contracted  rather  than  dilated — a  condi- 
tion opposed  to  that  stated  by  Glenard  to  be  usually  present.  Ewaldi  believes 
that  this  mass  is  the  pancreas  v/hich  has  been  uncovered  by  the  enteroptosis. 

Auscultation  of  the  belly  in  these  cases  often  reveals  a  large  number  of 
liquid  sounds,  and  if  the  patient  is  shaken  there  may  be  heard  succussion 
notes  and  sounds  which  may  be  called  "slopping." 

While  some  patients  with  moderate  enteroptosis  present  many  of  the 
symptoms  just  described,  it  is  a  fact  worthy  of  note  that  others  with  very 
marked  falhng  of  the  abdonu'nal  contents  often  have  no  complaint  to  make 
of  the  abdominal  state,  and  if  they  are  told  of  it  at  once  become  mentally 
"centred"  on  their  alimentary  tract,  and,  if  already  neurasthenic,  speedily 
drive  themselves  and  their  medical  attendant  almost  demented  by  their 
constant  discovery  of  new  symptoms. 

Treatment. — The  treatment  of  enteroptosis  is  manifestly  to  be  directed  to 
the  support  of  the  displaced  organs  and  their  replacement.  Not  rarely,  if 
the  physician  stands  behind  the  patient  and  presses  upon  and  lifts  the 
abdominal  contents  by  pressing  the  hands  in  front  of  the  abdomen,  relief 
from  the  sense  of  abdominal  relaxation  is  at  once  noticed. 

The  adjustment  of  a  properly  filled  abdominal  belt  or  binder  is,  therefore, 
a  valuable  aid  in  this  condition.  It  should  be  applied  every  morning  before 
rising  and  not  until  after  the  patient,  by  gentle  strokings  with  his  hands, 
has  placed  the  abdominal  contents  at  about  the  proper  level.  Its  greatest 
pressure  must  be  exercised  inward  and  upward  in  the  zone  below  the 
navel.  Sometimes  the  use  of  a  broad  flannel  binder  about  the  lower  zone 
may  be  sufficient,  but  the  support  must  be  upward  as  well  as  inward. 

Great  care  should  be  taken  as  to  diet.  Starches  and  milk,  both  of  which 
are  prone  to  produce  flatulence,  should  be  avoided.  If  starch  is  used  in  an 
easily  digested  form,  as  rice  and  cornstarch,  some  taka-diastase  should  be 


636  DISEASES  OF    THE  INTESTINES    ' 

given  with  it.  Cheese  and  beans  are  absolutely  forbidden,  and  fats  are  also 
harmful.  Small  quantities  of  green  vegetables  may  be  taken,  and  roast  or 
broiled  beef  and  mutton  allowed  at  each  meal.  Eggs  are  also  permissible. 
The  patient  should  be  warned  against  eating  heavily  at  any  one  time,  since 
an  overweighted  stomach  or  colon  will  make  the  ptosis  much  worse.  If 
gastric  dilatation  exists,  lavage  may  be  useful. 

In  the  way  of  drugs,  there  are  only  three  which  produce  much  benefit, 
namely:  nux  vomica  in  full  dose — say,  I  grain  four  times  a  day;  extract  of 
physostigma  in  the  dose  of  ^  grain  four  times  a  day,  and  capsicum,  1  grain 
three  or  four  times  a  day.  Sometimes  it  is  well  to  combine  all  of  these  in 
one  pill  or  capsule. 

In  the  way  of  digestants,  hydrochloric  acid  and  pepsin,  soda  and  pan- 
creatin,  and  taka-diastase  are  to  be  employed.  As  laxatives,  cascara  sagrada 
and  aloes  may  be  used,  1  grain  of  the  extract  of  the  former  and  -^  grain  of 
aloin  being  given  once,  twice,  or  thrice  a  day,  according  to  the  obstinacy  of 
the  bowels.  The  bitter  fluid  extract  given  in  capsules  is  the  best  preparation 
to  employ. 

In  cases  in  which  the  symptoms  are  so  severe  as  seriously  to  impair  health 
and  comfort  and  even  the  chances  of  life,  operative  interference  is  indicated; 
the  displaced  organs  being  fixed  by  suturing.  Up  to  the  present  time  quite 
a  number  of  such  cases  have  been  operated  on  by  different  methods.  Duret, 
in  a  case  in  which  the  stomach  came  within  four  inches  of  the  pubis,  placed 
stitches  through  the  lesser  curvature  of  the  stomach,  then  through  its  anterior 
wall,  and  made  it  fast  to  the  peritoneum  of  the  anterior  abdominal  wall. 
Recovery  followed.  In  other  cases  the  intestines  have  been  raised  by  taking 
a  reef  in  the  mesentery.  Rovsing  has  fastened  the  stomach  by  three  stout 
sutures  passed  through  the  abdominal  wall  and  through  the  outer  coats  of 
the  stomach,  with  the  result  that  the  patient  gained  forty  pounds  in  weight. 
Beyea  has  taken  tucks  in  the  gastrophrenic  and  gastrohepatic  ligaments,  with 
good  results,  and  Webster  has  treated  a  large  number  of  cases  by  excising 
the  tissues  between  the  recti  muscles  and  then  stitching  the  edges  of  these 
muscles  together,  thereby  affording  support  for  the  abdominal  contents. 


COLITIS. 

Acute  Colitis. — ^This  is  a  very  common  condition  and  follows  exposure  to 
cold,  particularly  if  the  abdominal  contents  have  been  the  parts  chiefly 
deprived  of  warmth.  The  inflammatory  process  chiefly  affects  the  lower 
part  of  the  colon  and  extends  to  the  rectum  as  well,  so  that  proctitis  is 
developed.  The  primary  hypersemia  of  inflammation  is  followed  by  an 
increasing  secretion  of  mucus,  with  the  throwing  off  of  dead  epithelial  cells 
mixed  with  white  and  red  blood  corpuscles  which  have  escaped  from  the 
engorged  vessels.  If  the  process  is  very  severe,  a  suppurative  state  may  be 
developed.  In  most  cases  the  tendency  is  to  rapid  recovery,  but  if  the 
inflammatory  process  persists,  one  of  two  conditions  may  be  developed, 
either  small  areas  of  necrosis  or  ulceration  occur,  or  there  is  deposited  in  the 
submucous  tissues  a  considerable  amount  of  connective  tissue,  which  may 


COLITIS  637 

by  its  contraction  impair  the  function  of  the  glands  and  perhaps  narrow  the 
caHbre  of  the  bowel. 

Symptoms. — The  symptoms  consist  in  severe  abdominal  fain,  with  tender- 
ness in  the  region  of  the  sigmoid  flexure,  and  in  frequent  movements  of 
the  bowels,  which  movements  soon  become  very  small,  so  that  they  finally 
consist  in  nothing  but  a  little  mucus,  which  is  passed  with  great  tenesmus. 

Treatment. — The  treatment  consists  in  the  use  of  absolute  rest  in  bed. 
The  application  of  a  mustard  plaster  over  the  sigmoid  flexure  and  the  injec- 
tion into  the  bowel  of  4  ounces  of  starch-water,  with  40  grains  of  potassium 
chlorate  and  30  drops  of  deodorized  laudanum,  every  three  or  four  hours. 

Acute  infectious  colitis  has  already  been  considered  in  the  article  on 
Dysentery. 

Mucous  Colitis.  Definition. — Under  the  name  of  mucous  colitis  physi- 
cians meet  with  a  condition  which  is,  next  to  dysentery,  the  most  common 
affection  of  the  colon,  and  in  temperate  zones  is  more  frequent.  It  affects 
persons  suffering  from  neurasthenia,  in  the  great  majority  of  cases,  and  is 
met  with  in  the  overworked  or  overwrought  of  both  sexes,  but  most  fre- 
quently in  women  of  from  twenty  to  forty  years  of  age. 

The  affection  is  a  chronic  one,  often  lasting  for  several  years,  and  during 
its  continuance  causing  a  great  impairment  of  nutrition  and  much  general 
ill-health.  Not  rarely  the  irritable  state  of  the  colon  causes  constant  abdom- 
inal distress.  Severe  colicky  pain  is  also  present,  and  a  state  of  hyper- 
peristalsis  of  the  small  bowel  exists,  so  that  food  is  often  hurried  on  into  the 
large  bowel  before  it  can  be  digested  and  absorbed,  the  patient  suffering  from 
lienteric  diarrhoea,  not  because  the  digestive  power  is  impaired,  but  because 
the  food  does  not  remain  in  one  part  of  the  small  bowel  long  enough  to  be 
digested.  The  stools  are  not  as  frequent  as  those  of  other  kinds  of  chronic 
diarrhoea. 

Mucus  in  considerable  amount  is  often  passed,  and  this  mucus  may 
be  so  thick  that  it  resembles  a  false  membrane,  whence  the  term  "muco- 
membranous  enteritis."  Not  rarely  the  patient  has  excessive  peristalsis 
every  time  food  is  taken. 

Blood  is  almost  never  passed  unless  there  are  hemorrhoids  which  bleed. 
There  is  no  fever,  but  profound  mental  depression.  Areas  of  marked 
tenderness  can  be  found  in  the  abdomen  on  palpation,  and  the  cutaneous 
sensibility  is  often  increased. 

Treatment. — The  treatment  of  mucous  colitis,  while  it  is  not  capable  of 
producing,  in  the  majority  of  cases,  very  marked  improvement  within  a 
short  time,  is  nevertheless  successful  in  a  large  proportion  of  patients,  pro- 
vided that  it  is  carefully  and  persistently  carried  out,  and  if  the  patient's 
mode  of  life  and  her  diet  is  arranged  in  such  a  way  as  to  be  favorable  in 
their  effects.  As  the  majority  of  these  patients  have  been  subjected  to 
nervous  stress  and  are  neurasthenic,  it  is  essential  that  they  shall  be  sub- 
jected to  the  rest  cure,  in  order  that  by  re-establishing  nervous  tone  and 
equihbrium  a  normal  intestinal  peristalsis  and  normal  digestive  functions 
may  be  established.  Without  rest  in  cases  of  this  character  other  treatment 
is  commonly  useless. 

In  order  that   the   greater  part  of  digestion   and   assimilation  may  be 


638  DISEASES  OF  THE  INTESTINES 

cai'ried  out  in  the  stomach  and  duodenum,  foods  easy  of  digestion  and 
readily  assimilated  should  be  given,  and  should  consist  chiefly  in  pro- 
teids,  that  is,  broiled  or  roasted  meats.  Green  vegetables  and  fatty  foods 
should  not  be  allowed.  Easily  digested  starches,  such  as  rice  and  corn- 
starch, may  be  given,  provided  that  pancreatin  or  taka-diastase  is  given  with 
them  to  hurry  their  digestion.  All  vegetable  foods  which  leave  a  bulky  resi- 
due should  be  forbidden,  as,  for  example,  oatmeal  and  wheaten  grits.  The 
patient  should  take  liquids  in  small  quantities  frequently,  rather  than  in 
large  quantities  at  long  intervals,  and  should  avoid  taking  liquids  with  her 
food.  She  should  also  avoid  taking  liquids  before  going  to  bed  at  night, 
as  not  infrequently  liquids  taken  at  this  time  seem  to  lie  in  the  bowel  unab- 
sorbed,  and  on  the  assumption  of  the  erect  posture  by  the  patient  in  the 
morning  a  morning  diarrhoea  is  developed.  All  fatty  articles  of  diet  should 
be  avoided. 

Continuous  counterirritation,  produced  by  frequently  repeated  appli- 
cations of  tincture  of  iodine  over  the  whole  abdominal  surface,  should  be 
maintained,  and  if  there  is  much  tenesmus  a  suppository  containing  5  to 
10  grains  of  iodoform  may  be  inserted  into  the  rectum  in  the  morning  after 
a  movement  of  the  bowels,  not  only  for  its  local  counterirritant  effect,  but 
for  the  beneficial  influence  of  the  iodine,  when  absorbed,  upon  tlie  catarrhal 
condition  of  the  bowel.  In  some  cases  where  the  colon  is  chiefly  at  fault, 
clysters  of  1  or  2  quarts  of  hot  normal  saline  solution,  or  of  pure  water  con- 
taining 20  grains  of  sulphocarbolate  of  zinc  to  the  pint,  should  be  gently 
given,  care  being  taken  that  the  fluid  does  not  run  in  so  rapidly  as  to  irritate 
the  bowel.  The  patient  should  lie  on  the  left  side  until  the  sigmoid  flexure 
is  filled,  then  turn  on  the  back  while  the  transverse  colon  is  filled,  and 
perhaps  after  this  turn  on  the  right  side  with  the  hope  that  the  fluid  will 
enter  the  ascending  colon. 

In  those  cases  in  which  there  is  a  history  of  repeated  mild  attacks  of 
appendicitis,  or  of  pain  in  the  right  iliac  region,  appendectomy  sometimes 
produces  excellent  results,  the  chronic  colitis  being  due  to  the  infection  of 
the  colon  by  small  quantities  of  pus  which  escape  from  the  appendix.  Prob- 
ably the  enforced  rest  which  follows  an  operation  for  the  removal  of  the 
appendix  also  is  advantageous  in  producing  a  cure  in  these  cases. 

Follicular  and  Croupous  Colitis. — Follicular  colitis,  sometimes  called 
nodular  colitis,  is  a  form  of  inflammation  of  the  colon  characterized  by 
marked  swelling  of  its  solitary  glands,  or  lymph  nodes,  rendering  these 
structures  unusually  protuberant.  After  this  primary  stage  of  enlargement 
necrosis  and  sloughing  ensue,  leaving  round  ulcers,  which  are  frequently 
numerous.  By  the  failure  of  these  to  heal  the  more  chronic  state  of  ordinary 
ulcerative  colitis  is  developed. 

Ulceration  of  the  colon  is,  of  course,  also  due,  in  many  cases,  to  the  typhoid 
bacillus,  the  tubercle  bacillus,  the  Amoeba  dysenteries,  and  sometimes  to  infec- 
tion by  Shiga's  bacillus.  It  also  develops  as  a  terminal  infection  in  some 
cases  of  chronic  renal  disease.  Ulcerative  processes  in  the  intestines  are 
very  common  in  the  insane,  and  they  have  been  associated  with  locomotor 
ataxia. 

Under  the  name  of  croupous  colitis,  a  condition  exists  in  which  the  mucous 


.     DILATATION  OF   THE  COLON  639 

membrane  of  the  colon  becomes  engorged  and  coated  with  a  false  membrane, 
and  the  underlying  tissues  becoming  filled  with  dead  leukocytes  and  fibrin. 
As  in  the  small  bowel,  so  here,  this  false  membrane  may  be  widely  diffused 
or  occur  in  patches.  After  the  formation  of  the  membrane  the  disease  either 
disappears  by  the  exfoliation  of  necrotic  material  or  the  deeper  coats  of 
the  bowel  are  affected,  so  that  areas  of  submucous  tissue  become  necrotic 
and  are  passed  in  the  stools  as  sloughs.  At  the  site  of  these  sloughs 
healing  by  cicatrization  develops,  or  the  process  extends  still  more  deeply 
to  the  peritoneum  and  causes  serious  secondary  lesions.  In  this  way  is 
formed  a  necrotic  colitis,  the  ulcerated  areas  being  gangrenous  in  appearance 
and  of  great  size.  A  large  number  of  pathogenic  organisms  have  been  found 
in  the  bowel  in  such  cases. 

Treatment. — This  consists  in  following  a  plan  identical  with  that  advised 
for  mucous  colitis,  and  in  addition  in  giving  an  injection  of  nitrate  of  silver 
in  the  strength  of  40  grains  to  the  quart  each  evening  in  place  of  the  normal 
saline  already  spoken  of. 

Pseudomembranous  Colitis. — ^This  is  a  condition  in  which  not  only  the 
large  intestine,  but  the  small  bowel  as  w^ell  is  affected  by  a  superficial  necrosis, 
which  may  be  diffuse,  but  is  more  commonly  distributed  in  patches.  The 
process  closely  resembles  croupous  colitis,  and  by  some  writers  the  two  con- 
ditions are  held  to  be  identical.  The  false  membrane  consists  of  dead 
epithelium,  mucus,  fibrin,  and  white  blood  cells  which  have  passed  out 
of  the  bloodvessels.  In  some  cases  the  false  membrane  is  almost  purely 
mucin-bearing  and  quite  fibrin  free;  the  latter  element  is  only  exceptionally 
abundant.  Not  rarely  the  submucous  tissues  may  be  infiltrated  by  serum 
and  leukocytes. 

Pseudomembranous  enteritis  develops  in  the  course  of  a  number  of  the 
acute  infectious  diseases,  in  pyaemia  and  septicaemia,  in  persons  who  suffer 
from  chronic  Bright's  disease,  and  occasionally  after  the  taking  of  poisons 
which  cause  gastrointestinal  irritation.  It  is  important  to  recall  the  fact 
that  this  pseudomembranous  condition  is  not  diphtheritic  in  the  sense  that 
it  is  due  to  the  Klebs-Loeffler  bacillus,  and  that  the  proportion  of  fibrinous 
exudate  is  far  less  than  in  the  membrane  of  that  specific  disease  called  diph- 
theria. Perhaps  the  most  common  cause  of  this  lesion  is  the  ingestion  of 
poisonous  quantities  of  arsenic,  for  this  drug  is  eliminated  by  the  mucous 
membrane  of  the  alimentary  canal  and  in  the  process  a  necrosis  of  the  lining 
epithelium  takes  place. 

DILATATION  OF  THE  COLON. 

Hale  White  places  dilatation  of  the  colon  in  four  divisions.  The  first  of 
these  is  that  type  of  dilatation  which  is  due  to  acute  distention  from  the 
accumulation  of  gas.  This  is  not  rarely  met  with  in  severe  infectious  dis- 
eases, as  in  the  pneumonia  of  drunkards  and  in  severe  cases  of  typhoid  fever 
with  toxsemia.  The  distention  of  the  colon  under  these  circumstances  often 
interferes  with  the  action  of  the  lungs  and  heart  by  mechanical  pressure 
against  the  diaphragm.  The  zone  of  the  abdomen  between  the  umbilicus 
and  the  ensiform  cartilage,  and  between  the  right  and  left  hypochondrium 


640  DISEASES  OF  THE  INTESTINES 

is  distinctly  bulging  and  tympanitic  on  percussion.  Tympanites  of  this 
kind  possesses  a  double  significance :  first,  it  is  an  evil  in  itself  by  reason 
of  the  pressure  which  it  produces,  and,  second,  its  presence  is  evil  in  that  it 
indicates  a  lowered  vitality  and  an  inability  of  the  intestine  to  expel  gas  which 
otherwise  would  not  be  allowed  to  accumulate,  and  which  in  health  would 
not  form. 

The  treatment  of  this  form  of  tympanites  consists  in  the  application  of  a 
hot  turpentine  stupe  over  the  abdomen  and  the  injection  into  the  rectum 
of  6  ounces  of  milk  of  asafoetida  containing  1  drachm  of  oil  of  turpentine, 
the  two  fluids  being  thoroughly  mixed  in  order  to  prevent  the  turpentine 
from  damaging  the  bowel.  In  other  cases,  where  it  is  considered  advisable  to 
stimulate  the  circulation  at  the  same  time  that  the  gas  is  expelled,  and  when 
it  is  feared  that  the  turpentine  may  be  absorbed  and  irritate  the  kidneys, 
excellent  results  will  follow  the  use  of  this  quantity  of  milk  of  asafoetida 
with  the  addition  of  ^  to  1  ounce  of  Hoffmann's  anodyne.  When  obstinate 
constipation  is  present,  and  the  sigmoid  flexure  is  filled  with  feces,  an  ordi- 
nary soapsuds  enema,  followed  by  1  ounce  of  sulphate  of  magnesium  in 
4  ounces  of  water  and  2  ounces  of  glycerin,  may  be  injected.  A  few  years 
ago  it  was  suggested  by  Ogle,  and  others,  that  puncture  of  the  bowel  through 
the  abdominal  wall  should  be  performed  in  those  cases  in  which  the  gas 
could  not  be  dislodged  and  when  it  was  causing  dangerous  pressure.  While 
this  advice  is  theoretically  good,  practically  it  is  of  little  value.  I  have  tried 
it  in  a  number  of  instances,  and  it  has  either  failed  entirely  or  has  permitted 
but  a  small  quantity  of  gas  to  escape  from  a  single  knuckle  of  intestine, 
the  bowel  contracting  in  such  a  manner  as  to  prevent  most  of  the  gas  from 
finding  its  way  to  the  aspirating  needle.  If  a  fine  needle  is  used  but  little 
gas  can  escape,  while  if  a  coarse  needle  is  employed  a  sufficiently  large 
puncture  may  be  made  in  the  bowel  to  permit  of  the  escape  of  gas  or  liquid 
into  the  peritoneal  cavity  after  the  needle  is  withdrawn. 

The  second  group  of  cases  depends  upon  the  accumulation  of  foreign 
bodies.  These  are  so  rare  in  human  beings  as  to  be  scarcely  worthy  of  con- 
sideration. Occasionally,  however,  the  dilatation  may  be  due  to  the  presence 
of  enormous  gallstones  which  have  been  still  further  increased  in  size  by 
fecal  additions.    Such  cases  are  to  be  treated  by  operation. 

The  third  form  is  that  due  to  obstruction  of  the  lower  part  of  the  colon,  so 
that  fecal  accumulation  and  secondary  ulceration  may  occur.  The  obstruc- 
tion may  be  due  to  volvulus,  to  a  band  or  to  a  coil  of  adherent  small  intestine. 
It  is  also  due  to  stricture  or  to  syphilitic,  cicatricial,  or  neoplastic  growths,  par- 
ticularly cancer.    These  cases  are  very  rare,  and  the  treatment  is  operative. 

Finally,  in  the  fourth  type  we  find  cases  of  so-called  idiopathic  dilatation 
of  the  colon,  which  are  also  exceedingly  rare.  Many  years  ago  Formad 
reported  an  extraordinary  case  of  this  character,  and  Hale  White  has  collected 
several  from  Hterature.  In  most  of  these  instances  the  enormously  dilated 
colon  is  loaded  with  accumulated  fecal  matter. 

Treatment  can  be  of  little  value  in  the  last  type  of  cases,  for  a  congenital 
defect  in  the  muscular  and  other  tissues  forming  the  wall  of  the  intestine  is 
responsible  for  the  condition.  Relief  may,  perhaps,  be  given  by  making 
an  artificial  anus  at  the  sigmoid  flexure. 


ACUTE  PERITONITIS  g41 

DISEASES  OF  THE  PEEITONEUM. 

ACUTE  PERITONITIS. 

Definition. — Peritonitis  is  a  term  applied  to  inflammation  of  the  serous 
membrane,  the  peritoneum,  lining  the  abdominal  cavity  and  covering  in 
its  reflections  the  organs  which  this  cavity  contains. 

Etiology. — Within  comparatively  recent  years  it  was  generally  considered 
that  acute  peritonitis  was  usually  idiopathic,  but  with  an  increasing  knowl- 
edge of  the  methods  by  which  infection  occurs,  we  have  come  to  learn  that 
most,  if  not  all,  cases  of  peritonitis  are  due  to  an  infection  which  has  come 
to  the  peritoneum  through  primary  disease  or  the  presence  of  infecting 
organisms  in  other  organs.  While  we  are  not  in  a  position  to  deny  the  exist- 
ence of  idiopathic  peritonitis,  we  should,  nevertheless,  always  doubt  it,  and 
use  every  effort  to  discover  the  source  of  the  infection  which  is  present,  even 
if  it  is  not  readily  found.  Nearly  half  a  century  ago  Habershon  found,  in 
an  analysis  of  501  autopsies  after  death  from  peritonitis,  that  over  50  per 
cent,  resulted  from  some  primary  disease  not  involving  the  peritoneum,  and 
more  recently  Kelynack,  in  studying  124  cases  of  acute  peritonitis,  found 
that  every  one  of  them  developed  the  disease  as  a  secondary  lesion. 

It  may  be  true  that  exposure  to  cold  and  severe  strain  are  productive  of 
peritonitis,  but  if  this  is  the  case  it  is  only  because  these  influences  diminish 
the  vital  resistance  of  the  peritoneum. 

The  two  great  causes  of  peritonitis  are  appendicitis  and  disease  of  the 
Fallopian  tubes.  In  both  of  these  instances  it  is  due  to  the  extension  of 
an  inflammatory  process,  which  in  turn  arises  chiefly  from  the  spread  of 
infecting  micro-organisms. 

The  method  by  which  pathogenic  micro-organisms  are  enabled  to  pass 
through  the  walls  of  an  inflamed  appendix  has  already  been  spoken  of  in 
the  article  on  Appendicitis,  and  it  is  worthy  of  note  that  any  cause  which 
seriously  interferes  with  the  health  of  even  a  small  part  of  the  intestinal 
wall  may  permit  the  escape  of  micro-organisms  into  the  general  peritoneal 
cavity.  Of  the  micro-organisms  which  commonly  produce  peritonitis  under 
these  circumstances,  the  Bacillus  coli  communis  is,  perhaps,  the  most  fre- 
quent, but  a  large  number  of  other  micro-organisms  are  often  present,  and 
there  is  every  reason  to  believe  that  they  are  active  in  the  production  of  the 
inflammatory  process.  Next  to  the  Bacillus  coli  communis  stands  the  Strep- 
tococcus and  the  Pneumococcus,  the  Staphylococcus  alhus,  and  the  Bacillus 
pyocyaneus.  The  Bacillus  aerogenes  capsulatus  is  also  not  infrequently 
present.  Occasionally  the  Bacillus  typhosus  seems  to  be  responsible  for 
the  process. 

When  infection  takes  place  by  means  of  the  Fallopian  tubes,  the  peri- 
tonitis may  be  due  to  the  gonococcus;  but  in  the  majority  of  instances 
the  inflammatory  process  is  not  due  to  this  organism,  but  to  the  strepto- 
cocci or  staphylococci  which  are  associated  with  it;  the  presence  of  which, 
perhaps,  enables  the  gonococcus  to  become  pathogenic  in  this  serous  mem- 
41 


642  DISEASES  OF   THE    PERITONEUM 

brane.  Bumm,  however,  believes  that  the  escape  of  the  gonococcus  into 
the  peritoneum  is  not  usually  followed  by  evil  results.  On  the  other  hand, 
pure  cultures  of  the  gonococcus  have  been  obtained  from  the  abdominal 
cavity  in  two  cases  of  acute  general  peritonitis  by  Young  and  Gushing. 

Subacute  or  chronic  peritonitis  is  often  due  to  the  Bacillus  tuberculosis 
and  acute  miliary  tuberculosis  of  the  peritoneum,  which  is  usually  looked 
upon  as  a  form  of  acute  peritonitis,  is  necessarily  the  result  of  the  infection 
by  the  tubercle  bacillus.  In  the  acute  peritonitis  following  labor,  the 
so-called  septic  peritonitis,  the  streptococcus  is  the  chief  factor.  Cases  of; 
peritonitis  due  to  the  pneumococcus  have  been  frequently  recorded. 

While  we  know,  therefore,  that  peritonitis  in  its  acute  forms  is  a  sec- 
ondary infection,  it  must  not  be  forgotten  that  in  a  very  large  number  of 
cases  the  peritoneum  is  capable  of  resisting  infection  and  of  destroying 
micro-organisms  which  may  gain  access  to  it.  Indeed,  the  vital  resistance 
of  this  membrane  when  in  health  is  very  remarkable,  and  a  number  of  inves- 
tigators have  shown  that  it  is  possible  to  place  in  the  peritoneal  cavity  con- 
siderable quantities  of  septic  material  without  serious  result,  provided  this 
serous  membrane  is  not  subjected  at  the  same  time  to  insult  whereby  its 
vitality  is  decreased. 

Certain  diseases  which  greatly  decrease  vital  resistance  greatly  increase 
the  susceptibility  to  peritonitis,  as,  for  example,  typhoid  fever,  Bright's 
disease,  and  advanced  arteriosclerosis. 

Peritonitis  in  children,  of  course,  develops  as  a  result  of  the  causes  already 
enumerated.  It  also  is  sometimes  seen  in  young  infants  suffering  from  con- 
genital syphilis,  and  in  those  who  have  intestinal  obstruction.  In  still  other 
cases  it  follows  infection  of  the  umbilicus  after  birth.  In  still  others  it  is 
due  to  an  extension  of  infection  in  empyema,  and  a  few  cases  are  on  record 
in  which  sewer-gas  poisoning  has  seemed  to  produce  an  epidemic  of  this 
character  among  children  exposed  to  its  influence. 

Striimpell  states  that  a  form  of  localized  peritonitis  in  the  left  groin  is 
occasionally  met  with  in  children,  that  it  is  prone  to  be  purulent,  and  that 
the  pus  usually  escapes  through  the  rectum. 

Pathology  and  Morbid  Anatomy. — The  characteristic  appearance  of  the 
peritoneum  in  primary  acute  peritonitis  is  hypersemia,  with  a  diminution  in 
the  normal  glossiness  of  the  membrane  involved.  This  is  followed  by  a  more 
or  less  copious  fibrinous  exudate,  which  may  be  well  distributed,  or  appear 
chiefly  in  patches,  upon  the  parietal  and  visceral  peritoneum.  In  many  cases 
there  is  little  fluid  exudate,  the  small  quantities  present  being  found  in 
pockets  formed  by  the  coils  of  intestine  which  become  agglutinated.  In 
other  instances  the  fluid  portion  of  the  exudation  is  very  much  more  copious, 
and  the  quantity  of  fibrin  thrown  out  is  also  of  considerable  amount,  so  that 
it  is  not  only  found  well  distributed  over  the  surface  of  the  membrane,  but 
free  flakes  may  be  found  floating  in  the  serous  exudate  as  well. 

When  the  infection  is  due  to  pyogenic  micro-organisms,  and  particu- 
larly in  those  cases  in  which  the  vital  resistance  of  the  patient  is  very 
low,  a  septic  peritonitis  speedily  develops.  It  is  usually  very  diffuse  in 
such  cases,  the  entire  peritoneum  being  involved.  The  quantity  of  exudate 
is  moderately  large,  and  is  often  offensive  in  character,  forming  what  has 


ACUTE  PERITONITIS  643 

been  called  "putrid  peritonitis."  In  other  cases  when  the  vital  resistance 
is  not  so  depressed,  the  presence  of  pyogenic  micro-organisms  produces  a 
peritonitis  in  which  pus  alone  is  present.  This  form  of  peritonitis  may  be 
widespread,  but  is  often  localized — the  so-called  loculated  or  circumscribed 
peritonitis  or  peritoneal  abscess — nature  being  able  to  wall  off  the  area  of 
acute  infection  by  a  plastic  exudate,  which  prevents  the  infection  from 
becoming  well  distributed  throughout  the  peritoneum.  In  those  cases  of 
septic  peritonitis  in  which  death  occurs  early,  the  physician  may  be  surprised 
on  opening  the  abdomen  at  autopsy  to  find  that  but  little  change  has  taken 
place  in  the  appearance  of  the  peritoneum  and  its  contents.  Save  for  some 
duskiness  of  the  peritoneum  and  the  presence  of  sanious  fluid,  the  abdominal 
contents  may  seem  to  the  naked  eye  to  be  but  little  altered. 

Occasionally  we  meet  with  what  is  known  as  hemorrhagic  peritonitis, 
which  may  follow  severe  septic  infection,  and  in  cancerous  and  tuberculous 
cases,  with  ulceration,  the  fluid  in  the  abdominal  cavity  may  be  blood- 
stained. 

Localized  peritonitis,  such  as  has  already  been  referred  to,  is  most  fre- 
quently found  in  connection  with  diseases  of  the  pelvic  organs  in  women 
and  with  cases  of  appendicitis.  It  may  be  considered  the  rule  rather  than 
the  exception,  for  the  disease  to  be  limited  by  an  inflammatory  exudate  in 
such  cases.  Other  forms  of  localized  peritonitis  which  are  not  so  frequently 
met  with  depend  upon  an  extension  of  infection  from  the  gall-bladder,  from 
perforation  or  infection  through  a  gastric  ulcer,  and  occasionally  we  find  a 
suppurative  peritonitis  in  the  lesser  peritoneum  as  the  result  of  disease  of  the 
pancreas  or  fat-necrosis.  In  other  instances  this  condition  arises  as  the  result 
of  renal  calculus  and  nephritic  abscess. 

Symptoms. — There  are  few  diseases  which,  when  well  developed,  produce 
a  train  of  symptoms  more  characteristic  than  are  those  of  acute  peritonitis. 
This  holds  true,  however,  only  when  the  disease  is  well  advanced,  and,  indeed, 
is  so  severe  that  there  is  grave  doubt  as  to  the  patient's  recovery.  In  most 
cases  of  peritonitis,  when  the  physician  is  first  called  to  the  patient,  severe 
pain  in  the  abdomen  is  the  chief  condition  which  is  complained  of.  The 
pulse  is  usually  quick,  small,  and  hard,  and  the  belly  wall  tender  on  palpa- 
tion, and  distinctly  rigid.  The  face  will  be  found  to  wear  an  expression  of 
anxiety,  which  seems  to  be  far  out  of  proportion  to  the  length  of  the  illness 
and.  its  severity.  In  many  instances,  even  when  the  pains  are  exceedingly 
severe,  the  patient  considers  that  he  is  suffering  from  acute  indigestion, 
but  acute  indigestion  is  often  relieved  by  pressure,  and  is  usually  accom- 
panied by  tumidity  of  the  abdomen;  whereas,  peritonitis  is  characterized 
by  great  abdominal  tenderness  and  by  a  flat  or  scaphoid  appearance  of 
the  belly  wall.  The  fever  is  usually  not  very  high.  The  pulse  is  tense  and 
rapid.  It  often  does  not  go  above  102°,  and  frequently  not  over  101°.  Vomit- 
ing is  frequently  present. 

After  the  pains  have  been  present  for  a  few  hours,  the  exquisite  tenderness 
of  the  abdomen  makes  the  weight  of  the  bed-clothes  insupportable,  and,  in 
order  to  obtain  some  relief  for  the  abdominal  tension,  the  patient  usually  lies 
on  his  back,  with  the  knees  drawn  up,  and  supports  the  bed-clothes  over  his 
abdomen  by  his  hands,  looking  with  dread  upon  the  approach  of  the  attendant 


644  DISEASES  OF  THE  PERITONEUM 

lest  he  touch  the  abdomen  or  jar  the  bed.  Thirst  which  cannot  be  reheved, 
because  of  constant  retching,  may  add  to  the  patient's  distress,  and  hiccough 
of  a  very  persistent  and  exhausting  character  often  develops. 

As  the  disease  progresses,  the  belly,  which  has  been  tense  and  scaphoid, 
becomes  hard,  not  from  muscular  spasm,  but  from  abdominal  distention.  In 
the  flanks  percussion  may  reveal  some  flatness  due  to  the  accumulation  of 
the  exudate  in  these  parts.  The  face  not  only  is  anxious  in  appearance,  but 
rapidly  becomes  pinched  and  peaked,  the  eyes  appear  sunken,  the  nostrils  are 
thill  and  drawJi,  the  skin  pale  and  livid,  and  the  tongue  dry  and  parched, 
the  typical  "Hippocratic  facies."  The  pulse  at  this  stage  is  exceedingly 
rapid,  running,  and  wiry,  and,  as  the  end  approaches,  loses  its  tense  char- 
acter.   A  cold  sweat  may  break  out  about  the  wrists  and  on  the  forehead. 

The  bowels  are  usually  obstinately  confined,  but  in  some  instances  diar- 
rhoea may  be  present,  particularly  if  diarrhoea  has  been  a  symptom  of  the 
case  prior  to  the  development  of  the  peritonitis.  The  respirations  are  usually 
a  little  quickened,  but  are  shallow  and  superficial,  in  order  that  the  abdom- 
inal movement  may  be  as  slight  as  possible.  A  remarkable  fact  in  connection 
with  these  cases  is  the  preservation  not  only  of  consciousness,  but  the  develop- 
ment of  intense  mental  activity,  which  in  some  cases  persists  up  to  the 
moment  of  death,  the  patient  showing  an  acuteness  of  mind  which  is  startling. 
In  some  instances  during  the  last  hours  there  may  be  a  mild  delirium,  or  even 
slight  stupor. 

In  septic  cases  pain  is  absent  in  the  majority  of  instances,  but  the  tem- 
perature in  the  early  stages  may  be  much  more  febrile  than  in  the  ordinary 
types  of  the  disease.  Sometimes  it  is  distinctly  like  that  of  early  septicaemia. 
By  the  time  that  the  septic  inflammation  is  well  developed,  however,  the 
fever  usually  falls  to  the  neighborhood  of  normal,  and  it  may  reach  sub- 
normal. 

Careful  examination  of  the  abdomen  in  cases  of  well-developed  peritonitis 
not  only  reveals  the  local  symptoms  already  described,  but  it  may  also  show 
localized  patches  of  tympany  where  gas  has  accumulated  in  the  coils  of 
intestine,  which  are  more  or  less  fixed  in  one  position  by  inflammatory  adhe- 
sions. These  coils,  partly  because  of  the  inflammation  and  partly  because 
of  distention,  may  soon  become  paralyzed,  so  that  distention  increases. 

When  the  peritonitis  is  due  to  a  perforation  of  the  intestine  or  of  the 
^  stomach,  the  accumulation  of  gas  in  the  peritoneal  cavity  may  mask  the 
area  of  liver  dulness  or  completely  obliterate  it.  At  one  time  this  was  consid- 
ered a  very  valuable  sign  in  the  diagnosis  of  perforation  with  secondary 
peritonitis,  but  we  now  know  that  in  many  instances  this  symptom  is 
absent. 

Complications  and  Sequelae. — Peritonitis  usually  runs  such  a  rapid  course, 
either  to  recovery  or  death,  that  complications  are  rarely  met.  The  most 
important  and  most  frequent  complication  of  a  serious  nature  is  pneumonia. 
In  100  cases  of  peritonitis  observed  in  the  London  Hospital,  Treves  found 
that  no  less  than  17  developed  pneumonia  or  pleurisy  after  the  peritonitis 
began.    Retention  of  urine  is  frequent. 

As  a  sequel  intestinal  obstruction  may  develop  as  the  result  of  adhesions 
or  by  strangulation  of  the  bowel,  produced  by  the  slipping  of  a  knuckle  of 


ACUTE  PERITONITIS  645 

intestine  through  an  opening  under  a  band  or  a  false  ligament,  or  by  the 
development  of  a  twist  of  the  bowel  through  interference  with  its  peristaltic 
movement. 

Diagnosis. — The  diagnosis  of  acute  diffuse  peritonitis  is  usually  readily 
made,  even  in  its  early  stages.  In  its  late  stages  its  symptoms,  except  in  the 
septic  form,  are  so  characteristic  that  the  diagnosis  can  be  made  on  a  most 
superficial  examination  of  the  patient. 

In  certain  cases  of  typhoid  fever  in  the  early  stages,  when  the  inflam- 
matory process  in  the  intestines  is  acute,  there  may  be  a  good  deal  of 
abdominal  pain  and  considerable  tenderness.  The  apathetic  expression  of 
the  face,  the  higher  temperature  of  typhoid  fever  in  the  stage  of  onset,  the 
tumid  belly,  and  the  coated  tongue,  with  red  edges,  will  aid  in  its  differ- 
entiation. 

The  separation  of  intestinal  obstruction  from  peritonitis  is  exceedingly 
difficult;  but  as  they  often  are  coincident,  the  one  following  the  other,  and 
the  treatment  of  such  cases  the  same,  differentiation  is  unnecessary.  The 
rapid  onset  of  severe  pain  of  a  cramp-like  character,  the  complete  ab- 
sence of  any  movement  of  the  bowels,  the  presence  of  intestinal  unrest, 
and  in  intussusception  the  palpation  of  a  mass  may  make  the  diagnosis 
possible. 

Certain  cases  of  hysteria  at  times  present  symptoms  so  characteristic  of 
peritonitis  that  even  the  most  skilful  may  be  misled.  Every  symptom  may 
be  presented,  yet  the  patient  always  recovers. 

Acute  hemorrhagic  pancreatitis  may  also  so  closely  resemble  peritonitis  that 
a  diagnosis  is  impossible,  but  this  malady  is  exceedingly  rare.  In  it  there 
may  be  a  preceding  history  of  gallstone  disease,  whereas  in  peritonitis, 
unless  perforation  of  the  gall-bladder  has  occurred,  there  is  no  such  history. 

The  pain  of  gallstone  colic  and  renal  colic  is  so  localized  that  much  diffi- 
culty in  diagnosis  does  not  exist,  as  a  rule. 

In  cases  of  perforation  of  the  stomach  with  secondary  pyopneumothorax 
subphrenicus,  the  differentiation  may  be  exceedingly  difficult,  save  that 
swelling  in  the  epigastrium  and  a  history  of  gastric  ulcer  may  be  present. 

When  perforation  of  the  stomach  has  occurred  without  the  formation  of 
abscess,  so  that  the  gastric  contents  and  gas  escape  into  the  peritoneum, 
great  tympany  and  modification  of  the  area  of  liver  dulness  is  found.  Not 
infrequently  in  subphrenic  abscess  a  pleural  effusion  exists,  so  that  serum 
may  be  drawn  from  this  level  and  pus  from  the  level  below  the  diaphragm. 

Occasionally,  in  children  suffering  from  pleurisy,  pericarditis,  and  pneu- 
monia, violent  pain  is  complained  of  in  the  abdomen,  which  may  mislead  the 
physician,  if  he  be  not  on  his  guard. 

Prognosis. — The  prognosis  in  every  case  of  well-developed  acute  diffuse 
peritonitis  is  distinctly  unfavorable.  If  the  physician  has  reason  to  believe 
that  the  peritonitis  is  localized,  the  outlook  becomes  more  promising.  A  good 
deal  depends,  too,  upon  the  cause  of  the  peritonitis,  and  upon  the  character 
of  the  infecting  micro-organism.  Thus,  if  it  follows  perforation  of  the 
stomach  or  bowels,  and  it  is  not  walled  off  from  the  general  peritoneal  cavity, 
and  again,  if  a  skilful  surgeon  is  not  at  hand  to  operate  at  once,  the  prognosis 
is  hopeless.    When  the  infection  after  perforation  is  localized,  the  mortality 


646  DISEASES  OF  THE  PERITONEUM 

is  not  so  great,  but  this  form  of  localized  peritonitis  is  far  more  fatal  than 
that  form  which  is  due  to  appendicitis. 

The  duration  of  life  in  fatal  cases  of  peritonitis  varies  very  greatly.  Death 
may  come  as  early  as  thirty-six  or  forty-eight  hours,  or  may  be  deferred  for 
a  week  or  ten  days,  or  even  longer. 

Treatment. — ^The  treatment  depends  so  entirely  upon  the  cause  of  the  peri- 
tonitis that  it  behooves  the  physician  to  study  the  case  most  carefully.  If 
seen  shortly  after  the  onset  of  the  malady,  the  physician  should  at  once  con- 
sider the  possibility  of  perforation  of  some  portion  of  the  alimentary  canal 
being  responsible,  and  should  examine  carefully  into  the  history  of  the  patient 
as  to  the  possible  presence  of  gastric  ulcer  or  intestinal  ulcer  due  to  typhoid 
fever  or  dysentery.  If  the  patient  is  an  adult,  careful  consideration  of  the 
possibility  of  extension  of  inflammation  from  the  gall-bladder  should  be 
followed^  It  is  hardly  necessary  to  state  that  as  appendicitis  and  diseases  of 
the  Fallopian  tubes  are  the  most  common  causes  of  peritonitis,  the  condition 
of  these  two  parts  should  be  most  carefully  inquired  into,  both  as  to  previous 
history  of  the  patient  and  as  to  the  physical  signs  which  may  be  present. 
If  the  peritonitis  is  diffuse  and  has  followed  perforation  or  strangulation,  the 
salvation  of  the  patient  depends  upon  immediate  surgical  interference, 
unless,  perchance,  shock  prohibits  operation,  when  it  is  permissible  to  wait 
two  or  three  hours,  in  the  hope  that  by  the  use  of  external  heat  and  stimulants 
the  patient  may  be  enabled  to  bear  operation.  If,  on  opening  the  belly,  a 
diffuse  general  peritonitis  is  found,  it  would  seem  best,  in  the  majority  of 
cases,  to  resort  to  the  plan  suggested  by  J.  B.  Murphy,  namely,  to  remove 
the  appendix  if  it  can  be  reached,  close  the  perforation  if  it  exists,  intro- 
duce a  drainage  tube  into  the  pelvis,  place  the  patient  in  a  semi-recumbent 
posture  and  give  a  quart  of  normal  saline  solution  by  the  rectum  every 
two  or  three  hours. 

When  it  is  due  to  appendicitis,  the  age  and  general  physical  condition 
of  the  patient,  must  largely  influence  the  decision  as  to  operative  inter- 
ference. I  agree  with  McCosh,  who  states  that  in  aged  persons,  particu- 
larly if  they  have  been  dissipated,  medical  treatment  gives  better  chances 
than  surgical  interference,  while  the  reverse  holds  true  in  young  persons. 
If  a  surgeon  of  experience  cannot  be  obtained,  medical  treatment  will 
always  give  the  best  results. 

The  question  as  to  the  procedure  which  should  be  followed  if  the  cause 
lies  in  the  appendix  has  already  been  discussed  in  the  article  on  that  dis- 
ease. Fulminating,  gangrenous,  or  perforative  appendicitis  should,  of  course, 
be  operated  upon  at  once;  whereas,  on  the  other  hand,  if  the  appendicitis  has 
simply  produced  an  adjacent  peritonitis,  temporizing  measures  should  be 
resorted  to,  and  operation  performed  in  the  period  of  quiescence.^ 

The  profession  has  passed  through  three  periods  of  fashion  in  regard 
to  the  drug  treatment  of  peritonitis  itself.  Twenty  or  thirty  years  ago 
it  was  extensively  taught  that  general  peritonitis  should  be  treated  by  the 
administration  of  massive  doses  of  opium,  which  were  not  only  sufficient 
to  relieve  pain  completely,  but  also  to  produce  mental  quiet.  Under  the 
leadership  of  Alonzo  Clark,  of  New  York,  enormous  doses  were  sometimes 
given,  as  much  as  258  grains  of  opium  being  given  in  a  day;. and  while 


CHRONIC  PERITONITIS  647 

it  is  undoubtedly  a  fact  that  patients  with  peritonitis  are  able  to  take  these 
doses  without  being  poisoned,  this  plan  of  treatment  received  its  deathblow 
with  the  discovery  that  nearly  all  cases  of  peritonitis  are  due  to  an  infection, 
and  that  the  source  of  infection  must  be  discovered,  and,  if  possible,  removed. 
It  has  therefpre  become  obsolete  because  it  masks  the  symptoms,  and  is 
thought  to  have  no  definite  influence  upon  the  progress  of  the  disease,  save 
that  it  diminishes  the  suffering  of  the  patient.  It  is  probably  safe  practice 
to  administer  a  sufficient  quantity  of  morphine  or  opium  to  diminish  agony, 
but  not  enough  to  mask  the  symptoms  or  make  the  patient  so  comfortable 
that  he  will  refuse  operative  interference  when  the  physician  thinks  it 
advisable. 

Soon  after  the  infectious  nature  of  peritonitis  was  recognized,  the  profes- 
sion went  to  the  extreme  of  purging  with  saline  cathartics,  and  even  with 
vegetable  cathartics,  all  cases  in  which  symptoms  of  acute  peritonitis  were 
manifest.  There  is  no  doubt  that  this  method  was  used  to  excess,  and  at 
the  present  time  we  know  that  it  is  unnecessary,  unless  there  is  reason  to 
believe  that  the  bowels  are  overloaded  with  fecal  matter.  In  the  writer's 
experience  cases  of  this  character  are  usually  relieved  by  the  bowels  expelling 
the  feces  in  the  early  stages  of  the  peritoneal  inflammation. 

The  opium  treatment  was  excessive,  the  purgative  treatment  was  also 
excessive,  when  either  of  these  plans  was  applied  to  every  case,  but  both  of 
them  used  in  moderation  may  be  advantageous  in  certain  cases. 

Counterirritation  applied  over  the  abdomen  in  the  shape  of  a  large 
number  of  leeches  may  be  useful  in  sthenic  cases.  In  other  instances  a. 
light  mustard  plaster  may  be  used  for  relief.  In  still  others  an  ice-bag  has 
been  employed.  Thirst  may  be  relieved  by  the  use  of  small  pieces  of  ice,  or, 
better  still,  by  rinsing  the  mouth  with  glycerin  1  part  and  water  3  parts, 
to  which  has  been  added  a  few  drops  of  lemon-juice.  Liquids  should  not 
be  swallowed,  as  they  increase  the  tendency  to  vomiting.  If  thirst  is  exces- 
sive, fluid  may  be  supplied  to  the  tissues  by  hypodermoclysis  or  by  rectal 
injection.  As  a  rule,  the  patient  does  not  live  long  enough  in  well-developed 
peritonitis  to  make  the  question  of  feeding  an  important  one.  If  the 
focus  of  infection  is  removed  by  operation,  the  feeding  is  that  used 
after  all  abdominal  sections. 


CHRONIC  PERITONITIS. 

Chronic  peritonitis  occurs  in  four  forms,  namely :  a  local  adhesive  process; 
a  diffuse  process;  one  characterized  by  a  proliferation  of  inflammatory  mate^ 
rial  and  connective  tissue;  and  in  a  hemorrhagic  form,  as  a  complication  of 
severe  disease  in  adjacent  organs  or  malignant  disease  of  the  serosa. 

The  local  adhesive  type  is  often  found  in  the  neighborhood  of  such  organs 
as  the  liver,  spleen,  and  stomach,  when,  as  a  result  of  an  acute  inflamma- 
tory process  in  the  visceral  peritoneum  covering  the  organ,  an  adhesion  takes 
place,  and,  perhaps,  thick  fibrous  bands  develop.  In  many  of  these  cases  this 
condition  is  not  even  suspected  during  life.  In  the  neighborhood  of  the 
pelvic  organs  this  type  of  peritonitis  is  exceedingly  common,  and  is,  perhaps, 


648  DISEASES  OF  THE  PERITONEUM 

the  most  frequent  peritoneal  lesion  met  with  by  the  gynecologist.  Sometimes 
intestinal  obstruction  results  from  a  slow,  chronic,  inflammatory  process, 
which  glues  a  knuckle  of  intestine  to  the  omentum  or  the  anterior  wall  of 
the  pertitoneum. 

In  the  diffuse  but  chronic  type  of  peritonitis  a  condition  closely  resembling 
that  of  fibrous  tuberculous  peritonitis  develops,  so  that  the  peritoneal  cavity 
is  practically  obliterated,  and  the  coils  of  intestine  are  often  matted  together 
so  that  it  is  impossible  to  separate  them.  The  parietal  layer  of  the  peritoneum 
is  greatly  thickened,  and  all  the  abdominal  organs  seem  to  be  constricted 
and  drawn  by  the  cicatricial  process. 

Closely  allied  to  the  last  type  is  the  proliferative  form,  in  which  the  changes 
are  not  very  different,  except  that  there  is,  in  addition,  a  considerable  quantity 
of  serum  in  the  abdominal  cavity.  Sometimes  this  may  be  present  in  such 
quantities  that  the  belly  is  greatly  distended.  The  omentum  is  rolled  up  as 
a  window-shade  is  rolled  up,  and  extends  across  the  upper  zone  of  the 
abdomen  in  a  round  mass.  The  intestines  may,  or  may  not,  be  adherent 
to  one  another,  the  presence  of  the  fluid  serving  to  separate  them  and  to 
prevent  dense  adhesi'ons  taking  place.  At  times  some  of  the  fluid  may  be 
divided  off  into  pockets  by  the  adhesions.  This  form  of  proliferative  peri- 
tonitis is  usually  due  to  tuberculosis,  and  not  infrequently  complicates 
alcoholic  cirrhosis  of  the  liver,  but  it  is  generally  believed  that  in  some  cases 
it  may  arise  from  other  causes  than  tuberculosis.  Even  if  the  cause  is  not 
tuberculosis  the  condition  may,  however,  very  closely  resemble  it  on  palpa- 
tion, because  nodules  may  be  found. 

In  cases  of  carcinoma  of  the  viscera  a  chronic  form  of  peritonitis  asso- 
ciated with  the  exudation  of  blood-stained  or  hemorrhagic  serum  is  occa- 
sionally met  with.  Indeed,  the  obtaining  of  such  serum  from  a  case  of 
ascites  is  always  to  be  considered  as  indicative  of  that  form  of  peritonitis 
depending  upon  malignant  growth.  As  a  rule,  the  chief  lesions  are  found 
in  the  pelvis,  or  there  may  be  present  a  general  carcinomatosis  of  the  peri- 
toneum. In  other  cases  the  pelvic  viscera  may  be  coated  with  fibrinous 
exudate,  which  undergoes  connective-tissue  changes,  and  becomes  highly 
vascularized. 

Friedreich  has  described  a  form  of  chronic  hemorrhagic  peritonitis  which 
follows  repeated  resort  to  paracentesis  abdominis,  the  entire  peritoneal 
surface  being  granular,  reddened,  and  dotted  with  extravasations  of  blood. 


CHRONIC  ADHESIVE  SCLEROTIC  PERITONITIS. 

This  is  a  very  rare  state,  apparently  met  with  more  frequently  in  Germany 
than  in  the  United  States.  It  was  described  by  Virchow  in  1853,  and  in  more 
recent  times  by  Riedel.  It  consists  in  an  extensive  subperitoneal  fibroid 
infiltration  or  sclerosis,  without  ascites  and  without  serous,  or  serofibrinous, 
or  purulent  fluid  in  the  abdomen.  In  other  words,  it  is  rather  a  disease 
primarily  involving  the  subperitoneal  connective  tissue  than  a  true  chronic 
peritonitis.  This  hyperplasia  results  in  a  sclerotic  process,  which  in  turn 
produces  contractions  and  retractions,  and,  by  the  formation  of  adhesions. 


OTHER  GROWTHS  OF  THE  PERITONEUM  649 

fastens  organs  to  the  abdominal  wall.  The  symptoms  are  those  of  the 
chronic  fibroid  type  of  tuberculous  peritonitis  already  described,  but  the  con- 
dition is  not  due  to  tuberculosis.  Wetherill  states  that  the  peritoneum 
shrinks  so  that  when  abdominal  section  is  performed  it  is  impossible  to 
approximate  its  edges  on  closing  the  wound. 

For  a  description  of  the  so-called  "iced  liver  of  Pick"  see  Adhesive 
Pericarditis. 

CANCER  OF  THE  PERITONEUM. 

This  is  an  exceedingly  rare  condition  as  a  primary  lesion.  In  all  proba- 
bility when  it  does  occur,  it  is  an  endothelioma  rather  than  an  epithelioma. 

Carcinoma  and  carcinomatosis  of  the  peritoneum  are  usually  if  not  always 
secondary  to  cancer  of  some  contained  viscus.  The  primary  growth  may  be 
so  small  as  to  escape  superficial  examination  even  at  autopsy,  and  is  com- 
monly in  the  stomach,  pancreas,  liver,  or  biliary  passages,  or,  less  frequently, 
in  the  rectum;  in  the  female  the  pelvic  organs  are  by  far  the  commonest  site 
of  the  primary  growth.  On  account  of  the  pervious  nature  of  the  diaphrag- 
matic lymphatics,  the  pleurae,  pericardium,  and  peritoneum  may  be  simul- 
taneously afi^ected,  or  invasion  of  one  may  be  quickly  followed  by  extension 
to  the  others. 

An  interesting  case  of  colloid  cancer  has  been  reported  by  Ferguson. 
Both  the  visceral  and  parietal  layers  of  the  peritoneum  were  involved,  as 
were  also  the  omentum.    The  mesentery  was  in  some  places  10  cm.  thick. 

The  symptoms  of  either  the  primary  or  secondary  carcinoma  of  the  peri- 
toneum are  emaciation,  ascites,  and,  it  may  be,  the  discovery  of  nodules,  or  of 
a  furled  omentum,  such  as  occurs  in  certain  types  of  peritoneal  tubercu- 
losis. The  fact  that  the  fluid  is  often  hemorrhagic  has  already  been  referred 
to.  In  the  colloid  cases  the  peritoneum  may  be  filled,  not  with  fluid,  but  with 
a  jelly-like  substance,  which  is  so  firm  that  it  will  not  fluctuate. 


OTHER  GROWTHS  OF  THE  PERITONEUM. 

Hydatid  cyst  of  the  peritoneum  is  occasionally  found,  although,  as  a 
rule,  it  develops  in  the  abdominal  organs  rather  than  in  the  peritoneum 
itself.  A  cyst  the  size  of  an  orange  has  been  reported  by  Jones  as  occurring 
in  the  mesocolon.  It  was  successfully  removed.  Rein  has  reported  a  mul- 
tiple hydatid  cyst  occurring  in  the  omentum  of  a  woman  in  the  third  month 
of  pregnancy.  She  was  operated  on  and  recovered.  Other  instances  have 
been  reported  by  various  clinicians,  the  largest  number  of  cases  collected 
being  those  of  Mon^ger,  who  has  reported  32.  He  tells  us  that  such  cysts 
are  nearly  always  secondary  to  rupture  of  cysts  in  neighboring  organs,  and 
there  is  usually  a  history  of  violent  pain  at  the  time  of  rupture.  Perhaps  the 
most  extraordinary  case  is  that  reported  by  MacDonald,  who  has  reported 
the  case  of  a  man  with  thirty  hydatid  cysts  of  the  peritoneum.  Other 
cysts  of  the  mesentery  are  chylous,  dermoid,  serous,  and  sanguineous. 

Very  rarely  sarcoma  and  cystic  adenoma  affect  the  peritoneum. 


650  DISEASES  OF   THE  PERITONEUM 


ASCITES. 


Definition. — The  term  ascites  is  applied  to  the  accumulation  of  serous 
fluid  in  the  abdominal  cavity.  In  some  cases  the  quantity  of  fluid  is  very 
small,  but  in  others  it  amounts  to  several  gallons.  In  the  majority  of 
instances  ascites  is  due  to  atrophic  cirrhosis  of  the  liver,  tuberculosis  of  the 
peritoneum,  or  cardiac  disease.  In  cases  of  chronic  Bright's  disease  of 
the  parenchymatous  type,  ascites  is  often  present  as  part  of  the  general 
anasarca.  It  also  develops  as  the  result  of  pressure  upon  the  abdominal 
bloodvessels,  whereby  the  blood  in  the  large  venous  trunks  is  obstructed  in 
its  flow. 

The  fluid  in  ascites  is  usually  of  a  light  straw  color,  and  does  not  coagulate 
when  exposed  to  the  air. 

Etiology. — The  intra-abdominal  causes  of  ascites,  as  just  stated,  are 
atrophic  cirrhosis  of  the  liver,  tuberculous  peritonitis,  and  morbid  growths, 
which,  by  pressure  upon  bloodvessels,  or  by  producing  changes  in  the  peri- 
toneum, result  in  a  transudation  of  fluid.  A  thrombophlebitis,  or  other 
form  of  venous  obstruction,  may  also  cause  ascites.  Thrombosis,  tubercu- 
losis, or  neoplastic  invasion  of  the  thoracic  duct,  or  its  obstruction  by 
parasites  (filarise) ,  or  other  causes,  and  also  wounds  of  the  duct  or  of  the 
receptaculum,-  or  larger  lymph-vessels  or  chyle-vessels  may  produce  an 
ascites  the  fluid  of  which  contains  chyle. 

Symptoms. — When  the  abdomen  of  a  patient  suffering  from  ascites  is 
exposed,  it  is  seen  to  be  greatly  enlarged,  this  enlargement  being  chiefly  in 
the  lower  and  lateral  zones,  although  if  the  intestines  are  by  chance  dis- 
tended by  gas  the  upper  and  middle  zone  may  be  most  enlarged.  The 
line  of  the  ribs  is  usually  sharply  defined,  by  reason  of  the  fact  that  they 
do  not  yield  readily  to  the  pressure  and  are  held  in  place  by  the  dia- 
phragm. 

If  the  ascites  be  due  to  hepatic  cirrhosis,  the  venules  about  the  navel  will 
often  be  found  engorged  (see  Cirrhosis  of  the  Liver),  and  in  all  forms  of 
ascites  due  to  venous  obstruction  the  veins  under  the  skin  in  the  right  and 
left  hypogastrium  and  groins  may  be  surcharged  with  blood  in  an  endeavor 
to  establish  a  collateral  circulation,  and  so  relieve  deep  pressure  in  the 
venous  trunks. 

The  signs  of  fluid  in  the  abdominal  cavity  are  dulness  on  percussion  in 
the  flanks,  and  in  the  suprapubic  region  when  the  patient  is  semi-recumbent, 
with  tympany  over  the  anterior  and  middle  zone  of  the  abdomen  extending 
upward  to  the  epigastrium,  owing  to  the  intestines  being  floated  up  against 
the  anterior  abdominal  wall  by  the  fluid  beneath.  If  the  hand  of  the  nurse 
is  placed  with  its  ulnar  edge  upon  the  middle  line  of  the  abdomen,  the  left 
hand  of  the  physician  placed  on  the  right  flank,  and  the  right  hand  used  to 
lightly  strike  the  left  flank,  distinct  fluctuations  will  be  felt  by  the  left  hand, 
the  impulse  being  transmitted  by  the  fluid  from  one  side  to  the  other,  the 
hand  of  the  nurse  being  used  to  prevent  the  transmission  of  this  impulse 
through  the  abdominal  wall.  Changing  the  patient's  position  from  the 
recumbent  to  the  erect   posture  will  change  the  area  of   dulness  on  per- 


ASCITES 


651 


cusslon  and  the  shape  of  the  abdomen,  owing  to  the  alteration  in  the  position 
of  the  fluid.  Palpation  will  reveal  fluctuation  if  the  belly  is  not  too 
tense.  Percussion  will  give  a  tympanitic  note  in  the  epigastrium  when  the 
patient  is  sitting  up  and  flatness  below  the  navel  and  at  the  sides  of  the 
abdomen. 

A  patient  who  has  ascites  to  any  considerable  degree  is  usually  unable  to 
lie  down  with  the  head  low,  because  if  this  attitude  is  assumed  the  pressure 
of  the  fluid  against  the  diaphragm  is  such  that  breathing  is  interfered  with. 
For  this  reason  he  usually  sits  propped  up  in  bed  or  in  a  reclining  chair. 
The  face,  which  is  usually  thinner  than  in  health  and  somewhat  haggard, 
forms  a  striking  contrast  to  the  large  abdomen,  which  is  "aldermanic"  in 


Ascites  due  to  cardiac  dropsy,  with  diastasis  of  the  recti  muscles,  so  that  there  is  a  subcutaneous 
hernia  in  the  tissue  around  the  umbilicus.  There  is  also  enteroptosis  due  to  great  relaxation  of  the 
abdominal  wall,  which  actually  overlies  the  thighs. 


appearance,  and  if  the  legs  be  dropsical  as  well,  the  massiveness  of  the  lower 
half  of  the  trunk,  as  compared  to  the  upper  half  and  to  the  neck  and  face, 
presents  a  striking  picture.  Not  rarely  the  face  bears  the  expression  known 
as  the  "abdominal  facies." 

Dyspnoea  may  not  be  noticeable  when  the  patient  is  at  absolute  rest,  but 
it  not  rarely  happens  that  so  slight  an  exertion  as  conversation  will  develop 
this  symptom,  particularly  if,  in  addition,  there  be  some  tendency  to  oedema 
at  the  bases  of  the  lungs.  As  a  rule,  men  are  more  uncomfortable  when 
suffering  from  ascites  than  are  women,  because  their  respiration  is  naturally 
more  diaphragmatic  than  that  of  women,  whose  respiratory  movement  is 
chiefly  costal. 


652 


DISEASES  OF  THE  PERITONEUM 


Diagnosis. — Ascites  must  be  differentiated  from  distention  of  the  abdomen 
due  to  a  large  ovarian  cyst.  This  can  usually  be  accomplished  by  palpation 
percussion,  and  vaginal  examination.  Inspection  of  a  case  of  a  cyst  will 
usually  reveal  somewhat  greater  distention  of  one  side  of  the  abdomen 
than  the  other.  The  area  of  dulness  on  percussion  will  not  be  in  the  lower 
zone  of  the  abdomen  alone,  but  will  extend  upward  toward  the  ribs  and  will 
include  part  of  the  area  in  the  anterior  and  middle  zone  of  the  belly,  which 
in  ordinary  ascites  is  tympanitic.  Further  than  this,  a  large  ovarian  cyst 
of  this  character  will  usually  be  tense  and  will  offer  more  resistance  when 
the  abdomen  is  palpated  with  both  hands. 


Fig.  87 


Case  of  enormous  ascites  due  to  atrophic  hepatic  cirrhosis. 


From  enlargement  of  the  spleen  in  chronic  leukaemia  ascites  may  be  differ- 
entiated, by  reason  of  the  fact  that  in  this  disease  the  area  of  dulness  is  chiefly 
in  the  upper  zone  instead  of  in  the  lower  zone  of  the  belly,  that  tympany  is 
usually  not  present  in  the  middle  line  if  the  spleen  extends  so  far,  and  that  the 
edge  of  the  spleen  can  be  readily  palpated.  In  some  cases,  however,  in  which 
the  spleen  is  enlarged  in  leukaemia,  ascites  is  also  present,  and  it  may  be 
impossible  to  feel  the  edge  of  the  spleen  until  some  of  the  fluid  is  removed. 
This  removal  may  be  more  difficult  than  in  an  ordinary  case  of  ascites, 
because  the  spleen  may  be  so  close  to  the  anterior  abdominal  wall  and  may 
extend  so  far  down  toward  the  pubis  that  ordinary  paracentesis  cannot  be 
readily  performed  without  danger  of  puncturing  the  spleen.  Ascites  must  also 
be  separated  from  great  enlargement  of  the  liver,  as  in  hypertrophic  cirrhosis. 
Here,  again,  the  presence  of  dulness  in  the  right  upper  zone  of  the  abdomen 


INFLAMMATION   OF   THE   LIVER  653 

and  the  ability  to  feel  the  lower  edge  of  the  large  liver  will  aid  materially  in 
the  differentiation.  In  both  enlargement  of  the  spleen  and  enlargement  of 
the  liver  the  area  of  dulness  and  of  tympany  is  not  materially  altered  by 
changing  the  posture  of  the  patient  as  it  is  in  ascites. 

Treatment. — The  treatment  of  ascites  depends  to  some  extent  upon  its 
cause.  If  it  is  due  to  interference  with  the  circulation  by  pressure,  as  in 
atrophic  hepatic  cirrhosis,  little  can  be  done  except  to  remove  the  fluid 
by  paracentesis,  for  the  purpose  of  giving  the  patient  relief  from  distention. 
If  it  is  due  to  cardiac  disease  an  improvement  in  the  condition  of  the  heart 
by  the  use  of  digitalis  and  rest,  and  the  judicious  administration  of  saline 
purges,  may  remove  the  fluid.  In  renal  disease  the  use  of  purgatives  may 
also  be  of  value,  but  paracentesis  has  usually  to  be  resorted  to  if  the  fluid  is 
present  in  large  amount.  In  peritoneal  tuberculosis  paracentesis  may  be  of 
value,  but  the  best  method  of  producing  cure  is  to  resort  to  abdominal 
section,  permitting  the  fluid  to  escape  through  the  incision,  and  then 
maintaining  drainage. 

Before  performing  paracentesis  abdominis  the  patient  should  be  made  to 
evacuate  his  bladder,  in  order  that  by  no  possibility  can  it  be  punctured  by 
the  trocar.  If  the  patient  be  a  woman,  great  care  should  be  taken  that  an 
ovarian  cyst  is  not  punctured.  Puncture  of  a  papillomatous  cyst  not  infre- 
quently results  in  the  speedy  death  of  the  patient. 


DISEASES  OF  THE  LIVER. 

INFLAMMATION  OF  THE  LIVER. 

Acute  Hepatitis  or  Hepatic  Abscess.  Definition.— Acute  exudative 
hepatitis  is  a  state  of  inflammation  of  the  liver  in  which,  after  a  stage 
of  hypersemia  with  exudation,  the  area  involved  undergoes  necrosis,  and 
abscess  results. 

Etiology. — Inflammation  of  the  liver,  severe  enough  to  result  in  suppura- 
tion, may  arise  from  injury,  from  inflammation  of  the  portal  vein  or  of  the 
bile-ducts,  or  from  adhesions  to  neighboring  organs  which  are  infected  and 
from  which  infection  may  spread,  as,  for  example,  in  cases  of  gastric  ulcer. 

Suppuration  within  the  substance  of  the  liver  beneath  its  capsule  or  in 
the  bile  passages  occurs  under  many  varying  conditions. 

Traumatic  Abscess. — Liver  abscess  may  result  from  traumatism.  The 
traumatism  may  be  a  severe  blow  or  contusion,  or  a  penetrating  wound  in 
or  near  the  liver  from  a  bullet,  knife,  or  other  weapon.  Traumatic  abscess 
of  the  liver  is  usually  single.  When  it  occurs  as  a  result  of  contusion  in 
the  absence  of  direct  infection,  the  injury  acts  by  lessening  resistance  and 
permitting  colonization  of  pyogenic  bacteria  brought  to  the  organ  by  the 
portal  vein  or  hepatic  artery. 


654  DISEASES  OF   THE  LIVER 

Pyemic  Abscesses. — Pyaemic  abscesses  are,  as  a  rule,  multiple.  One 
group  of  cases  arises  from  pyogenic  embolism  of  the  portal  vein.  There  is 
phlebitis  or  thrombophlebitis  of  the  portal  trunk  or  its  branches,  the  infection 
being  due  to  ulcerations  in  the  colon  and  rectum,  or  to  appendicitis,  ulcera- 
tions and  suppurative  processes  about  the  neck  of  the  bladder,  and  typhoid 
fever.  Another  group  of  cases  arises  from  embolism  of  the  hepatic  artery, 
as  in  ulcerative  endocarditis  and  other  pyeemic  conditions.  Infe<2tion 
may  also  reach  the  liver  through  the  lymphatics.  Abscess  may  also  arise 
from  the  direct  extension  of  infection  from  the  gall-bladder  and  the 
biliary  ducts.  Ascarides,  liver  flukes,  echinococcus,  and  the  Balantidium 
coli  may  also  cause  abscess  of  the  liver,  and  it  has  also  been  observed  as  a 
sequel  to  measles,  epidemic  influenza,  and  ulcer  of  the  stomach. 

Aaicebic  Abscess  of  the  Liver. — In  the  consideration  of  the  etiology  of 
tropical  abscess,  we  find  predisposing  and  direct  causes.  As  a  predisposing 
cause,  the  passive  congestion  of  the  liver  which  exists,  to  some  extent,  in  a 
large  proportion  of  colonists  in  the  tropics,  must  be  remembered.  Other 
predisposing  factors  in  the  production  of  tropical  abscess  are  malaria  and 
exposure  to  cold  and  wet.  Abuse  of  alcohol  is  probably  an  important 
predisposing  cause.  In  Waring's  careful  study  of  the  subject  of  abscess  of 
the  liver,  he  found  a  clear  history  of  the  abuse  of  alcohol  in  65  per  cent,  of 
the  cases. 

The  direct  cause  of  tropical  abscess  is  the  aoemhce  dysenterioe  which  may 
or  may  not  have  previously  excited  intestinal  lesions.  Various  observers 
have  found  that  tropical  abscess  of  the  liver  has  been  preceded  by 
dysentery  in  from  72  to  97  per  cent,  of  all  cases.  Woodward,  in  3680 
dysentery  autopsies,  found  liver  abscess  in  779,  or  21  per  cent.  Boston  col- 
lected data  of  2430  autopsies,  with  486  abscesses,  or  20  per  cent.  Legrand, 
of  Alexandria,  found  that  in  109  cases  of  hepatic  abscess  which  occurred  in 
children  31  were  due  to  dysentery.  Hepatic  suppuration  may  develop  very 
shortly  after  the  dysentery,  or  may  be  delayed  for  years.     (See  Dysentery.) 

Pathology  and  Morbid  Anatomy. — Abscess  of  the  liver  usually  occurs  either 
in  one  or  two  large  purulent  collections  or  in  a  number  of  small  abscess 
cavities. 

The  single  large  abscess  is  usually  the  result  of  dysentery,  and  the  infec- 
tion reaches  the  liver  through  the  veins,  which  closely  anastomose  with 
the  hemorrhoidal  plexus.  If  the  cause  be  dysentery  of  the  amoebic  type, 
the  amoeba  is  found  in  the  wall  of  the  abscess,  and  less  constantly  in  the 
abscess  contents.  In  still  other  cases  an  examination  of  the  pus  reveals  the 
presence  of  the  Bacillus  coli  communis,  or  the  Streptococcus  pyogenes  or 
a  pyogenic  staphylococcus.  In  still  other  cases,  if  the  abscess  be  very  chronic, 
the  pus  may  be  sterile. 

In  tropical  abscesses  the  lesion  is  solitary  in  about  60  per  cent  of  the  cases ; 
it  is  single,  from  coalescence,  or  double  in  about  15  per  cent,  of  the  cases,  and 
the  remainder  are  multiple.  The  abscesses  vary  in  size  from  a  pigeon 's  egg 
to  a  cocoanut. 

The  single  abscess  may  be  very  large,  and  often  fills  an  entire  lobe  of 
the  liver.  The  right  lobe  is  usually  affected,  and  as  the  abscess  gradually 
nears  the  surface  of  the  organ  it  bursts  through  the  capsule  into  the  peri- 


INFLAMMATION  OF   THE  LIVER 


655 


toneal  cavity,  or,  as  is  far  more  common,  the  advancing  inflammatory  zone 
causes  the  surface  of  the  hver  to  become  adherent  to  adjacent  structures, 
so  that  when  rupture  takes  place  the  pus  breaks  into  the  bowel,  as  in  a  case 
recently  under  my  care,  or  through  the  diaphragm  into  the  pleura,  or  even 
into  the  lung,  so  that  the  pus  from  the  liver  escapes  by  the  respiratory  tract. 
Accumulations  of  pus  in  burrowing  a  way  for  escape  often  cause  extra- 
ordinary effects,  and  cases  are  on  record  in  which  the  pus  from  one  of  these 
abscesses  has  escaped  into  the  pericardium,  and  even  into  the  pelvis  of  a 
kidney.  Still  other  instances  have  occurred  in  which  the  pus  has  found  its 
way  into  the  great  veins  of  the  abdomen  or  into  the  gall-bladder.  Rupture 
externally  is  not  common. 


Fig.  88 


Liver,    amcebic   abscess   of  right  lobe;  case  of  dysentery.      Note  the  shaggy  necrotic  wall   and   that   the 
abscess  has  approached  the  superior  surface  of  the  organ. 

The  pus  from  such  an  abscess  is  often  very  offensive,  and  it  generally  differs 
from  ordinary  pus  in  appearance,  being  thin  instead  of  creamy,  reddish 
instead  of  yellow,  and  oftentimes  it  is  quite  green  from  the  presence  of  bile. 
Sometimes,  however,  the  pus  is  quite  like  that  commonly  found  in  abscesses. 

The  lining  of  the  abscess  cavity  is  shaggy,  because  of  the  pieces  of  dead 
hepatic  tissue  which  hang  upon  it  (Fig.  88).  In  abscesses  of  long  standing 
more  or  less  imperfect  encapsulations  of  the  pus  may  occur. 

Large  multiple  abscesses  are  sometimes  met  with  as  the  result  of  suppura- 
tion about  an  echinococcus  cyst. 

Small  multifile  abscesses  are  usually  pytemic — i.  e.,  of  metastatic  origin. 
Septic  emboli,  or  micro-organisms,  from  septic  foci  elsewhere  are  carried 
by  the  blood  into  the  liver  and   cause   multiple    areas   of    necrosis,  and 


656 


DISEASES  OF   THE  LIVER 


suppuration.  The  liver,  therefore,  presents  not  one  large  abscess,  but  a 
large  number  well  distributed  through  its  tissues.  These  abscesses  vary 
in  size.  Several  small  necrotic  cavities,  which  may  hold  several  drachms 
of  pus,  may  be  present,  or  a  number  may  coalesce  to  form  one  large 
abscess.  Although  each  abscess  seems  isolated,  it  is  usually  in  communica- 
tion through  a  branch  of  the  portal  vein  with  others,  so  that  by  this  vascular 
pathway  the  whole  gland  is  riddled  with  pus.  The  pus  may  vary  from  foul, 
reddish,  or  greenish  material  to  the  character  of  what  used  to  be  called,  in 
preantiseptic  days,  "laudable  pus." 

When  the  infection  takes  place  along  the  bile-ducts,  as  the  result  of  the 
entrance  of  micro-organisms,  the  introduction  of  which  is  facilitated  by  the 
presence  of  gallstones,  it  is  often  found  that  the  pus  is  not  only  distributed 


Fig.  89 


Chart  showing  septic  fever  and  marked  leukocytosis  in  case  of  hepatic  abscess.    (Bassett-Smith.) 

widely  through  the  organ,  but,  in  addition,  that  the  gall-bladder  is  full  of  pus 
as  well,  so  that  the  entire  biliary  tract  is  involved  in  the  suppurative  process. 

Small  multiple  abscesses  may  be  due  not  only  to  the  ordinary  organisms  of 
suppuration,  but  to  infection  by  the  Amceba  dysenterice. 

Symptomatology. — The  symptoms  of  hepatic  suppuration  are  usually 
marked.  In  some  cases,  however,  even  with  the  existence  of  large  abscesses, 
the  lesion  is  latent,  and  the  disease  is  not  suspected  until  rupture  of  the 
abscess  occurs.  The  chief  symptoms  are  fever,  sepsis,  enlargement  of  the 
liver,  and  pain. 

The  pain  is  felt  not  only  in  the  right  hypochondrium,  but  in  the  region  of 
the  right  shoulder  blade,  and,  as  the  abscess  approaches  the  surface  and 
causes  inflammation  of  the  peritoneum,  the  pain  may  be  sharp  and  even 
severe. 


INFLAMMATION  OF  THE  LIVER  657 

There  is  loss  of  weight  and  strength  and  pronounced  feebleness  in  mus- 
cular effort.  Dyspeptic  symptoms  become  marked.  There  is  anorexia, 
nausea,  morning  vomiting,  with  a  heavily  coated  tongue.  The  patient  becomes 
ancemic  and  gradually  takes  on  a  peculiar  subicteric  color.  The  fever 
begins  early  and  is  the  most  constant  symptom.  At  first  it  does  not 
run  high,  but  later  an  evening  temperature  of  from  104°  to  105°  is  not 
uncommon.  The  fever  is  irregular  or  intermitting  in  type.  It  is  preceded 
by  a  chill  and  then  followed  by  a  sweat.  These  sweats  are  very  severe  and 
contribute  greatly  to  the  depression  and  exhaustion  of  the  patient.  They 
follow  the  fastigium  of  the  fever  and  are  prone  to  come  on  during  sleep,  whether 
it  be  by  day  or  night ;  so  that  they  may  be  properly  called  sleeping  sweats 
rather  than  night  sweats. 

Enlargement  of  the  liver  is  constant.  It  is  symmetrical,  and  in  extreme 
cases  may  reach  as  high  as  the  third  rib  in  front  and  may  extend  as  far 
down  as  the  crest  of  the  ilium,  or  over  as  far  as  the  umbilicus.  The 
right  hypochondrium  may  appear  full  and  bulging,  and  there  may  be 
an  apparent  fulness  or  sleekness  of  the  right  side,  and  in  marked  cases 
obliteration  of  the  lower  intercostal  spaces. 

When  pus  approaches  close  to  the  surface  it  is  always  preceded  by  an 
oedema  of  the  skin  overlying  the  abscess,  and  in  cases  with  large  abscess 
fluctuation  may  be  present.  Auscultation  over  the  liver  may  reveal  peritoneal 
or  liver  friction. 

Occasionally  sharp  pain  is  felt  in  the  oesophagus,  when  a  food  bolus 
passes  the  level  of  the  diaphragm.  A  dry,  hacking,  unproductive  cough  is 
very  commonly  present  and  frequently  leads  to  error  by  directing  attention 
to  the  lungs  rather  than  to  the  liver. 

The  decubitus  of  the  patient  is  characteristic.  He  lies  on  his  right  side 
with  that  shoulder  drawn  down  and  knee  drawn  up  to  relieve  the  tension  on 
the  abdominal  muscles. 

Jaundice  is  not  common  and  only  appears  when  the  enlarged  liver  or 
abscesses  make  pressure  on  the  bile-duct.  Pressure  on  the  portal  vein  may 
cause  a  moderate  degree  of  ascites. 

Pneumonia  of  the  right  base  often  occurs  when  the  abscess  is  high  up  in 
the  dome  of  the  liver. 

Diagnosis. — The  condition  which  in  all  probability  most  closely  resembles 
hepatic  abscess  is  infection  of  the  gall-duct  or  gall-bladder,  produced  by  the 
presence  of  a  stone  or  stones,  for  here,  too,  there  is  septic  absorption,  high 
fever,  chills,  sweats,  and  tenderness  about  the  liver,  although  pus  may  not 
be  actually  present.  In  this  condition,  however,  there  is  a  history  of  gallstone 
colic  in  most  instances,  and  of  jaundice.  Further,  the  emaciation  and 
anaemia  are  not  so  marked,  nor  is  the  liver  so  generally  increased  in  size.  A 
marked  leukocytosis  is  present  in  either  case. 

The  absence  of  marked  swelling  of  the  spleen,  of  any  history  of  malarial 
infection,  and  the  lack  of  the  malarial  parasite  in  the  blood,  combined  with 
the  fact  that  the  fever  does  not  yield  to  quinine,  all  go  to  prove  the  febrile 
state  not  malarial.  The  blood  condition  may  also  aid  in  the  diagnosis. 
There  is  usually  a  marked  leukocytosis,  which  ranges  from  12,000  to  53,000. 
Unfortunately,  this  symptom  is  not  constant,  but  when  it  does  occur  it 
42 


558  DISEASES  OF   THE  LIVER 

makes  a  clear  distinction  between  this  disease  and  malaria.  Other  condi- 
tions that  simulate  liver  abscess  are  hepatic  colic  with  fever,  suppuration 
in  and  about  the  gall-bladder,  suppuration  in  or  near  the  right  kidney, 
subdiaphragmatic  abscess,  empyema  or  pneumonia  of  the  right  base,  and 
ulcerative  endocarditis. 

An  empyema  or  pleural  effusion  on  the  right  side  can  be  excluded  by  the 
decrease  in  vocal  resonance  and  vocal  fremitus  caused  by  that  state,  and  by 
the  presence  of  Skodaic  resonance  just  above  the  area  of  dulness  on  per- 
cussion. 

It  is  important  to  remember  that  amoebic  abscesses  may  be  present  with- 
out diarrhoea  or  dysentery,  the  amoebae,  nevertheless,  being  present  in  the 
stools  and  in  the  liver. 

In  all  obscure  cases  attended  by  the  signs  of  hepatic  disease  and  sepsis, 
an  effort  should  be  made  to  establish  the  condition  of  the  liver  by  explora- 
tory operation. 

Prognosis. — The  prognosis  of  abscess  of  the  liver  depends  on  two  factors, 
the  number  of  abscesses  and  the  time  when  the  case  is  brought  to  operation. 
Eighty  to  90  per  cent,  of  single  abscess  brought  to  early  operation  should 
recover,  but  often  operation  is  postponed  too  long.  In  cases  of  sponta- 
neous rupture  into  the  colon  50  per  cent,  recover.  The  prognosis  is  not  so 
good  where  rupture  takes  place  into  the  lung  or  pleura.  Recovery  occa- 
sionally takes  place  when  two  and  three  abscesses  are  present. 

In  162  fatal  cases  of  hepatic  abscess  the  mortality  is  given  as  due  to  the 
following  causes:  severity  of  the  accompanying  dysentery,  125  cases;  burst- 
ing of  abscess  into  the  peritoneum  12  cases,  into  the  pleura  11  cases;  gan- 
grene of  the  abscess  wall,  3  cases ;  rupture  of  adhesions,  2  cases ;  pneumonia, 
2  cases;  and  rupture  into  the  pericardium,  1  case.  The  prognosis  in  multiple 
abscess  is  hopeless,  for  manifest  reasons. 

Treatment. — The  treatment  of  hepatic  abscess  consists  in  sustaining  the 
patient's  strength  by  good  food  and  by  iron  and  arsenic,  and,  if  the  abscess 
is  single,  by  opening  and  draining  it  as  soon  as  its  existence  is  determined. 

Exploratory  puncture  should  not  be  practised  unless  the  surgeon  is 
prepared  to  go  ahead  and  operate  at  once.  If  pus  be  found,  the  puncture 
may  spread  infection  or  cause  a  leak  along  the  wound.  This  is  especially  a 
danger  with  large  needles,  and  large  needles  must  be  used  on  account  of  the 
thickness  and  viscosity  of  the  abscess  contents  in  some  cases. 


CIRRHOSIS  OF  THE  LIVER. 

Definition. — Cirrhosis  of  the  liver  is  a  state  in  which  there  is  an  overgrowth 
of  connective  tissue  of  the  gland.  In  some  instances  this  overgrowth  results 
in  an  atrophy  and  shrinkage  of  the  organ  (atrophic  cirrhosis) ;  in  others  the 
liver  becomes  greatly  enlarged  (hypertrophic  cirrhosis). 

Recently  Kretz,  MacCallum,  Kelly,  and  others  have  called  attention  to 
regenerative  changes  in  the  liver  cells  as  being  a  prominent  feature  of  cir- 
rhosis. They  do  not  regard  the  normal  liver  as  made  up  of  distinct  lobules 
but  as  consisting  of  continuous  mantles  of  cells  surrounding  the  blood- 


CIRRHOSIS  OF   THE  LIVER 


659 


vessels.  In  cirrhosis,  following  degenerative  changes,  these  cells  regenerate 
and  rearrange  themselves  and,  according  to  Kretz,  cirrhosis  is  consequently 
to  be  regarded  as  a  focal  recrudescent  chronic  atrophy  of  liver  cells  modified 
by  parenchymatous  regeneration  and  not  as  a  disease  entity.  He  believes 
that  practical  extension  of  our  knowledge  on  this  subject  is  to  come  from 
investigating  the  causes  of  degeneration  of  Hver  cells  rather  than  from 
attempts  further  to  differentiate  and  classify  so-called  types  of  developed 
cirrhosis. 

Cirrhosis  of  the  liver  derives  its  name  from  the  Greek  word  ^^^<tc,  mean- 
ing yellow  or  tawny.  The  term  cirrhosis  was  first  applied  by  Laennec, 
because  the  liver,  when  cirrhotic,  is  yellow  or  tawny  in  color.  Cirrhosis  is  an 
unfortunate  term,  in  that  it  in  no  way  describes  the  pathological  state  which 


Fig.  90 


Liver,  advanced  cirrhosis;  typical  hob-nailed  organ.     A.  Gall-bladder. 


is  present.  Further  than  this,  the  word  cirrhosis  is  now  applied  to  patholog- 
ical states  of  other  organs  in  which  no  yellow  hue  is  seen. 

Atrophic  Cirrhosis. — The  liver  in  cases  of  atrophic  cirrhosis  is  often 
enlarged  in  the  early  stage  of  the  disease,  but  after  this  primary  change 
it  undergoes  a  diminution  in  size,  so  that  eventually  it  is  much  smaller 
than  normal.  This  primary  enlargement,  which  does  not  always  occur,  is 
perhaps  due  to  hypersemia,  cellular  infiltration,  and  oedema.  The  charac- 
teristic picture  of  atrophic  cirrhosis  is.  however,  that  of  a  small,  contracted 
liver,  tawny  in  hue,  and  possessing  a  roughened  surface,  which  in  some  cases 
may  be  so  irregular  as  to  be  called  "hob-nail"  liver,  because  of  its  resem- 
blance to  a  rough  shoe  the  sole  of  which  is  filled  with  hob-nails  (Fig.  90). 

Atrophic  cirrhosis  of  the  liver  is  a  not  uncommon  malady  in  adults,  and 


660  DISEASES  OF   THE  LIVER 

it  is  by  far  the  most  frequent  of  all  the  types  of  cirrhosis  which  affect  this 
organ. 

Etiology. — The  causes  of  atrophic  cirrhosis  of  the  liver  are  chronic  alcohol- 
ism and  other  chronic  intoxications,  of  which  lead  is  certainly  one  of  the  most 
important.  There  is  good  reason  to  believe  that  prolonged  gastrointestinal 
indigestion  and  disorders  of  nutrition,  such  as  gout  and  its  allied  states,  may 
exert  a  similar  effect.  Experimental  cirrhosis  has  been  produced  in  animals 
by  acetic,  lactic,  butyric,  and  valerianic  acid,  all  of  which  are  present  in 
cases  of  gastrointestinal  disorder.  Syphihs  may  cause  it  (see  Syphilis  of 
the  Liver),  and  hepatic  cirrhosis  has  been  known  to  develop  after  severe 
infectious  fevers.  Cardiac  disease,  with  great  and  prolonged  hepatic  conges- 
tion, may  also  produce  cirrhotic  changes,  and  it  is  a  noteworthy  fact  that 
cirrhosis  in  ay  be  present  as  a  part  of  a  general  fibroid  process  involving  the 
bloodvessels  and  the  kidneys. 

Pathology  and  Morbid  Anatomy. — In  cirrhosis  of  the  liver  the  dominant 
lesion  is  an  increase  in  its  connective  tissue.  This  overgrowth  varies  very 
greatly  in  different  cases.  Although  the  fibrous  overgrowth  may  penetrate 
the  lobules,  it  is  principally  increased  at  the  periphery  of  these  structures. 
Again,  it  may  be  equally  distributed  throughout  the  entire  liver  or  affect 
certain  areas  very  much  more  than  others,  and,  finally,  the  overgrowth 
of  fibrous  tissue  may  be  so  great  that  bands,  both  large  and  small,  may 
traverse  the  liver  substance,  separating  it  into  masses  of  compressed  gland- 
ular tissue. 

The  fibrous  tissue  formed  in  this  process,  like  fibrous  tissue  formed 
elsewhere  in  the  body,  undergoes  cicatricial  contraction,  and  by  this  means 
fatty  degeneration  or  atrophy  of  the  liver  cells  composing  the  lobules  is 
facilitated.  These  changes  are  due,  not  only  to  the  pressure  exerted  on  the 
lobules,  so  that  their  cells  are  flattened  and  deformed,  but  also  to  the  effects 
produced  on  the  circulation  of  blood  in  the  liver. 

It  will  be  recalled  that  the  hepatic  artery  carries  to  the  liver  the  blood 
which  is  to  nourish  its  cells,  just  as  the  bronchial  arteries  carry  the  blood 
which  is  to  nourish  the  lungs.  The  blood  from  the  branches  of  this  vessel  in 
performing  its  nutritive  function  passes  through  the  so-called  interlobular 
vessels,  and  from  these  into  the  intralobular  vessels,  which  carry  blood 
from  the  digestive  organs. 

The  overgrowth  of  fibrous  tissue  in  the  interlobular  spaces,  in  the  fibrous 
sheath  of  the  interlobular  veins,  and  sometimes  even  between  the  cells  about 
the  intralobular  veins  results  in  obstruction  to  the  flow  of  blood.  The 
arterial  supply  is  little  affected,  but  the  venous  flow  is  interfered  with,  and  in 
this  manner  the  cells  suffer,  not  only  from  the  pressure  of  the  fibrous  tissue, 
but  from  the  pressure  in  the  vessels  and  the  lack  of  fresh  blood  as  well. 
Nor  is  this  all,  for  the  fibrous  tissue  obstructs  the  smaller  bile-ducts  and  so 
prevents  the  escape  of  bile,  with  the  result  that  atrophy  takes  place  from 
retained  secretion,  and  the  tissues  of  the  liver  become  bile-stained. 

Many  pathologists  adhere  to  the  view  that  the  destruction  of  the  paren- 
chyma of  the  organ  takes  place  first,  and  that  the  overgrowth  of  the  con- 
nective tissue  already  described  is  secondary  to  this  change. 

The  remote  effects  of  the  interference  with  the  circulation  of  blood  in  the 


CIRRHOSIS  OF   THE  LIVER  661 

liver  is  catarrh  of  the  stomach  and  duodenum,  due  to  the  obstruction  of  the 
blood  in  the  portal  veins.  This  state,  finally,  may  cause  varicosities  in 
the  gastric  or  oesophageal  vessels,  and  hajmatemesis  may  ensue,  or  it  may 
cause  fatal  hemorrhage  from  the  bowels  because  of  similar  varicosities 
in  the  intestinal  wall.  The  marked  portal  obstruction  leads  to  trans- 
udation from  the  peritoneal  vessels,  constituting  the  ascites  of  hepatic 
cirrhosis. 

Not  rarely  in  well-developed  cases  of  hepatic  cirrhosis  the  veins  of  the 
abdominal  wall  will  be  found  enlarged  in  an  endeavor  to  supplement  the 
deep  abdominal  veins  in  the  transfer  of  blood  from  the  portal  area  to 
the  vessels  of  the  thorax.  Still  another  state,  called  the  " caput  medusae" 
is  the  development  of  a  bunch  of  enlarged  veins  about  the  umbilicus.  This 
has  been  generally  considered  as  due  to  the  stasis  in  the  paraumbilical  vein 
or  in  the  umbilical  vein,  which  has  not  closed,  as  it  usually  is  after  birth. 
As  a  result  a  collateral  circulation  is  established  by  an  anastomosis  with 
the  internal  mammary,  epigastric,  and  cutaneous  veins. 

From  the  description  which  has  just  been  given  of  the  effect  of  cicatricial 
contraction,  it  is  easily  seen  why  the  liver  presents  upon  its  surface  so  many 
excrescences  or  projections  (the  so-called  "hob-nail  liver"),  for  parts  of  the 
gland  are  pressed  out  of  place,  or  irregular  bands  pulled  in,  by  the  ever- 
growing fibrous  bands.     (See  Fig.  90.) 

The  atrophy  of  the  parenchyma  of  the  liver  in  the  true  atrophic  form 
causes  a  very  great  diminution  in  the  size  of  the  organ,  so  that  the  organ  may 
be  less  than  one-half  its  natural  dimensions. 

The  spleen  is  usually  enlarged,  and  arteriosclerotic  changes  are  often 
present.    Secondary  fibroid  changes  in  the  pancreas  have  also  been  described. 

In  the  so-called  fatty  cirrhosis,  in  which  the  deposit  of  fat  is  more  pro- 
nounced than  the  cicatricial  contraction  of  fibrous  tissue,  the  gland  may  not 
be  decreased  in  size,  and  it  may  be  very  much  larger  than  the  normal.  Such 
a  liver  is  rarely  hob-nailed,  but  smooth,  or  but  slightly  roughened. 

Peritoneal  and  pleural  tuberculosis  is  a  very  common  complication  of 
atrophic  cirrhosis  of  the  liver. 

Symptoms. — The  symptoms  of  atrophic  cirrhosis  of  the  hver  are,  to  a  large 
degree,  dependent  upon  the  obstruction  to  the  circulation  of  blood  in  the 
intralobular  and  interlobular  vessels,  and  if  the  effects  of  this  obstruction  are 
relieved,  or  prevented  from  developing,  by  the  establishment  of  an  efficient 
collateral  circulation,  there  may  be  no  symptoms  at  all  for  many  months,  or. 
indeed,  for  years.  Occasionally  we  meet  with  cases  in  which  an  extreme 
degree  of  atrophy  of  the  liver  seems  to  be  present  with  no  symptoms  of 
any  importance,  and  yet  the  patient  is  taking  far  more  alcohol  than  is  good 
for  him.  It  is  scarcely  conceivable  that  the  establishment  of  a  collateral 
circulation  can  be  responsible  for  the  absence  of  all  systemic  disturbance, 
but  there  is  no  other  explanation  for  it. 

When  obstruction  to  the  flow  of  blood  in  the  portal  vessels  is  produced 
gastric  catarrh  develops,  and  this  causes  indigestion  and  distress  in  the 
epigastrium,  with  morning  nausea  and  vomiting.  Usually  the  patient  loses 
strength  and  is  prone  to  become  spare  and  lean  if  previously  stout. 

The  occurrence  of  hemorrhage  from  the  stomach,  and  bowel  has  already 


662  DISEASES  OF   THE  LIVER 

been  mentioned  when  discussing  the  secondary  lesions  of  the  disease,  as 
has  also  the  presence  of  enlarged  abdominal  veins  and  the  cayut  medusce  on 
the  abdominal  wall.  (See  also  the  article  on  Hsematemesis.)  The  skin  of 
the  trunk  is  often  more  sallow  and  yellow  than  normal,  but  it  is  rarely  dis- 
colored by  a  true  jaundice.  At  times  the  temperature  may  be  subnormal, 
and  at  others  slightly  febrile. 

In  some  cases  which  have  manifested  few  or  none  of  these  symptoms,  the 
patient,  with  little  warning,  develops  a  state  of  delirium,  which  is  often  of  a 
noisy  and  joyous  type,  but  he  soon  sinks  into  a  state  which  proceeds  to  coma, 
and  then  to  death.  To  this  state  the  term  "  hematic  coma"  has  been  applied. 
It  was  thought  at  one  time  to  be  due  to  cholestersemia,  but  this  view  has  now 
been  cast  aside  without  any  satisfactory  explanation  of  the  state  being  offered. 
I  have  so  often  seen  this  condition  follow  free  drainage  of  ascites  that  I  believe 
this  operation  predisposes  to  its  development. 

The  physical  signs  of  atrophic  cirrhosis  consist  in  an  inability  to  palpate 
the  lower  margin  of  the  liver  by  ordinary  effort,  and  in  the  small  area  of 
hepatic  dulness  on  percussion.  In  those  cases  in  which  ascites  is  marked,  it 
is  often  impossible  to  discover  the  state  of  the  liver  until  the  fluid  is  with- 
drawn. 

Some  have  held  that  the  ascites  is  really  the  result  of  an  associated  low- 
grade  peritonitis. 

Hess  has  lately  directed  attention  to  obliterating  endophlebitis  of  the 
hepatic  veins  as  producing  symptoms  almost  identical  with  those  of  cir- 
rhosis. Most  of  the  23  cases  on  record,  as  also  the  one  he  reports,  were 
diagnosed  cirrhosis  of  the  liver.  The  signs  leading  one  to  suspect  oblitera- 
tion of  the  hepatic  veins  are  absence  of  the  history  of  a  cause  of  cirrhosis, 
pain  over  the  hepatic  area  or  localized  in  the  upper  abdomen,  and  rapid 
swelling  of  the  liver  and  development  of  ascites. 

Prognosis. — The  prognosis  as  to  the  duration  of  life  depends  entirely  upon 
the  degree  of  obstruction  to  the  circulation  and  upon  the  severity  of  the 
patient's  symptoms.  If  ascites  is  well  developed  the  outlook  for  more  than 
a  few  months  of  life  is  bad,  yet  there  are  cases  on  record  in  which  repeated 
tappings  have  resulted  in  the  prevention  of  recurrence  of  ascites  and  in  the 
apparent  recovery  of  the  patient.  Probably  in  these  cases  the  ascites  was  not 
due  to  the  cirrhosis,  or  the  relief  of  pressure  has  permitted  the  establishment 
of  a  collateral  circulation.  The  occurrence  of  hemorrhages  is  always  a  most 
grave  omen,  yet  patients  often  live  for  months  after  severe  bleedings.  On  the 
other  hand,  I  know  of  one  case  in  which  a  man,  in  apparently  perfect  health, 
while  washing  in  his  bath-room  bled  so  freely  from  the  stomach  as  to  die  in 
half  an  hour,  although  he  had  never  had  a  hemorrhage  before. 

Treatment. — The  treatment  consists  in  removing  the  cause  of  the  disease, 
if  it  be  alcohol,  and  in  an  endeavor  to  prevent  intestinal  fermentation  and 
disorder  by  mild  purgatives,  digestive  stimulants,  acids,  and  antiseptics. 
Each  morning  the  patient  should  have  the  bowels  well  moved  by  a  glass  of 
hot  Hunyadi  or  Carlsbad  water,  and  while  this  is  acting  he  should  receive  a 
few  drops  of  Fowler's  solution  for  the  nausea  and  lack  of  appetite  at  break- 
fast. During  breakfast,  luncheon,  and  supper  he  should  take  a  capsule 
made  up  as  follows: 


CIRRHOSIS  OF   THE  LIVER  663 

JJ  — Pancreatin, 

Taka-diastase, 

Sodii  bicarbonat aa     gr.  ij.— M. 

S. — Take  with  each  meal. 

In  some  cases  the  catarrhal  state  of  the  stomach  and  bowels  is  benefited 
by  the  use  of  small  doses  of  iodide  of  potassium,  5  grains  three  or  four  times 
a  day,  or  of  ammonium  chloride  in  the  same  amount. 

Within  the  last  few  years  it  has  been  proposed  by  Talma  and  others  that 
an  endeavor  be  made  to  relieve  the  obstructive  symptoms  of  atrophic  cirrhosis 
by  establishing  a  collateral  circulation  by  surgical  procedure.  The  anterior 
surface  of  the  liver,  of  the  spleen,  and  of  the  parietal  peritoneum  and  intes- 
tines are  roughened  by  being  rubbed  with  surgical  gauze,  and  the  omentum 
is  attached  to  the  parietal  peritoneum  of  the  anterior  abdominal  wall  by 
sutures.  By  this  means  it  is  hoped  to  cause  adhesions  through  which  the  col- 
lateral circulation  may  be  established.  According  to  Greenough's  statistics, 
only  9  cases  have  been  cured  in  105  operated  upon.  The  operation  is  not 
devoid  of  danger  because  of  the  malnutrition  of  the  patient. 

Ascites  should  be  treated  by  tapping.  (See  Ascites.)  The  use  of  violent 
hydragogue  cathartics,  in  the  hope  that  the  quantity  of  fluid  will  be  materially 
decreased,  is  not  very  successful,  as  a  rule,  and  may  weaken  the  patient.  It 
is,  however,  important  to  keep  the  bowels  opened  freely  to  avoid  distention 
and  pressure. 

Hypertrophic  Cirrhosis.  Definition. — Hypertrophic  cirrhosis  is  a  condi- 
tion in  which  the  liver  is  very  much  enlarged,  its  surface  is  smooth,  jaundice 
develops,  but  ascites  is  absent.  It  is  called  by  the  French  cirrhose  hyper- 
trophique  avec  ictere,  or  hypertrophic  cirrhosis  with  jaundice. 

Etiology. — The  causes  of  this  malady  are  unknown.  Alcohol  is  not  a 
factor.  In  the  cases  I  have  seen  a  history  of  severe  and  prolonged  malarial 
infection  has  been  present  in  several  instances.  It  is  a  disease  of  young  adult 
and  early  middle  life,  but  cases  occur  in  children  of  tender  years. 

Pathology  and  Morbid  Anatomy. — An  essential  difference  between  atrophic 
and  hypertrophic  cirrhosis  is  that  in  the  former  the  connective  tissue  which 
is  developed  undergoes  contraction,  whereas  in  the  hypertrophic  form  it 
remains  more  cellular  and  does  not  contract.  The  second  difference  lies  in 
the  fact  that  in  hypertrophic  cirrhosis  there  is  a  very  considerable  increase  of 
connective  tissue  about  the  biliary  ducts  (biliary  cirrhosis),  with  compara- 
tively little  or  no  increase  of  this  tissue  about  the  bloodvessels.  For  these 
reasons  we  do  not  find  any  marked  decrease  in  the  blood  supply  of  the  gland, 
but  we  do  find  jaundice  because  the  biliary  ducts  are  obstructed.  In  the 
atrophic  form,  therefore,  venous  obstruction  causes  ascites;  in  the  hyper- 
trophic form  biliary  obstruction  causes  jaundice,  but  there  is  usually  no 
ascites.  Between  these  two  types  of  cirrhosis  intermediate  cases  develop, 
in  which  sufficient  overgrowth  of  connective  tissue  about  the  bloodvessels 
may  be  present  to  cause  ascites,  for  in  hypertrophic  cirrhosis  there  is  an 
overgrowth  of  connective  tissue  about  the  interlobular  vessels,  and  even 
between  the  cells  of  the  lobules. 

Although  the  liver  is  enlarged,  it  does  not  present  the  hob-nailed  appear- 
ance of  atrophic  cirrhosis   because  contraction  does  not  occur.     On  cross- 


664  DISEASES  OF   THE  LIVER 

section  it  presents  a  firm  surface  of  a  yellowish-green  hue,  and  strands  of 
connective  tissue  can  be  seen  traversing  it. 

It  has  been  shown  that  in  some  instances  hypertrophic  cirrhosis  is  a 
secondary  condition  arising  from  disease  of  the  bile-ducts,  and  that  in 
others  it  is  a  primary  state  without  connection  with  any  direct  cause  yet 
discovered.  As  a  consequence,  some  writers  have  divided  this  disease  into 
two  types  and  have  asserted  that  these  are  separate  entities.  The  patholog- 
ical changes  in  each  case  are  so  nearly  identical  that  this  separation  is  not 
justifiable.  To  the  primary  form  the  term  "  Hanot's  cirrhosis  "  has  been 
applied.  In  this  form  there  is  pigmentation  of  the  skin  in  addition  to  jaun- 
dice, there  is  usually  more  pain  than  in  the  commoner  variety,  and  the 
spleen  is  usually  very  large.  It  is  better  to  call  such  cases  instances  of 
Hanot's  type  of  hypertrophic  cirrhosis. 

Symptoms. — ^The  predominant  symptom  of  this  disease  is  enlargement  of 
the  liver,  which  often  extends  to  a  lower  level  than  that  of  the  navel  and  far 
to  the  left  of  the  middle  line.  When  the  liver  is  palpated  it  is  found  to  be 
hard  and  its  surface  fairly  smooth,  its  edges  rounded,  and  its  movement 
heavy  and  difficult  when  it  is  pressed  upon.  Percussion  reveals  the  fact  that 
it  not  only  extends  downward,  but  upward  far  above  the  ordinary  hepatic 
level,  and  laterally  even  to  the  sixth  rib,  pushing  the  diaphragm  and  lung 
before  it.  The  spleen  is  usually  considerably  enlarged.  Jaundice  is  generally 
present  and  varies  from  a  faint  lemon-yellow  to  a  dark-olive  hue,  but  it  is  a 
noteworthy  fact  that  the  stools  are  not  without  bile,  as  in  ordinary  jaundice. 
The  urine,  of  course,  contains  bile.  At  times  attacks  of  severe  hepatic  pain 
develop,  and  the  liver  may  seem  more  enlarged  than  usual  at  these  periods. 
Pruritus  is  often  a  most  persistent  symptom,  and  xanthoma  may  be  developed 
to  an  extraordinary  degree.  In  a  case  now  under  my  care  the  yellow  xan- 
thomatous patches  about  the  eyes  form  a  striking  contrast  to  the  dark-olive 
hue  of  the  rest  of  the  face.  More  or  less  disturbance  of  digestion,  due  to  gastric 
catarrh,  from  an  impaired  circulation  in  the  stomach,  is  nearly  always  present. 

Diagnosis. — An  enlarged  liver,  like  that  seen  in  hypertrophic  cirrhosis,  is 
also  seen  in  leukaemia,  but  the  association  of  profound  anaemia  and  pallor 
of  the  skin  separate  it  from  the  condition  now  under  consideration.  Great 
enlargement  of  the  liver  also  occurs  in  heart  disease  from  hepatic  congestion, 
and  in  cases  of  adherent  pericardium.  The  state  of  the  heart  makes  the 
diagnosis  possible  in  this  instance.  Malignant  growth  of  the  liver  can  often 
be  differentiated  by  the  presence  of  a  primary  growth  in  the  gall-bladder  or 
stomach,  and  by  the  nodules  felt  in  the  liver  substance. 

Prognosis. — The  prognosis  as  to  cure  is  hopeless.  As  to  duration  of  life, 
it  varies  from  one  to  ten  years.  Death  comes  from  some  terminal  infection, 
from  a  hemorrhage  into  the  bowel  or  stomach,  or  from  an  ever-increasing 
feebleness.    At  times  coma  develops. 

Treatment. — There  is  no  treatment  for  the  disease  itself.  The  digestion 
should  be  kept  in  good  order  by  the  line  of  treatment  outlined  for  this 
function  under  Atrophic  Cirrhosis. 

Syphilitic  Cirrhosis. — Syphilis  may  produce,  in  its  inherited  form  or  ter- 
tiary stage,  a  remarkable  degree  of  cirrhotic  change  in  the  liver.  The  over- 
growth of  connective  tissue  in  this  type  projects  itself  everywhere  between 


PERIHEPATITIS  665 

the  lobules  and  between  their  cells,  or  forms  large  bands  which,  as  they  con- 
tract, produce  extraordinary  irregularities  in  its  surface,  so  that  the  organ 
appears  to  be  as  well  covered  with  knobs  as  a  tuberous  root  is  covered  by 
projections,  a  polylobed  organ.     (See  Syphilis.) 

Because  of  the  frequency  of  syphilis,  this  form  of  cirrhosis  is  not  very  rare. 
The  importance  of  recognizing  it  lies  in  the  fact  that  while  we  cannot  cure 
the  state  already  developed,  by  active  antisyphilitic  treatment  we  may  be  able 
to  arrest  or  delay  its  progress,  and  in  this  sense  the  prognosis  is  better  than 
in  the  non-syphilitic  type.  In  some  cases,  however,  this  peculiar  nodular 
formation  does  not  occur,  and  the  course  of  the  disease  may  be  identical 
with  ordinary  atrophic  cirrhosis.  Sometimes  tumors  due  to  the  formation 
of  gummata  can  be  felt.  The  symptoms  differ  in  no  way  from  those  of 
ordinary  cirrhosis,  except  when  gummata  are  present. 

Treatment. — The  treatment  of  syphilitic  cirrhosis,  while  it  presents  greater 
opportunities  than  are  offered  by  therapeutic  measures  in  ordinary  cirrhosis, 
cannot  be  expected  to  produce  very  remarkable  alterations  in  the  liver. 
Wonderful  as  are  the  effects  of  the  iodides  and  mercury  in  the  treatment 
of  syphilis,  they  cannot  regenerate  tissues  which  have  been  destroyed,  and 
the  most  that  we  can  expect  from  them  is  that  they  will  do  something  to 
arrest  the  progress  of  the  disease,  and,  perhaps,  cause  a  removal  of  some  of 
the  cells  which  have  been  proliferated,  but  which  have  not  as  yet  become 
organized  tissue.  In  those  cases  in  which  there  are  any  evidences  of  active 
syphilis,  it  is  hardly  necessary  to  state  that  the  specific  treatment  should  be 
carried  out  most  thoroughly.     (See  Syphilis.) 


PERIHEPATITIS   (CAPSULAR  CIRRHOSIS). 

Inflammation  of  the  capsule  of  the  liver  and  of  the  tissues  immediately 
beneath  it,  when  it  occurs  in  a  chronic  form,  may  be  associated  with  chronic 
peritonitis  and  with  hepatic  cirrhosis.  More  rarely  it  develops  as  a  result 
of  chronic  pleurisy  on  the  right  side.  The  thickening  which  ensues  may, 
by  its  contraction,  result  in  deformity  of  the  surface  of  the  liver.  This 
effect  is  increased  by  the  fact  that  abnormal  projections  of  connective  tissue 
dip  downward  from  the  capsule  into  the  liver  substance  and  divide  it  into 
masses  of  parenchyma,  which  undergo  atrophy  from  pressure.  The  condi- 
tion is,  therefore,  in  some  cases,  at  least,  not  very  different  from  that  met 
with  in  ordinary  atrophic  syphilitic  cirrhosis. 

The  condition  is  very  rare  and  is  thought  by  Hale  White  to  be  due  •  to, 
or  a  sequence  of,  contracted  kidney.  Unlike  most  instances  of  chronic 
contracted  kidney,  the  patient  often  has  marked  ascites  because  of  the 
state  of  the  liver.  As  already  stated,  it  sometimes  happens  that  the 
capsule  of  the  liver  is  secondarily  involved  in  cases  of  chronic  peritonitis, 
particularly  in  cases  of  adherent  pericardium  and  chronic  inflammatory 
changes  in  the  mediastinum.    (See  Adherent  Pericardium  and  Mediastinitis.) 


666  DISEASES  OF   THE  LIVER 


AFFECTIONS  OF  THE  HEPATIC  BLOODVESSELS. 

These  consist,  aside  from  those  already  considered  when  discussing  the 
subject  of  cirrhosis,  in  three  chief  changes. 

Hyperoemia  occurs  physiologically  whenever  the  liver  is  actively  engaged 
in  disposing  of  foodstuffs.  Pathologically,  it  probably  takes  place  when 
an  extra  amount  of  stimulating  food  and  irritant  drink  are  taken.  Neither 
condition  is  capable  of  being  diagnosticated. 

A  much  more  important  state  is  the  congestion  due  to  cardiac  disease,  or 
to  other  causes  which  retard  the  egress  of  blood  from  the  gland.  We  find, 
therefore,  that  all  the  causes  which  tend  to  result  in  interference  with  the  free 
flow  of  blood  in  the  inferior  vena  cava  above  the  liver  may  cause  hepatic  con- 
gestion. Disease  at  the  tricuspid  orifice  of  the  heart,  pulmonary  emphysema, 
fibroid  lung,  bronchiectasis,  and  valvular  disease  of  the  left  side  of  the  heart, 
with  secondary  obstruction  in  the  right  side,  all  produce  it. 

The  congestion  is,  of  course,  due  not  to  an  increase  of  blood  in  the 
portal  vein  but  in  the  hepatic  veins.  As  a  result  of  this,  the  centre  of 
each  lobule  is  congested,  and  its  periphery  contains  relatively  less  blood. 
Frequently  the  cells  in  the  areas  of  greatest  congestion  are  pigmented.  As 
a  result  of  this,  the  homogeneous  hue  of  the  normal  liver  is  altered,  and  it 
presents  what  is  called  a  "nutmeg"  appearance,  particularly  if  the  cells  at 
the  periphery  become  still  paler  from  fatty  changes.  In  some  cases,  however, 
nothing  more  than  the  appearance  of  intense  congestion  is  present.  When 
the  continued  pressure  by  the  excess  blood  causes  atrophy  of  hepatic  cells, 
the  condition  is  known  as  "red  atrophy"  of  liver. 

During  life  the  congested  liver  is  usually  much  larger  than  normal,  and 
may  attain  enormous  dimensions,  but  not  rarely,  when  the  congestion  has 
lasted  for  a  long  time,  it  grows  smaller  than  it  is  in  health,  and  its  surface 
may  be  roughened,  so  that  it  may  somewhat  resemble  the  roughened  sur- 
face seen  in  early  stages  of  atrophic  cirrhosis.  In  fact  the  connective 
tissue  is  usually  increased. 

A  third  vascular  change  is  thrombosis  of  the  portal  vein.  The  formation 
of  this  thrombus  may  be  due  to  pressure  on  the  vein  produced  by  a  tumor, 
by  gallstones,  by  traumatism,  and  in  some  instances  it  may  arise  from 
septic  infection.  When  the  thrombus  forms  from  pressure,  and  is  not  infec- 
tious, it  may  become  organized  and  gradually  close  the  vessel  permanently. 
This  does  not  necessarily  work  much  havoc  in  the  liver,  because  the 
nutrition  of  this  organ  is  carried  out  by  the  branches  of  the  hepatic 
artery,  which  speedily  enter  into  anastomosis  with  the  neighboring  vessels. 
While  the  liver  itself  may  not  suffer  very  greatly,  the  abdominal  circula- 
tion is  usually  much  disturbed  by  obstruction  of  the  portal  vein,  and  the 
spleen,  the  kidneys,  and  the  veins  of  the  entire  abdominal  network  become 
engorged,  so  that  ascites  usually  occurs  and  hsematemesis  or  bloody  stools 
may  be  produced. 

If  the  thrombus  is  infectious  (suppurative  pylephlebitis),  the  pathological 
and  clinical  picture  is  quite  different,  for  in  this  case  the  clot  does  not  act  as. 


AMYLOID  LIVER  667 

a  mechanical  obstruction  alone,  but  as  a  source  of  septic  disease.  Necrosis 
and  suppuration  take  place  in  the  wall  of  the  infected  vessel  and  in  the 
hepatic  tissues  around  it.  The  thrombus  may  break  down  and  minute 
pieces  of  the  infected  mass  pass  into  smaller  divisions  of  the  portal  vein,  and 
so  spread  the  disease  until  multiple  abscess  of  the  liver  develops. 

The  sources  from  which  such  septic  infections  arise  are  found  in  ulcer  of 
the  stomach  and  bowels,  appendicitis  and  suppuration  of  the  lymph  nodes 
in  the  mesentery.  Another  origin  is  suppurative  angiocholitis.  (See  Abscess 
of  the  Liver.)     In  infants  infection  may  take  place  by  way  of  the  umbilicus. 

Symptoms. — The  symptoms  of  congested  liver  consist  in  finding  its  lower 
margin  below  the  ribs  to  an  abnormal  degree  and  distinct  tenderness  on 
pressure,  particularly  in  the  epigastrium.  Pain  in  this  region  is  often  com- 
plained of  by  the  patient  even  when  he  is  at  rest.  If  tricuspid  regurgitation 
is  present,  the  liver  may  have  systolic  expansile  pulsation,  which  must  not 
be  confounded  with  movement  of  the  liver  due  to  direct  transmission 
of  the  impulse  of  the  apex  beat  of  the  heart.  In  some  cases  distinct  evi- 
dences of  gastrointestinal  catarrh  develop,  and  the  congestion  of  the  gastric 
vessels  may  be  so  great  as  to  cause  rupture  and  hoematemesis.  Ascites  due 
to  the  interference  with  the  venous  return  in  the  lower  parts  of  the  body,  and 
oedema  of  the  legs  from  the  same  cause  may  be  present. 

Treatment. — The  treatment  consists  in  unloading  the  gastroduodenal  and 
hepatic  glands  and  bloodvessels  by  a  full  dose  of  blue  mass  (10  grains), 
followed,  if  need  be,  by  a  saline  purge.  This  is  to  be  followed  by  the  use 
of  digitalis  to  support  the  heart,  and,  if  the  arterial  tension  is  high,  by  the 
administration  of  nitroglycerin,  to  lower  the  arterial  pressure  and  so  relieve 
the  heart  of  work.    (See  Valvular  Disease  of  the  Heart.) 


AMYLOID  LIVER. 

Amyloid  disease  of  the  liver  occurs  as  the  result  of  severe  and  prolonged 
suppurative  changes  in  other  parts  of  the  body,  as  in  chronic  bone  disease, 
in  pulmonary  tuberculosis,  and  in  syphilis,  particularly  if  the  latter  disease 
has  caused  suppuration  over  a  long  period  of  time.  The  liver  is  usually  very 
large  and  may  be  easily  felt  far  below  the  ribs,  presenting  a  smooth  surface. 
Occasionally  an  amyloid  liver  is  small.  When  it  is  cut  across  it  is  found  to 
be  hard  and  infiltrated  by  amyloid  material,  which  stains  a  mahogany  hue 
when  it  is  touched  with  a  watery  solution  of  iodine. 

Symptoms. — The  symptoms  are  not  typical.  Indeed,  it  may  be  said  that 
the  changes  in  the  liver  produce  no  manifestations  that  call  attention  to 
hepatic  disease,  for  there  is  no  jaundice  and  no  pain,  neither  is  there  any 
ascites.  The  presence  of  enlargement  of  the  liver,  with  a  smooth  surface  of 
the  gland,  and  the  presence  of  a  suppurative  focus,  combined  with  an  absence 
of  any  of  the  signs  of  hypertrophic  cirrhosis  and  morbid  growth,  make  the 
diagnosis  easy. 

Treatment. — There  is  no  treatment  for  amyloid  liver,  except  the  removal, 
if  possible,  of  the  suppurating  area,  which  is  the  underlying  cause  of  the  dis- 
ease, and  in  the  maintenance  of  as  great  a  degree  of  health  as  possible  by  the 
use  of  fresh  air,  sunshine,  iron,  arsenic,  and  good  food. 


66g  DISEASES  OF  THE  LIVER 


FATTY  LIVER. 

Fatty  liver,  like  fatty  heart,  occurs  in  two  forms,  namely,  as  a  true  fatty 
degeneration  of  the  hepatic  cells  and  as  an  infiltration  of  fat  into  the 
cells.  The  true  fatty  degeneration  without  cirrhosis  is  rarely  met  with, 
except  as  a  result  of  the  ingestion  of  some  poison,  such  as  phosphorus,  anti- 
mony, iodoform,  sulphate  of  copper,  and  carbolic  acid.  A  similar  change  is 
present  in  acute  yellow  atrophy  of  the  liver. 

In  uncompUcated  fatty  infiltration  the  liver  is  enlarged  and  smooth.  On 
autopsy  it  is  pale  and  yellow  and  renders  the  incising  knife  greasy.  Its 
specific  gravity  is  so  low  that  the  organ  may  almost  float  in  water.  No 
distinctive  hepatic  symptoms  are  present. 

Often  fatty  infiltration  is  part  of  general  obesity,  and  the  large  deposit  of 
fat  in  the  abdominal  wall  and  in  the  tissues  near  the  liver  make  a  diagnosis 
difficult. 

Large,  fatty,  cirrhotic  livers  have  been  recorded,  and  fatty  liver  accom- 
panying alcoholism,  severe  anaemia,  and  cachexia,  as  in  tuberculosis,  also 
occurs.    In  such  cases  the  change  is  thought  to  be  due  to  faulty  oxidation. 


TUMORS  OF  THE  LIVER. 

The  most  important  morbid  growth  in  the  liver  is  carcinoma.  It  is 
rarely  primary. 

Secondary  carcinoma  is  quite  common  and  is  nearly  always  due  to  metas- 
tasis from  the  alimentary  viscera,  as  from  carcinoma  of  the  gall-bladder, 
of  the  stomach,  of  the  pancreas,  or  of  the  intestines.  In  rare  instances  the 
metastasis  is  from  more  distant  organs,  as  the  uterus  or  mammary  gland. 

Carcinoma  of  the  liver  rarely  occurs  as  a  solitary  nodule.  Usually 
it  is  in  the  form  of  multiple  growths,  which  vary  in  size  from  a  small  seed 
to  an  orange.  When  these  growths  are  immediately  subcapsular  they 
appear  as  large  protuberances  on  the  surface  of  the  organ,  which  may  be  felt 
as  nodules  through  the  belly  wall,  or  they  lie  buried  in  the  tissue  of  the 
liver  and  present  a  disk-like  surface  upon  the  level  of  the  capsule,  so  that 
they  may  be  felt  in  thin  persons  as  a  slightly  flattened  or  umbilicated  eleva- 
tion. The  nodules  are  sometimes  very  hard,  at  other  times  quite  soft,  and 
in  the  centre  softening  may  take  place,  so  that  an  apparent  cyst  is  formed 
(Fig.  91). 

The  liver  is  sometimes  enormously  enlarged  and  may  extend  far  below  the 
navel,  thereby  causing  great  distention  of  the  belly.  A  very  rare  form  of 
hepatic  cancer  is  that  in  which  the  liver  diminishes  in  size  with  the  develop- 
ment of  the  growth. 

Sarcoma  of  the  liver  is  rarely  encountered. 

Cavernous  angiomata  have  been  described,  and  cysts,  single  and  large,  or 
multiple  and  small,  have  been  found  in  this  organ.  The  latter  are  congenital, 
the  so-called  "  cystic  disease  of  the  liver."     (See  also  Hydatid  Disease.) 


TUMORS  OF   THE  LIVER 


669 


Symptoms. — The  evidences  of  tumor  of  the  liver  may  be  so  easily  observed 
in  many  cases  that  there  is  no  difficulty  in  making  a  diagnosis,  particularly 
if  emaciation,  anj3emia,  and  profound  cachexia  are  present.  In  other  cases 
the  fact  that  the  patient  is  still  well  nourished,  and  the  growths  deeply 
situated,  may  render  it  impossible  to  discover  the  existence  of  a  mass  by 
palpation.  In  some  instances  there  is  present  nothing  more  than  a  vague 
sense  of  distress  in  the  hypochondrium,  with  loss  of  weight  and  strength. 
In  still  others,  if  the  gall-ducts  are  obstructed,  jaundice  may  come  on,  and  if 
the  pancreas  is  involved,  fatty  stools  may  be  present,  or  glycosuria  is  found. 
Pain  may  be  severe,  but  usually  it  is  not.  At  times  the  veins  of  the  leg 
on  the  right  side  may  be  obstructed  by  a  thrombus,  or  a  phlebitis  may  be 
present.     Moderate  fever  may  occur. 


Fig.  91 


Liver,  secondary  carcinoma. 


Even  the  smaller  nodules  show  more  or  less  umbilication,  which  is 
marked  in  the  larger  masses. 


Diagnosis. — The  diagnosis  requires  that  we  exclude  hypertrophic  cirrhosis, 
which  can  be  done  by  the  more  rapid  development  of  the  enlargement  of  the 
liver  in  carcinoma,  and  by  the  presence  of  cancerous  cachexia.  From 
echinococcus  cyst  it  must  be  separated,  by  the  fact  that  the  cyst  usually 
fluctuates,  or,  at  least,  is  not  so  hard  as  is  nodular  cancer.  From  gumma 
of  the  liver  other  tumors  can  be  differentiated  only  by  the  history  of  the 
patient  and  the  response  to  antisyphilitic  treatment. 

Prognosis. — When  the  growth  is  malignant,  the  outlook  is,  of  course,  hope- 
less as  to  recovery. 

Treatment.^If  the  growth  is  a  gumma,  antisyphilitic  treatment  is  of  great 
value.     (See  Syphilis.)    If  it  is  a  cyst  or  non-malignant,  surgical  interference 


670  DISEASES  OF  THE  LIVER 

is  a  possible  source  of  relief.     If  it  is  malignant,  no  efficient  treatment 
except  the  relief  of  pain  can  be  instituted. 


ACUTE  YELLOW  ATROPHY  OF  THE  LIVER. 

Definition. — Acute  yellow  atrophy  of  the  liver  is  a  condition  characterized 
by  marked  fatty  degeneration  of  the  organ  and  violent  headache  and 
delirium.    It  is  a  very  rare  disease. 

Etiology. — The  causes  of  acute  yellow  atrophy  are  unknown,  but  it  occurs 
more  frequently  in  women  than  in  men,  and  has  been  associated  in  many 
instances  with  the  puerperal  state.  A  micrococcus  has  been  found  in  the 
liver  in  some  cases,  but  the  suspected  bacterial  origin  of  the  disease  has  not 
been  proved.  Some  pathologists  regard  it  as  a  local  state  representing  a 
general  infection,  and  others  as  a  distinctly  local  disease,  but  its  toxic  nature 
is  generally  admitted. 

Pathology  and  Morbid  Anatomy. — The  changes  which  take  place  in  the 
liver  are  a  rapid  decrease  in  its  size  due  to  necrosis,  fatty  degeneration,  and 
cellular  fragmentation.  So  rapid  may  be  the  process  that  after  three  or  four 
days  the  organ  is  not  one-half  its  normal  size.  The  gland  is  soft  and  its  cap- 
sule shrivelled,  as  if  it  were  too  large  for  the  organ.  If  an  incision  is  made 
into  the  viscus  the  lobules  will  be  found  almost  destroyed,  and  the  cut  surface 
is  mottled,  softened,  and  gray,  red,  or  yellow,  according  to  the  stage  of  the 
disease.  In  the  gray  areas  the  forms  of  the  hepatic  cells  are  recognizable, 
and  their  protoplasm  is  granular  in  appearance.  In  the  yellow  areas  the 
cells  are  more  or  less  filled  with  fatty  globules  and  yellow  pigment,  and  in 
the  red  areas  the  cell  outline  may  be  lost,  and  only  cell  debris,  or  the  remains 
of  broken-down  cells,  may  be  found.  The  spleen  is  usually  enlarged,  the 
kidneys  are  the  seat  of  parenchymatous  degeneration,  and  the  heart  muscle 
is  also  degenerated.  Hemorrhagic  extravasations  may  occur,  not  only  in 
the  liver,  but  in  the  stomach,  bowels,  bladder,  and  kidneys  as  well.  When 
death  has  been  long  delayed,  evidences  of  universal  tissue  degeneration  may 
be  found. 

If  the  urine  is  examined,  it  will  be  found  loaded  with  bile  and  an  excessive 
quantity  of  leucin  and  tyrosin,  or,  perhaps,  only  one  of  these  products. 
Leucin  appears  in  round  disks,  and  the  tyrosin  in  needle-shaped  crystals, 
which  are  usually  bunched  together. 

Symptoms. — The  symptoms  of  this  malady  are  jaundice,  severe  headache, 
vomiting,  and  finally  delirium,  fibrillary  muscidar  tremors,  convulsions,  and 
death.  As  a  rule,  there  is  little  or  no  fever,  but  cases  with  high  temperature 
have  been  recorded.  Petechial  spots  and  large  hemorrhages  may  develop 
beneath  the  skin. 

Diagnosis. — The  development  of  what  might  be  called  fulminating  jaun- 
dice in  a  woman  during  the  puerperium  should  awaken  a  suspicion  of  this 
disease  at  once,  but  such  an  onset  does  not  necessarily  prove  the  presence  of 
acute  yellow  atrophy,  unless  there  is  marked  decrease  in  the  size  of  the  liver, 
and  leucin  and  tyrosin  are  present  in  the  urine.  Even  these  additional  signs 
are  not  pathognomonic.     Particular  care  must  be  taken  that  the  coma  of 


ACUTE   CATARRH   OF   THE  BILE-DUCTS  671 

hypertrophic  cirrhosis  is  not  taken  for  acute  yellow  atrophy  of  the  liver,  for 
sometimes  hypertrophic  cirrhosis  belies  its  name,  in  that  the  liver  is  not 
greatly  enlarged,  and  acute  yellow  atrophy  may  occur  without  the  liver  being 
greatly  decreased  in  size. 

Prognosis. — Death  nearly  always  occurs.  A  few  cases  are  said  to  have 
recovered. 

Treatment. — Beyond  the  use  of  mild  purgatives,  diuretics,  and  stimulants 
there  is  no  treatment  for  this  malady. 


DISEASES  OF  THE  BILIARY  TRACT. 

1.  Acute  Catarrh  of  the  Bile-ducts,  or  Acute  Cholangitis. — As  its  name 
indicates,  this  is  a  condition  in  which  the  mucous  membrane  lining  the  gall- 
ducts  becomes  inflamed  and  swollen,  and  its  secretion  thick  and  tenacious. 
These  two  conditions  produce  partial  or  complete  occlusion  of  the  ducts, 
which  in  turn  results  in  biliary  stasis  and  jaundice.  In  the  liver  itself 
marked  pigmentation  also  occurs,  because  of  the  accumulation  of  pigment 
granules  in  its  cells.  When  the  inflammatory  process  affects  the  gall- 
bladder, it  is  called  catarrhal  cholecystitis.  Acute  catarrh  of  the  bile-ducts 
is  the  cause  of  most  attacks  of  jaundice  which  last  for  a  few  days. 

Etiology. — This  condition  nearly  always  arises  from  a  primary  catarrh 
of  the  duodenum,  which  extends  to  the  common  bile-duct.  It  may  follow 
exposure  to  cold,  particularly  if  the  exposure  follows  heavy  eating  and  drink- 
ing. It  usually  accompanies  the  presence  of  gallstones  if  they  arise  in 
or  enter  the  common  or  hepatic  duct.  It  also  is  a  result  of  infection  in 
many  cases,  as  in  influenza,  or  more  rarely  in  pneumonia.  Still  more 
rarely  jaundice  occurs  after  a  severe  fright  or  a  paroxysm  of  intense  anger. 
Any  cause  which  interferes  with  the  circulation  in  the  liver  and  duodenum 
may  also  indirectly  produce  this  state,  as,  for  example,  mitral  stenosis. 

In  nearly  all  cases  the  inflammation  does  not  extend  beyond  the  lower  part 
of  the  larger  ducts. 

Symptoms. — The  symptoms  vary  very  greatly.  In  some  persons  a  well- 
marked  jaundice  develops,  with  such  slight  general  symptoms  that  the  patient 
does  not  know  he  is  ill  until  he  sees  his  reflection  in  a  glass  or  a  friend 
remarks  upon  his  yellow  hue.  In  other  cases  the  patient  may  feel  and  seem 
wretchedly  ill,  probably  because  he  has  in  the  intestine  certain  substances 
which,  in  the  absence  of  bile,  develop  toxic  materials  which  the  torpid  liver 
does  not  destroy.  Headache  is  often  marked,  and  profound  weakness  may 
be  felt.  The  stools  are  putty  color  because  of  lack  of  bile,  and  the  urine  is 
the  hue  of  porter,  because  of  the  presence  of  this  secretion  in  excess.  The 
color  of  the  skin  varies  from  a  faint  lemon  to  a  much  deeper  hue,  but  the 
deep  olive-green  jaundice  of  chronic  hepatic  disease  is  not  met  with.    The 


672  DISEASES  OF   THE  BILIARY   TRACT 

pulse  and  respiration  are  remarkably  slow,  owing  to  the  pathological  action 
of  the  retained  biliary  salts.  The  temperature  may  be  subnormal,  but  if  the 
condition  is  due  to  an  acute  infection  it  may  reach  102°  or  more.  The 
liver  on  palpation  and  percussion  is  usually  found  to  be  moderately  enlarged, 
about  two  to  three  fingers'  breadth  below  the  ribs,  and  it  is  often  tender  on 
pressure. 

Catarrhal  jaundice  usually  lasts  from  a  few  days  to  several  weeks.  After 
the  patient  has  been  ill  for  some  days  he  usually  loses  weight  very  rapidly. 
There  is  no  mild,  brief  acute  illness  which  causes  a  greater  loss  of  weight  in 
a  few  days  than  this  affection. 

Diagnosis. — ^The  development  of  jaundice  in  persons  under  forty  without 
any  signs  of  grave  disease  renders  a  diagnosis  of  acute  catarrh  of  the  bile- 
ducts  probable.  In  older  persons,  particularly  if  the  jaundice  develops 
gradually,  the  possibility  of  malignant  growth  being  present  must  be  excluded. 
In  other  cases  when  jaundice  comes  on  suddenly,  the  cause  may  be  gall- 
stone, and  in  such  instances  a  history  of  colic  may  be  given.  If  distinct 
enlargement  of  the  gall-bladder  is  present,  the  probability  of  carcinoma  is 
great.     (See  Tumors  of  the  Gall-bladder.) 

Prognosis. — In  cases  of  acute  catarrh  of  the  simple  form  the  prognosis  is 
always  good. 

Treatment. — In  acute  catarrh  of  the  bile-ducts  the  treatment  consists  in 
placing  the  patient  in  bed,  and  in  the  application  of  hot  compresses  over  the 
liver,  renewing  the  compresses  as  rapidly  as  they  become  cooled.  In  some 
instances  it  is  advantageous  to  wet  the  compresses  with  hot  water  which 
contains  a  drachm  of  dilute  nitromuriatic  acid  to  the  pint;  or,  in  other  cases, 
for  the  purpose  of  producing  counterirritation,  a  turpentine  stupe  may  be 
employed. 

The  kidneys  should  be  kept  acting  freely  by  the  administration  of  large 
quantities  of  Vichy  water,  or  in  other  instances  Poland  water,  if  Vichy  water 
is  not  to  be  had.  In  some  instances,  if  the  kidneys  are  inactive,  it  is 
advantageous  to  add  to  the  water  5  grains  of  bicarbonate  of  potash  in 
each  glass. 

If  the  bowels  are  at  all  confined,  as  they  are  prone  to  be,  they  are  best  moved 
by  one  of  the  saline  purgatives,  of  which  sodium  phosphate  is  usually  con- 
sidered most  advantageous.  This  may  be  given  in  quantities  varying  from 
20  grains  to  a  drachm  in  half  a  glass  of  hot  water  every  two  hours  until  the 
bowels  are  thoroughly  moved. 

The  administration  of  calomel  in  the  early  stages  of  catarrhal  jaundice 
is  not  rational.  The  object  of  the  physician  is  to  re-establish  biliary  flow, 
and  the  difficulty  which  exists  is  that  the  liver  is  unable  to  get  rid  of  the  bile 
which  it  secretes.  To  stimulate  this  gland  to  a  greater  secretion  of  bile  by 
calomel,  when  its  ducts  are  blocked,  is  manifestly  not  good  therapeutics. 

After  the  acute  stages  of  jaundice  have  passed  by,  it  is  often  advantageous 
to  give  broken  doses  of  calomel,  in  order  to  overcome  the  natural  inactivity 
of  the  liver  after  acute  inflammation  in  its  bile-ducts,  and  these  should  be 
followed  by  the  doses  of  phosphate  of  sodium,  already  named. 

Patients  with  jaundice  frequently  insist  upon  getting  up  and  going  about. 
This  is  not  a  safe  thing  for  them  to  do,  as  it  is  entirely  possible  for  them,  if 


SUPPURATIVE  INFLAMMATION  OF   THE  BILE-DUCTS  673 

the  cause  be  gallstones,  to  convert  an  attack  of  acute  catarrhal  jaundice 
into  one  of  acute  cholecystitis. 

In  regard  to  diet,  the  patient  had  better  subsist  upon  nutritious  broths, 
thickened  it  may  be  with  barley  or  rice,  partly  digested  with  pancreatin, 
and  well  flavored  with  salt.  Milk  is  usually  not  well  digested  by  patients 
suffering  from  this  condition,  particularly  if  it  contains  any  considerable 
quantity  of  cream.  All  fatty  articles  of  food  should  be  avoided,  as  the 
emulsification  of  fats  in  the  intestines  in  the  absence  of  bile  is  imperfectly 
carried  out. 

2.  Chronic  Catarrh  of  the  Bile-ducts.— This  state  rarely  arises  as  a 
sequence  of  the  acute  type  just  described.  More  commonly  it  is  due  to 
obstruction  of  the  common  duct  caused  by  the  presence  of  gallstones, 
growths,  or  stricture.  Two  results  ensue  from  such  a  state,  depending 
upon  the  degree  of  obstruction.  When  the  duct  is  totally  blocked,  we  find 
on  opening  it  that  it  is  not  filled  with  bile,  but  with  clear  or  slightly  tinged 
mucus  which  is  devoid  of  bile,  and  that  the  mucous  membrane  is  not 
much  affected,  for  it  remains  smooth.  Such  patients  present  marked  and 
'persistent  jaundice,  the  skin  often  being  olive-green  in  hue.  When  the 
duct  is  not  quite  occluded,  the  retained  mucus  is  bile-stained;  it  is  cloudy, 
not  clear,  and  it  may  contain  micro-organisms  from  the  bowel.  Because  of 
the  infection  of  this  mucus  from  the  bowel  marked  fever  may  be  present, 
characterized  by  sharp  intermittency,  and  associated  with  fever  and  sweats, 
just  like  those  met  with  in  the  suppurative  type  about  to  be  described. 

Treatment. — Chronic  catarrh  of  the  bile-ducts  cannot  be  materially  modi- 
fied by  medicinal  measures.  Prolonged  counterirritation  in  the  form  of 
tincture  of  iodine  over  the  liver  may  be  tried,  but  it  must  be  continued  for 
long  periods  of  time  before  any  possible  influence  can  be  expected  from  it. 
If  constipation  exists,  the  bowels  should  be  relieved,  preferably  by  saline 
purgatives,  of  which  the  phosphate  of  sodium,  Hunyadi  water,  or  some 
similar  mild  purgative,  are  considered  the  best. 

The  diet  should  be  composed  of  easily  digested  meats  and  easily  digested 
starches,  the  digestion  of  which  should  be  aided  by  the  use  of  pancreatin  and 
taka-diastase.  Milk  and  fatty  foods  are  usually  not  well  digested  by  such 
patients,  and  are  prone  to  cause  fermentation  and  distention  of  the  bowels 
by  gas.  The  best  treatment  for  these  patients  is  operative  interference, 
for  the  presence  of  fever  indicates  infection  and  hints  at  the  existence 
of  pus. 

3.  Suppurative  Inflammation  of  the  Bile-ducts. — When  infection  of 
the  mucous  membrane  results  from  the  growth  of  the  Bacillus  coli  com- 
munis, or  more  rarely  the  Streptococcus  pyogenes  or  other  pyogenic  organ- 
isms, suppuration  occurs.  It  is  sometimes  called  "  suppurative  cholangitis." 
The  solution  of  continuity  in  the  mucous  membrane  which  permits  infec- 
tion may  be  due  to  gallstones.  In  some  cases  typhoid  fever,  cholera, 
typhus  fever,  or  pyeemia  may  be  the  cause. 

This  form  of  inflammation  extends  much  farther  into  the  smaller  biliary 
passages  than  the  acute  catarrhal  form,  and  by  this  means  the  liver  may  be- 
come generally  infected,  the  ducts  containing  pus  and  the  gall-bladder  also 
being  filled  with  the  same  material.     In  some  cases  the  suppurating   ducts 
43 


574  DISEASES  OF   THE  BILIARY   TRACT 

may  cause  small  abscesses  in  the  liver  substance  outside  their  walls,  and  these 
again  may  grow  large  enough  to  communicate,  and  so  abscesses  of  consider- 
able size  develop.  \Vhen  the  process  is  severe  the  ducts  may  be  perforated, 
and  the  pus  and  bile  escape  into  the  peritoneal  cavity,  causing  peritonitis, 
or  fistulous  tracts  may  communicate  with  the  bowel  or  the  exterior  of  the 
body. 

Symptoms. — ^The  symptoms  are  usually  so  sharply  developed  that  there  is 
little  difficulty  in  deciding  that  pus  is  present  in  the  liver.  The  fever  ranges 
from  high  to  low,  as  in  sepsis;  the  liver  is  enlarged  and  very  tender;  the  gall- 
bladder may  be  palpable,  and  jaundice  is  also  well  marked  in  some  cases, 
but  slight  in  others.  The  presence  of  pus  in  so  vascular  and  important  an 
organ  causes  profuse  sweats  and  rapid  loss  of  flesh,  but  pain  is  usually  not 
severe. 

Diagnosis. — Suppurative  cholangitis  must  be  differentiated  from  abscess 
of  the  liver,  and,  more  important  than  all,  from  severe  catarrhal  cholangitis 
without  the  formation  of  pus. 

In  hepatic  abscess  there  will  be  found,  on  careful  examination  of  the 
patient's  history,  that  at  some  time  in  the  near  or  remote  past  there  has  been 
an  attack  of  dysentery  or  of  an  infection  in  some  part  of  the  body  from 
which  pyogenic  micro-organisms  have  been  carried  to  the  liver.  Very 
rarely  there  may  be  a  history  of  trauma.  While  such  a  history  may  be 
found  in  a  case  of  suppurative  cholangitis  it  is  much  more  indicative  of 
abscess.  A  history  of  gallstone  colic  is  indicative  of  cholangitis,  and  it  must 
be  recalled  that  only  moderate  attacks  of  pain  in  the  hepatic  or  gastric  region 
may  be  present  in  cases  of  gallstones.  In  other  words,  every  person  that 
has  passed  a  gallstone  does  not  give  a  history  of  severe  colic.  Finally,  the 
presence  of  jaundice  is  a  sign  of  cholangitis,  for  this  symptom  is  usually 
absent  in  abscess.  In  both  cases  the  liver  is  enlarged  and  there  is  a  distinct 
leukocytosis. 

From  severe  catarrhal  cholangitis  suppurative  cholangitis  is  separated 
by  the  facts  that  in  the  former  state  the  leukocytosis  is  not  so  marked  as  in 
the  suppurative  type,  there  are  no  marked  chills,  sharp  fevers,  or  sweats, 
nor  is  there  so  much  tenderness  and  enlargement  of  the  liver. 

Treatment. — There  is  no  medicinal  treatment  for  this  condition.  The 
same  rule  holds  good  in  regard  to  pus  here  as  for  pus  elsewhere ;  whenever  it 
is  present,  the  safety  of  the  patient  demands  that  it  should  be  given  an  exit, 
but  if  the  suppurative  process  is  diffuse  this,  of  course,  cannot  be  done. 

4.  Occlusion  and  Constrictions  of  the  Bile-ducts. — Occlusion  of  the 
bile-ducts  sometimes  takes  place  by  the  entrance  of  an  intestinal  worm,  by 
the  impaction  of  a  gallstone,  or  by  the  pressure  produced  by  an  aneurysm,  a 
carcinoma,  or  other  growth,  such  as  enlargement  of  the  lymph  nodes, 
enlargements  or  tumors  of  the  head  of  the  pancreas,  inflammation  and 
fibroid  changes  around  the  ducts,  and  twisting  or  angulation,  caused  by 
hepatoptosis  or  other  changes  in  the  visceral  relations.  If  the  cystic  duct 
is  obstructed  the  gall-bladder  is  greatly  enlarged,  but  no  jaundice  is  present, 
but  if  the  common  or  biliary  ducts  are  closed,  intense  jaundice  is  developed. 
(See  Tumors  of  the  Gall-bladder.) 

Congenital  occlusion  of  the  ducts  sometimes  is  met  vnth..    When  it  is  com- 


ACUTE  CHOLECYSTITIS  675 

plete  death  occurs  within  a  few  weeks  after  birth.  Hemorrhages  from  the 
navel  and  other  parts  of  the  body  are  usually  present  in  these  cases. 

Sjmaptoms. — The  symptoms  are  those  met  with  in  chronic  catarrh  of  the 
bile-ducts  and  vary  as  these  vary  with  the  degree  of  obstruction  and  the 
degree  of  infection.  Cases  occur,  however,  in  which  life  is  prolonged  for 
long  periods  if  the  ducts  are  not  completely  closed  and  infection  does  not 
take  place.  A  remarkable  instance  of  this  character  has  been  reported  by 
Cocking,  of  Sheffield,  in  which  a  woman  was  jaundiced  for  fifty  years  from 
her  third  week  of  life,  yet  was  in  perfect  health  otherwise. 

Treatment. — ^The  treatment  is  surgical. 


ACUTE  CEOLECYSTITIS. 

Definition. — ^This  is  a  state  in  which  the  gall-bladder  suffers  from  an  acute 
inflammatory  process,  which  varies  from  catarrh  of  the  mucous  mem- 
brane to  suppuration,  and  even  to  phlegmonous  change  in  the  walls  of  the 
viscus.  The  process  may  be  catarrhal,  pseudomembranous,  gangrenous,  or 
suppurative.  It  may  be  restricted  to  the  lining  mucosa  and  submucosa, 
or  extend  to  all  the  coats.  When  the  overlying  serosa  is  affected  the  process 
is  called  pericholecystitis  or  paracholecystitis. 

Etiology. — Cholecystitis  arises  from  the  presence  of  gallstones,  which,  by 
injuring  the  gall-bladder,  permit  infection  to  occur,  and  by  the  entrance  of 
pathogenic  organisms,  which,  by  reason  of  lowered  vitality  of  the  patient, 
or  other  causes,  are  able  to  produce  more  or  less  severe  inflammatory  changes 
by  their  presence.  The  time  at  which  the  micro-organism  enters  the  gall- 
bladder and  that  at  which  it  makes  its  presence  felt  may  be  widely  sepa- 
rated ;  for  while  it  is  true  that  bile  is  antiseptic  in  its  influence  under  certain 
conditions,  the  genu  may  remain  alive  but  quiescent  for  months  or  even  for 
years,  and  produce  its  effects  only  when  some  illness  or  other  cause  offers 
an  opportunity  for  it  to  develop.  This  period  of  inactivity,  so  far  as  inflam- 
matory action  is  concerned,  may  be  utilized  in  the  formation  of  gallstones 
about  the  nucleus  formed  by  those  bacilli  which  have  become  agglutinated. 
(See  Cholelithiasis.)  The  organisms  found  in  the  gall-bladder  are  very 
numerous  as  to  kind.  The  typhoid  bacillus,  the  tubercle  bacillus,  the  Bacil- 
lus svbtilis,  the  streptococcus,  the  staphylococcus,  and  the  colon  bacillus 
have  all  been  found  here,  although  it  is  probable  that  the  latter  does  not 
remain  active,  except  for  a  short  time. 

Morbid  Anatomy. — ^The  gall-bladder  is  found  to  be  filled  with  dark,  muco- 
purulent material,  in  which,  if  the  wall  of  the  gall-bladder  is  seriously  involved, 
there  may  be  traces  of  blood.  Occasionally  the  distention  of  the  gall-bladder 
is  due  not  only  to  blocking  of  the  cystic  duct  by  a  stone,  but  the  canal  is 
closed  by  the  intense  inflammatory  process.  Perforation  of  the  gall-bladder 
or  gangrene  of  its  walls  may  develop  if  the  inflammation  is  very  severe,  and 
it  not  rarely  happens  that  adhesions  form  between  it  and  the  nearby  tissues. 

Riedel  states  that  such  adhesions  develop  in  no  less  than  75  per  cent,  of 
cases  of  cholecystitis.  These  adhesions  are  of  importance  because  as  a 
result  of  their  formation  a  gallstone  perforating  the  gall-bladder  may  find 


676  DISEASES  OF   THE  BILIARY   TRACT 

its  way  into  adjacent  organs.  (See  below.)  Riedel  also  states  that  the  adhe- 
sions depend  as  to  their  location  to  a  large  extent  upon  the  position  at  which 
the  stone  exists.  Thus,  if  it  be  in  the  gall-bladder  the  adhesions  are  between 
this  viscus  and  the  colon  or  the  omentum.  If  it  be  in  the  cystic  or  common 
duct  the  adhesion  is  to  the  stomach,  in  the  region  of  the  pylorus.  These 
adhesions  are  also  of  importance  because  they  may  cause  pain  or  obstruc- 
tion of  the  pylorus  or  duodenum. 

Symptoms  and  Diagnosis. — The  symptoms  are  those  of  acute  inflammation 
in  the  hepatic  area,  varying  in  severity  from  a  slight  discomfort  and  soreness 
to  violent  and  alarming  pain  and  collapse.  There  is  tenderness,  particularly 
about  the  region  of  the  gall-bladder,  and  this  speedily  may  amount  to 
exquisite  pain  on  pressure.  The  point  at  which  the  greatest  tenderness  is 
felt  is  where  the  lower  third  of  a  line  drawn  from  the  navel  to  the  ninth 
rib  joins  the  middle  third.  With  these  symptoms  there  is  fever,  often 
ushered  in  by  a  chill.  When  the  development  of  the  condition  is  sudden, 
as  it  very  frequently  is,  the  patient  may  be  seized  with  nausea  and  vomiting, 
threatened  collapse,  and  other  symptoms  of  fulminant  abdominal  disease. 

The  pulse  is    rapid;  the  belly  is  distended  and  its  walls  rigid. 

Diagnosis. — Unless  the  pain  is  so  localized  as  to  aid  materially  in  diagnosis, 
and  unless  the  physician  is  provided  with  a  history  of  gallstone  colic,  or  of 
an  inflammation  in  the  gall-bladder  after  one  of  the  acute  fevers,  as  typhoid 
fever,  the  symptoms  may  mislead  him  into  a  diagnosis  of  intestinal  obstruc- 
tion or  acute  appendicitis;  for  paralysis  of  the  bowel  may  be  present,  on 
the  one  hand,  and  in  appendicitis  the  pain  is  often  referred  to  the  region 
of  the  epigastrium  or  liver.  In  certain  cases  of  appendicitis,  with  a  history 
of  recurrent  attacks  or  of  a  recent  attack,  the  physician  must  also  recall 
the  fact  that  pain  in  the  hypochondrium  may  arise  from  a  septic  focus, 
carried  there  from  the  appendix  by  the  lymphatics.  So,  too,  a  gastric  ulcer 
with  perforation  and  subdiaphragmatic  abscess  may  simulate  acute  chole- 
cystitis. When  palpation  reveals  an  elongated  gall-bladder  projecting 
below  the  edge  of  the  liver,  which  is  very  tender  on  palpation,  the  diag- 
nosis is  readily  made.  Jaundice  may  or  may  not  be  present.  It  is  often 
absent.  It  is  important  to  bear  in  mind  the  fact  that  attacks  of  hepatic  colic 
may  occur  in  cases  of  cholecystitis  without  any  gallstones  being  present. 

But  in  hepatic  colic  an  examination  of  the  blood  will  not  reveal  leuko- 
cytosis of  polymorphonuclear  cells,  which  will  be  notably  increased  by 
the  presence  of  an  acute  inflammatory  process  in  or  about  the  gall- 
bladder. In  questioning  the  patient  as  to  the  possible  presence  of  gall- 
stones it  should  be  remembered  that  mild  attacks  of  pain  in  this  region 
may  be  as  indicative  of  the  passage  of  these  bodies  as  a  history  of  typical 
gallstone  colic.  Acute  cholecystitis  is  rarely  characterized  by  the  sud- 
denness of  onset  of  pain  and  abdominal  tenderness  which  are  met  with 
in  acute  pancreatitis  or  perforation  of  the  stomach  due  to  ulcer.  If  these 
symptoms  are  present  they  may,  however,  be  due  to  perforation  of  the  gall- 
bladder due  to  chronic  cholecystitis  arising  from  gallstones.  (See  Chole- 
lithiasis.) Sometimes  when  there  is  an  infection  of  the  gall-bladder,  as  in 
the  third  or  fourth  week  of  typhoid  fever,  the  onset  of  cholecystitis  may  be 
as  severe  as  that  of  perforation.     Occasionally  during  the  course  of  acute 


CHOLELITHIASIS  677 

ulcerative  endocarditis  with  secondary  cardiac  failure  the  liver  becomes 
enlarged  and  tender  and  chills  and  fever  are  met  with.  Pyopericardium 
must  also  be  excluded  if  possible. 

Treatment. — The  treatment  in  all  cases  in  which  the  symptoms  are  severe 
is  prompt  operative  interference.  Temporizing  measures  consist  in  the 
use  of  rest  in  bed,  counterirritation  over  the  region  of  the  gall-bladder,  and 
the  use  of  gentle  saline  purges  to  unload  the  bowels. 


CHOLELITHIASIS. 

Definition. — ^The  term  cholelithiasis  is  applied  to  a  condition  in  which  the 
gall-bladder  or  the  other  parts  of  the  biliary  passages  contains  one  or  more 
gallstones. 

Etiology  and  Pathology. — The  predisposing  causes  of  gallstone  formation 
are  all  conditions  which  produce  catarrh  of  the  stomach  and  duodenum  and 
biliary  passages.  A  sedentary  life  with  high  living  is  a  factor.  So,  too, 
enteroptosis  may  aid  in  its  development.  The  condition  is  commonly  met 
with  after  forty  years  of  age,  but  cases  have  been  seen  in  childhood  and  even 
in  the  newborn.  More  than  75  per  cent,  of  all  cases  occur  in  women,  and 
90  per  cent,  of  these  women  have  been  pregnant  one  or  more  times. 

Biliary  calculi  are  formed  as  the  result  of  the  deposit  of  certain  of  the 
ingredients  of  the  bile  about  a  nidus,  which  we  now  know  is  often,  if  not 
always,  an  accumulation  of  micro-organisms.  The  presence  of  these  infecting 
agents  has  already  been  discussed  in  the  article  on  Cholecystitis,  but  it  is 
particularly  important  to  bear  in  mind  the  fact  that  typhoid  bacilli  are  fre- 
quently the  origin  of  stone,  probably  because  they  often  remain  in  the  gall- 
bladder for  years,  and  because,  when  they  agglutinate,  they  form  with 
epithelial  cells  a  good  nidus  for  the  deposition  of  biliary  materials.  That 
micro-organisms  play  this  part  is  now  proved  not  only  by  many  observations 
on  man,  but  by  experiments  on  animals. 

The  mere  presence  of  micro-organisms,  however,  is  not  sufficient  for  the 
formation  of  stone.  It  is  necessary  that  a  catarrhal  state  of  the  mucous 
membrane  be  present,  since  in  this  condition  three  ingredients  of  the  stone 
are  excreted  by  the  walls  of  the  gall-bladder,  namely,  mucus,  cholesterin, 
and  a  substance  called  "bilirubin  calcium."  Healthy  bile  prevents  the  depo- 
sition of  bilirubin  calcium,  but  if  albumin  is  present  this  action  is  arrested 
and  the  deposit  is  made.  When  inflammation  is  present  enough  albumin 
enters  the  bile  from  the  diseased  mucous  membrane  to  permit  of  this  effect, 
and  the  small  quantity  of  cholesterin  present  in  normal  bile  is  also  much 
increased.  It  is  evident,  then,  that  for  the  deposit  of  the  materials  forming 
a  gallstone  an  unhealthy  mucous  membrane  is  primarily  essential. 

Gallstones  when  composed  chiefly  of  cholesterin  are  transparent  or  slightly 
tinged  by  bile.  If  broken,  such  a  stone  appears  crystalline,  with  radiating 
lines.  In  other  cases  the  stone  is  composed  not  only  of  cholesterin,  but  of 
biliary  pigment  and  salts  of  magnesium  and  calcium.  Such  stones  are 
usually  dark  in  color,  brown  or  green.  They  may  be  round  or  marked  by 
facets,  due  to  attrition,  where  they  have    rubbed    against   other  stones. 


678  DISEASES  OF  THE  BILIARY   TRACT 

In  these  stones  also  a  radiating  crystalline  formation  is  present  on  fracture. 
These  dark-faceted  stones  are  the  ones  commonly  found.  More  rarely 
stones  of  small  size  are  found,  composed  almost  entirely  of  bile  pigment. 
Calcium  carbonate  stones  are  still  less  frequently  met  with. 

In  size  gallstones  vary  from  fine  gritty  sand  to  masses  as  large  as  a  small 
banana. 

In  the  vast  majority  of  cases  of  cholelithiasis  biliary  calculi  are  formed 
in  the  gall-bladder.  Very  rarely  small  particles  of  biliary  sand  form  in  the 
bile-ducts  of  the  liver  itself.  The  large  stones  found  in  the  cystic  and  common 
duct  have  formed  in,  and  then  slipped  from,  the  gall-bladder. 

The  number  of  stones  found  in  the  gall-bladder  may  vary  from  one  or  two 
to  several  thousand,  if  the  tiny,  sand-like  pieces  are  counted.  When  the 
number  is  large,  they  usually  show  signs  of  lateral  pressure,  but  sometimes 
several  may  exist  without  facets  being  developed. 

If  a  gallstone  lodges  in  the  common  gall-duct  so  as  to  completely  occlude 
it,  there  is  usually  found  at  autopsy  a  condition  of  dilatation  of  this  duct, 
which  is  filled  with  a  clear,  mucus-like  fluid.  (See  Occlusion  of  the  Bile- 
ducts.)  If  the  obstruction  is  not  complete  and  infection  of  the  duct  takes 
place,  the  state  is  one  of  cholangitis,  already  described,  or  even  of  sup- 
purative angiocholitis. 

When  the  cystic  duct  is  completely  obstructed  by  a  stone,  the  gall-bladder 
may  be  greatly  enlarged  and  filled  with  clear  fluid  or  with  other  gallstones. 
If  the  gall-bladder  is  infected  suppurative  cholecystitis  develops,  and  perfor- 
ation may  occur.  (See  Symptoms.)  In  other  cases  the  gall-bladder  undergoes 
atrophy,  and  may  be  so  shrunken  as  to  be  nothing  but  a  small  mass  of  fibrous 
tissue  the  size  of  a  large  nut,  hidden  in  the  hollow  naturally  occupied  by 
the  gall-bladder.  Less  commonly  a  process  of  calcification  is  developed,  and 
the  gall-bladder  becomes  coated  or  infiltrated  by  lime-salts. 

Symptoms. — It  is  important  to  bear  in  mind  the  fact  that  the  mere  presence 
of  gallstones  in  the  gall-bladder  does  not  necessarily  cause  any  symptoms 
whatever.  The  records  of  autopsies  in  Germany,  in  particular,  show  that  a 
very  large  proportion  of  all  women  who  come  to  autopsy  in  the  later  years 
of  life  have  gallstones,  and  yet  there  has  been  no  suspicion  of  their  existence 
prior  to  death.  Only  about  5  per  cent,  suffer  from  distinct  symptoms  due 
to  this  cause.  On  the  other  hand,  if  the  biliary  tract  becomes  infected,  or 
if  an  acute  congestion  of  its  mucous  membrane  occurs,  more  or  less  severe 
symptoms  may  be  at  once  produced  and  fever  may  develop;  or  if  a  stone 
becomes  dislodged  from  the  gall-bladder  and  slips  into  the  cystic  or  common 
duct,  this  mechanical  difficulty  may  at  once  produce  biliary  colic. 

The  symptoms  of  biliary  colic  usually  consist  in  severe  fain,  which  amounts 
to  an  agony  in  most  instances.  Occasionally,  however,  the  pain  is  very 
moderate,  and  is  thought  to  be  due  to  indigestion.  The  patient  often 
vomits  and  sweats  profusely.  The  pain  manifestly  originates  in  the  gall- 
bladder, but  is  radiated  to  the  right  shoulder-blade  and  to  the  epigastrium. 
The  facial  expression  is  one  of  anguish  and  anxiety,  and  the  color  of  the 
skin  is  pallid. 

After  the  attack  has  lasted  for  some  hours,  or  on  the  day  after  an  attack, 
a  moderate  degree  of  jaundice  may  appear,  but  it  is  rarely  well  marked 


CHOLELITHIASIS  679 

unless  the  attack  lasts  for  several  days  or  the  obstruction  is  persistent.  If 
the  stone  is  in  the  cystic  duct,  no  jaundice  occurs  unless  the  neighboring 
mucous  membrane  in  the  common,  or  hepatic  duct,  becomes  swollen  and 
inflamed,  or  unless  the  stone  is  so  placed  in  the  cystic  duct  that  it  presses 
upon  the  hepatic  duct.  The  presence  of  jaundice  in  a  case  which  suffers 
from  severe  pain  in  the  region  of  the  gall-bladder  is  a  positive  diagnostic 
sign  of  much  value,  but  the  absence  of  jaundice  does  not  in  the  slightest 
degree  negative  the  view  that  gallstone  is  present.  Kehr  states  that  in 
720  cases  operated  on  for  gallstone,  80  per  cent,  showed  no  jaundice. 

The  urine,  if  the  stone  is  in  the  common  duct,  may  soon  show  the 
presence  of  bile,  and  not  rarely  albumin  is  found  in  it.  In  still  other 
cases  red  blood  cells  may  be  found  in  the  urine,  and  this  may  lead  us  into 
the  belief  that  the  pain  is  due  to  renal  colic. 

An  attack  of  biliary  colic  lasts,  as  a  rule,  for  but  a  few  hours,  but  occa- 
sionally the  patient  suffers  from  a  prolonged  seizure  lasting  over  several 
days  and  marked  by  temporary  remissions,  which  are,  perhaps,  due  to  ex- 
haustion of  the  irritated  gall-bladder  or  to  temporary  restoration  of  biliary 
flow. 

The  presence  of  a  stone  or  stones  in  the  common  or  cystic  duct  produces 
not  only  symptoms  of  biliary  colic  in  some  cases,  but  other  signs  as  well, 
which  may  be  of  use  in  diagnosis.  If  the  stone  blocks  the  common  duct 
completely,  the  jaundice  which  develops  is  persistent  and  well  marked,  and 
further  attacks  of  colic  may  never  occur,  or,  indeed,  there  may  not  be  a 
single  attack  in  the  patient's  history.  Febrile  movement  is  usually  absent, 
because  the  complete  obstruction  of  the  duct  prevents  infection  from  the 
intestine.    The  gall-bladder  is  usually  not  distended. 

When  the  common  duct  is  not  completely  closed,  and  in  the  majority 
of  cases  it  is  not  occluded,  the  attacks  of  biliary  colic  are  more  frequent, 
and  the  degree  of  jaundice  varies.  This  is  due  to  the  fact  that  at 
times,  when  the  mucous  membrane  surrounding  the  stone  is  not  acutely 
inflamed  or  congested,  bile  is  permitted  to  escape  into  the  bowel,  so  that 
the  pressure  is  relieved  and  the  stools  become  bile-stained.  Such  a  condition 
of  repeated  attacks  of  colic  with  varying  degrees  of  jaundice  may  also  be 
due  to  the  stone  becoming  so  fixed  in  the  ampulla  of  Vater  that  it  forms  a 
ball-valve,  which  sometimes  permits  the  passage  of  bile  and  sometimes  pre- 
vents it.  In  rarer  instances  the  stone  becomes  encysted  in  the  wall  of  the  duct, 
and  so  acts  as  a  valve,  and  in  still  other  cases  it  may  become  lodged  at 
the  junction  of  the  cystic  and  hepatic  duct,  and  by  pressure  cause  symptoms 
characteristic  of  obstruction  in  both  the  cystic  and  common  duct. 

These  cases  of  partial  obstruction  difi'er  from  those  of  complete  obstruction, 
in  the  fact  that  they  not  rarely  develop  fever,  owing  to  infection  of  the  com- 
mon and  hepatic  duct  by  micro-organisms  from  the  bowel.  The  febrile 
attacks  which  ensue  may  be  so  irregular  or  so  intermittent  in  type  that  they 
closely  resemble  those  of  malarial  fever,  but  they  are  in  reality  septic  fever, 
the  so-called  "intermittent  hepatic  fever  of  Charcot."  Such  attacks  may 
persist  for  years  with  no  more  serious  changes  in  the  ducts  than  a  chronic 
catarrh  with  thickening  and  the  proliferation  of  an  exudate  about  the  parts. 
In  some  cases,  however,  the  degree  of  infection  is  so  severe  that  suppura- 


680  DISEASES  OF  THE  BILIARY  TRACT 

tion  takes  place,  not  only  in  the  common  duct,  but  in  the  hepatic  duct  as 
well,  and  even  in  the  gall-bladder,  producing  suppurative  cholecystitis  and 
suppurative  angiocholitis.  (See  Suppurative  Inflammation  of  the  Bile-ducts 
and  Acute  Cholecystitis.) 

The  additional  symptoms,  to  those  of  biliary  colic,  which  arise  when  the 
cystic  duct  becomes  the  lodging-place  for  a  stone  are  chiefly  enlargement  of 
the  gall-bladder  from  distention  and  the  negative,  but  nevertheless  valuable, 
evidence  of  absence  of  jaundice.  The  size  of  the  gall-bladder  in  cases  in 
which  the  obstruction  is  complete  is  sometimes  marvellous.  Instances  have 
been  recorded  in  which  the  enlarged  gall-bladder  has  been  mistaken  for  an 
ovarian  tumor,  and  not  rarely  the  enlarged,  pear-shaped  mass  can  be  felt 
near  the  median  line  of  the  abdomen.  (See  Diagnosis.)  On  the  other 
hand,  the  facts  in  regard  to  atrophy  of  the  gall-bladder,  already  named  in 
the  discussion  of  the  pathology  of  this  affection,  should  be  recalled;  in  other 
words,  the  absence  of  a  large  gall-bladder  does  not  exclude  obstruction  to 
the  cystic  duct. 

If  the  gall-bladder,  which  is  distended  by  retained  bile  and  gallstones,  can 
be  palpated,  it  may  be  possible  to  produce  what  is  called  "gallstone  crepitus" 
by  the  rubbing  of  the  stones  one  upon  the  other. 

Complications  and  Sequelae.  —  A  stone  may  perforate  the  gall-bladder, 
and,  by  way  of  an  adhesion,  gain  the  cavity  of  the  duodenum  and 
escape  with  the  feces.  In  still  other  cases  the  perforation  takes  place 
through  an  adhesion  to  the  colon,  but  very  rarely  does  the  stone  escape 
into  the  srrlall  bowel  below  the  duodenum.  In  other  instances  the  gall- 
bladder becomes  adherent,  by  an  inflammatory  exudate,  to  the  abdom- 
inal wall,  and  the  stones  finally  escape  from  the  fistulous  opening.  I  had 
a  case  in  my  clinic  at  the  Jefferson  Hospital  some  years  since  in  which  the 
patient  passed  almost  daily  a  little  pus  and  a  little  bile  with  one  or  more 
stones  through  such  an  opening,  yet  seemed  in  excellent  health,  probably 
because  nature  had  established  free  drainage.  More  commonly  the  perforation 
takes  place  so  that  the  stone  enters  the  peritoneal  cavity  and  then  the  asso- 
ciated infectious  material  causes  fatal  peritonitis.  When  the  gall-bladder 
becomes  adherent  to  the  diaphragm  and  perforation  ensues,  the  stone  with 
pus  and  bile  may  escape  into  the  pleura  or  into  the  lung.  In  the  Transactions 
of  the  Association  of  American  Physicians  for  1897,  Graham,  of  Toronto, 
reports  10  cases  of  cholelithiasis  perforating  into  the  lung,  and  in  4  of  them 
the  stone  passed  through  an  adhesion  which  existed  between  the  gall-bladder, 
the  diaphragm,  and  the  pleura. 

The  spitting  of  bile,  with  a  distressing  cough,  and  dulness  on  percussion  in 
the  area  just  above  the  liver,  where  pulmonary  resonance  is  usually  present, 
make  the  diagnosis  certain. 

Gallstones  have  been  carried  far  away  from  the  gall-bladder  by  suppura- 
tion after  perforation,  and  have  even  been  found  in  the  urinary  bladder  as 
a  result  of  this  process.  Perforation  of  the  gall-bladder  with  fatal  syncope 
has  been  reported  during  an  attack  of  biliary  colic. 

Diagnosis. — ^This  is  not  difficult  if  we  are  able  to  exclude  appendicitis, 
diaphragmatic  pleurisy,  gastric  ulcer,  gastralgia,  the  gastric  crisis  of  ataxia, 
and  renal  stone.     Appendicitis  is  detected  by  finding  even  greater  pain  on 


CHOLELITHIASIS  681 

palpation  in  the  appendicular  area;  pleurisy  is  excluded  by  careful  auscul- 
tation to  reveal  a  friction  sound.  In  gastric  ulcer  there  is  a  history  of  pain 
immediately  after  the  taking  of  food,  and  perhaps  of  hsematemesis ;  and  the 
patient  is  usually  a  young  woman,  whereas  gallstones  are  usually  present 
in  women  past  forty  years  of  age.  A  person  with  an  ulcer  is  usually  poorly 
nourished  and  anaemic,  whereas  the  patient  with  gallstones  is  usually  plump 
and  possessed  of  a  thick  abdominal  wall,  Hyperchlorhydria  is  present  in 
ulcer,  but  absent  in  cholelithiasis,  as  a  rule.  In  those  cases,  however,  in 
which  there  are  adhesions  between  the  gall-bladder  or  its  duct  and  the 
pylorus  or  duodenum,  these  differential  signs  may  fail  because  pyloric 
obstruction  causes  pain  after  taking  food  and  produces  hyperchlorhydria. 
Gastralgia  is  pointed  to  by  the  fact  that  the  patient  is  subject  to  neuralgia, 
and  is  neurotic  in  type,  rather  than  stout,  as  are  most  gallstone  cases.  An 
attack  of  gastric  crisis  in  ataxia,  while  often  associated  with  vomiting, 
can  be  detected  by  the  history  of  an  ataxic  gait  and  by  the  presence  of  an 
Argyll-Robertson  pupil  or  other  signs  of  that  disease.  Renal  stone  causes 
pain  to  be  radiated  to  the  inside  of  the  thigh  and  to  the  testicle.  Movable 
kidney  may,  by  dragging  or  pressing  upon  the  common  biliary  duct,  cause 
obstruction,  and  so  produce  an  attack  of  biliary  colic  and  jaundice  not  due 
to  stone.  Further,  the  pain  due  to  twisting  of  the  ureter  in  such  a  case  may 
simulate  hepatic  colic.  The  finding  of  a  floating  kidney  clears  up  the 
diagnosis.  A  new-growth  may  produce  similar  symptoms,  and  it  may  be 
impossible  to  differentiate  the  obstruction  from  that  due  to  gallstones.  In 
none  of  these  states  is  the  greatest  degree  of  pain  on  pressure  over  the  gall- 
bladder. 

It  is  essential  that  attention  be  paid  to  one  very  important  differential 
point,  which  must  always  be  borne  in  mind,  the  so-called  "  Courvoisier's 
law,"  namely,  that  an  enlarged  gall-bladder  with  jaundice  is  a  sign  of 
malignant  growth  of  the  gall-bladder  rather  than  that  of  obstruction  due 
to  stone. 

Treatment. — The  treatment  of  biliary  colic,  like  that  of  renal  colic,  con- 
sists in  the  administration  of  a  hypodermic  injection  of  |  of  a  grain  of  mor- 
phine, with  3-|-g-  of  atropine,  and  yw  ^f  a  grain  of  nitroglycerin,  to  relieve 
pain  and  to  relax  spasm.  If  the  first  injection  does  not  give  relief  at  the  end 
of  fifteen  or  twenty  minutes  it  may  be  repeated,  the  atropine  being  left  out. 
After  the  attack  is  over  the  patient  should  rest  quietly  in  bed  for  two  or 
three  days,  in  order  to  hasten  the  disappearance  of  the  inflammation  of  the 
mucous  membrane,  which  is  usually  associated  with  the  attack,  and  thereby 
decrease  the  danger  of  a  subacute  or  chronic  inflammatory  process  develop- 
ing in  the  gall-bladder  or  common  duct. 

No  medicines  have  any  effect  upon  the  gallstones  which  are  already 
formed,  but  a  number  of  remedies  may  be  given  to  patients  who  suffer 
from  gallstones,  with  the  object  of  preventing  the  formation  of  others,  and 
with  the  hope  that  by  their  use  catarrh  and  irritation  of  the  mucous  mem- 
brane lining  the  gall-bladder  and  the  common  duct  may  be  materially 
diminished.  These  remedies  consist  in  the  mild  saline  purgatives,  such 
as  the  various  imported  purgative  waters,  which  are  gentle  in  their  action, 
and  which  may  be  preferably  taken  hot  in  the  dose  of  one  or  two  teacupfuls 


682  DISEASES  OF   THE  BILIARY  TRACT 

before  breakfast.  Chloride  of  ammonium,  in  the  dose  of  5  to  10  grains  three 
times  a  day,  is  useful  for  its  effect  upon  mucous  membranes,  and  is,  perhaps, 
best  given  in  equal  parts  of  fluid  extract  of  licorice  and  water. 

Until  within  recent  years  the  physician  was  content  when  a  case  of  chole- 
lithiasis escaped  month  by  month  from  a  return  of  biliary  colic,  deeming  it 
inexpedient  that  any  radical  measure  of  relief  should  be  instituted.  With  our 
present  knowledge,  however,  it  cannot  be  doubted  that  the  question  of  opera- 
tive interference  must  be  carefully  considered  in  every  case  in  which  a  positive 
diagnosis  of  cholelithiasis  can  be  made.  The  time  for  operation  is,  of  course, 
during  a  period  of  quiescence,  since  at  the  time  of  an  attack  the  acute  inflam- 
mation which  exists  in  and  around  the  gall-bladder  may  seriously  complicate 
the  work  of  the  surgeon. 

The  question  as  to  how  frequently  the  patient  should  be  allowed  to 
suffer  from  gallstone  colic  before  operative  interference  is  urged  is  one  which 
varies  with  each  individual  case.  If  the  jaundice  which  is  present  with  the 
first  attack  is  not  severe  and  lasts  but  a  very  short  time,  and  if  the  temper- 
ature of  the  patient  is  not  disturbed,  or  returns  to  normal  within  a  period 
of  twenty-four  hours,  and  if,  again,  palpation  in  the  neighborhood  of  the 
gall-bladder  some  days  after  the  attack  fails  to  reveal  evidence  of  a  low-grade 
inflammation,  as  manifested  by  tenderness  or  pain,  it  is  then  permissible, 
and,  indeed,  advisable,  that  the  patient  should  not  be  operated  upon.  Even 
when  as  many  as  two  or  three  such  mild  attacks  have  occurred  at  long  inter- 
vals, the  condition  may  not  be  such  as  to  require  that  the  physician  should 
strongly  recommend  surgical  aid.  When,  however,  the  attack  of  biliary  colic 
is  violent  or  repeated,  when  the  jaundice  persists  for  a  long  period,  and 
when  distinct  evidence  of  persistent  cholecystitis  continues,  then  operation 
should  be  resorted  to,  particularly  if  a  mass,  caused  by  the  gall-bladder  being 
distended  by  stones,  can  be  distinctly  felt.  To  delay  operation  in  a  case  of 
this  kind  until  frequent  attacks  have  resulted  in  the  formation  of  a  large 
amount  of  inflammatory  material  about  the  gall-bladder  is  very  unwise.  By 
this  means  cases  which  would  offer  under  ordinary  circumstances  no  surgical 
diflSculties  may  become  almost  inoperable,  and  what  should  be  an  easy  con- 
valescence may  be  instead  a  difficult  and  prolonged  illness,  testing  the  skill 
of  both  the  physician  and  surgeon  to  the  utmost. 

Mayo  has  performed  510  operations  for  gallstone,  with  a  mortality  of 
only  3  per  cent.  On  208  cases  in  which  stones  were  present  in  the  gall- 
bladder alone,  and  which  were  uncomplicated  by  any  other  condition,  there 
were  2  deaths — a  mortality  of  less  than  1  per  cent. 

Grouping  together  all  cases  complicated  by  the  presence  of  stones  in  the 
common  or  cystic  ducts,  cases  of  cholelithiasis  in  which  infection  occurred, 
cases  of  biliary  infection  and  malignant  disease,  Mayo  finds  the  mortality 
to  be  5  per  cent.,  or  16  deaths  out  of  326  cases  which  he  operated  on.  He 
believes  these  figures  to  be  a  strong  argument  in  favor  of  early  operation  in 
cases  of  cholelithiasis. 


MALIGNANT  GROWTHS  OF  GALL-BLADDER  AND  BILIARY  PASSAGES    683 


MALIGNANT  GROWTHS  OF  THE  GALL-BLADDER  AND  BILIARY 

PASSAGES. 

Etiology. — The  cause  of  the  development  of  morbid  growths  in  these  parts 
is  unknown,  and  only  some  of  the  predisposing  causes  are  recognized. 

In  the  case  of  carcinoma  of  the  biliary  ducts  and  the  gall-bladder,  there  can 
be  no  doubt  that  age  has  a  very  distinct  influence.  The  growth  usually 
develops  later  in  life  than  does  carcinoma  in  any  other  part,  namely,  about 
the  fifty-sixth  year;  whereas,  the  period  of  greatest  frequency  of  cancer  of 
the  mammary  gland  is,  according  to  Kelynack,  about  the  fortieth  year.  It 
would  also  seem  probable  that  gallstones  very  distinctly  predispose  to  the  devel- 
opment of  carcinoma  in  these  parts,  for  they  are  found  present  in  from  90  to 
95  per  cent,  of  all  cases;  whereas,  the  frequency  of  gallstones  in  persons 
dying  from  other  diseases  than  cancer  of  these  parts  is  from  6  to  12  per  cent. 
(Kelynack).  On  the  other  hand,  it  has  been  claimed  that  the  presence  of 
carcinoma  of  the  gall-bladder  leads  to  the  rapid  formation  of  stone.  Prob- 
ably the  pathological  condition  of  the  mucous  membrane  which  aids  in  the 
formation  of  stone  (see  Cholelithiasis)  also  predisposes  to  the  development 
of  a  morbid  growth,  and  this  effect  may  be  increased  by  the  irritation  pro- 
duced by  the  stones  after  they  are  formed. 

In  women  carcinoma  of  the  gall-bladder  is  far  more  common  than  it  is  in 
men.  Musser,  in  his  classical  paper  upon  this  subject,  found  that  out  of  98 
cases  75  were  in  women  and  only  23  in  men,  and  other  clinicians  have  noted 
an  even  greater  percentage  among  women.  Curiously  enough,  this  is  not  the 
case  when  the  growth  affects  the  biliary  passages  other  than  the  gall-bladder, 
for  in  such  instances  the  number  of  men  and  women  affected  is  practically 
the  same. 

Pathology  and  Morbid  Anatomy. — Carcinoma  of  the  gall-bladder  is  usually 
of  the  type  of  cylindrical-cell  epithelioma,  but  in  statistics  there  is  much 
contradiction  as  to  this  point.  This  form  of  cancer  is  also  the  type  which 
most  commonly  affects  the  biliary  ducts.  When  the  gall-bladder  is  affected 
the  fundus  is  the  part  that  usually  suffers.  If  the  biliary  passages  are  in- 
volved, the  common  duct  is  the  part  that  is  usually  affected,  and  that 
portion  of  it  where  it  enters  the  bowel  is  the  favorite  site  of  the  growth. 
(See  Fig.  92.) 

When  cancer  attacks  the  gall-bladder,  as  already  pointed  out  in  the  article 
on  Cancer  of  the  Liver,  the  liver  is  affected  in  a  large  percentage  of  cases 
by  secondary  growths  (Musser  says  54  per  cent.).  The  pancreas  is  also 
very  commonly  involved.  When  the  growth  is  in  the  biliary  ducts,  metas- 
tasis to  other  parts  is  rare. 

Carcinoma  of  the  gall-bladder  may  also  result  in  the  formation  of 
adhesions,  by  which  it  becomes  attached  to  the  abdominal  wall,  the  colon, 
and  even  the  stomach  and  small  intestines.  In  other  instances  a  suppurative 
cholecystitis  may  develop. 

Symptoms. — The  symptoms  of  cancer  of  the  gall-bladder  are  most  varied. 
If  the  growth  is  so  situated  that  it  interferes  with  biliary  flow,  the  manifes- 
tations of  hepatic  disease  may  develop  while  it  is  still  a  very  small  mass; 


684 


DISEASES  OF   THE  BILIARY   TRACT 


whereas,  if  no  pressure  is  produced,  the  tumor  may  reach  a  very  considerable 
size  before  its  presence  is  suspected. 

As  soon  as  the  tumor  reaches  any  size  it  can  be  palpated  below  the  border 
of  the  last  rib  in  most  instances,  particularly  if  it  affects  the  fundus  of  the 
gall-bladder,  as  it  does  in  the  majority  of  cases.  Its  position  is  usually 
along  the  outer  edge  of  the  right  rectus  muscle  and  about  the  neighborhood 
of  the  normal  gall-bladder.  It  may  extend  downward  toward  the  pelvis,  or 
it  may  be  erect  and  protrude  through  the  abdominal  wall,  as  an  aneurysm 
protrudes  from  the  chest.  The  tumor  feels  hard  and  is  usually  somewhat 
pear-shaped.  It  varies  in  size  from  that  of  a  child's  head  to  that  of  a  small 
walnut. 


Pig.  92 


Primary  carcinoma  of  the  duodenal  papilla  seen  at  the  upper  end  of  the  rod  running  through 
the  duct.     (Kast  and  Rumpler.) 

If  the  growth  is  so  placed  near  the  neck  of  the  gall-bladder  that  it  pre- 
vents the  cystic  duct  from  draining  that  viscus,  the  resulting  distention  of 
the  gall-bladder  may  cause  the  formation  of  a  greatly  distended  sac,  which 
may  extend  far  below  the  ribs,  and  by  its  pressure  upon  the  bowel  cause 
intestinal  obstruction. 

Jaundice  and  pain  are  very  constant  symptoms  of  cancer  of  the  gall- 
bladder. Musser  found  jaundice  in  69  per  cent,  of  his  cases,  and  pain  in 
62  per  cent.  When  the  growth  invades  the  gall-bladder  alone,  it  does  not 
of  itself  cause  icterus,  but  the  neighboring  glands  are  often  involved  very 


MALIGNANT  GROWTHS  OF  GALL-BLADDER  AND  BILIARY  PASSAGES    685 

early,  and  by  this  means,  or  by  secondary  growths  in  the  common  duct,  jaun- 
dice is  produced.  In  this  connection  " Courvoisier's  law"  is  to  be  recalled, 
namely,  that  given  an  enlarged  gall-bladder  with  jaundice  the  cause  is 
carcinoma,  not  gallstone. 

Wasting  is  usually  well  marked,  not  only  by  reason  of  the  malignant 
growth,  but  because  of  the  jaundice  and  gastroduodenal  catarrh  which  are 
usually  present.  Ascites  may  develop  (18  per  cent,  of  cases,  Musser).  Death 
is  due  to  exhaustion,  and  sometimes  to  cholsemia. 

Diagnosis. — A  growth  in  the  gall-bladder  can  usually  be  differentiated 
from  one  in  the  bile-ducts  by  its  size,  the  readiness  with  which  it  can  be  pal- 
pated, and  the  absence  of  jaundice  until  it  is  of  some  size.  Given  a  case  in 
which  jaundice  develops  in  a  woman  well  along  in  years,  in  which  the  jaun- 
dice remains  persistent  and  in  which  no  tumor  can  be  felt,  and  the  diagnosis 
is  in  favor  of  growth  in  the  duct.  If  metastatic  masses  can  be  found  in 
the  liver,  the  primary  growth  is  probably  in  the  gall-bladder,  for  they  rarely 
develop  from  a  growth  in  the  duct. 

An  even  more  important  differential  point  is  that  between  cancer  of  the 
gall-bladder  with  cystic  enlargement  and  enlargement  due  to  hydrops 
of  the  gall-bladder.  In  the  latter  case  the  gall-bladder  is  distended  with  a 
clear  fluid  as  the  result  of  the  presence  of  stone  or  other  cause,  completely 
closing  the  cystic  duct.  As  Courvoisier  found  this  state  of  hydrops  79  times 
in  91  cases  of  impacted  gallstone,  it  is  not  a  very  rare  condition.  The  dif- 
ferentiation between  these  two  states  is  made  as  follows:  In  hydrops  of  the 
gall-bladder  there  is  usually  no  jaundice,  and  the  tumor  presents  a  smooth, 
pear-shaped  surface,  and  there  may  be  a  history  of  gallstone  colic.  Bile  is 
present  in  the  stools  and  the  degree  of  wasting  is  not  marked. 

In  some  rare  cases  the  gall-bladder  undergoes  thickening  and  presents  a 
small,  hard  mass,  which  may  be  palpated.  This  has  already  been  described 
elsewhere  as  calcification  of  the  gall-bladder.  The  absence  of  metastasis 
and  of  other  signs  of  cancer  also  aids  us  in  excluding  the  morbid  growth 
in  these  cases. 

Other  causes  of  tumor  in  the  region  of  the  gall-bladder  are  aneurysm, 
cancer  of  the  pylorus,  cancer  of  the  head  of  the  pancreas,  and  tumor  of  the 
kidney.    A  fecal  mass  in  the  bowel  may  also  mislead  the  physician. 

Prognosis. — Life,  in  a  case  of  cancer  of  the  gall-bladder,  usually  does  not 
last  beyond  a  year,  and  in  many  instances  death  comes  earlier  than  this. 

Death  usually  comes  much  earlier  in  cases  of  malignant  growth  in  the 
duct  than  of  malignant  growth  in  the  gall-bladder. 

Treatment. — The  treatment  of  malignant  growth  of  the  gall-bladder,  of 
necessity,  does  not  offer  much  promise  for  ultimate  and  complete  recovery, 
for  medicinal  measures  are,  of  course,  entirely  useless,  except  for  the  pur- 
pose of  relieving  pain.  Operative  procedures,  even  if  they  result  in  the 
complete  removal  of  the  diseased  gall-bladder,  are  nearly  always  followed 
by  the  development  of  secondary  growths  in  neighboring  parts,  where  they 
are  inoperable  and  where  they  straightway  proceed  to  destroy  the  patient. 
Nevertheless,  given  a  case  in  which  the  gall-bladder  is  greatly  enlarged,  and 
in  which  evidences  of  the  presence  of  a  growth  in  nearby  parts  is  not  marked, 
it  is  certainly  permissible,  and,  indeed,  advisable,  that  operation  shall  be 


636  DISEASES  OF   THE  BILIARY  TRACT 

performed,  with  the  hope  that  the  growth  can  be  removed,  or  that  the  opera- 
tion will  reveal  the  fact  that  the  enlargement  of  the  gall-bladder  is  not  can- 
cerous in  origin,  but  dependent  upon  the  presence  of  gallstone,  or  other 
cause,  or  obstruction  of  the  cystic  or  common  duct. 

In  all  of  these  cases  in  which  jaundice  is  present,  the  very  grave  influence 
of  this  complication  upon  operative  procedure  must  be  taken  into  considera- 
tion, for  while,  on  the  one  hand,  we  are  learning  every  year  that  operations 
upon  the  gall-bladder  can  be  performed  with  a  surprising  degree  of  impunity, 
we  have  also  learned  with  increasing  experience  that  jaundiced  persons 
withstand  operations  badly,  and  that  the  presence  of  bile  in  the  blood  pre- 
disposes the  patient  to  obstinate  and  persistent  capillary  hemorrhage  during 
and  after  operation.  This  has  not  infrequently  resulted  in  death,  although 
the  mere  operative  procedure  itself  was  a  success. 

When  the  growth  involves  the  bile-duct  the  outlook  is,  of  course,  even 
more  discouraging,  for  the  bile-duct  cannot  be  excised,  and  the  jaundice  is 
usually  so  extreme  that  the  condition  of  the  patient  scarcely  justifies  opera- 
tive interference.  The  most  that  can  be  done  for  a  patient  with  a  malignant 
growth  in  the  bile-duct  is  to  operate  with  the  idea  of  providing  drainage  and 
relieving  pressure. 

ICTERUS  NEONATORUM. 

Jaundice  of  the  newborn  is  a  very  common  condition,  and  usually  appears 
about  the  third  or  fourth  day  after  birth.  It  is  noticeable  in  the  skin  and  in 
the  conjunctiva,  but  it  is  never  intense,  and  in  many  cases  may  be  so  slight 
as  to  be  overlooked.  Holt  states  that  it  occurred  300  times  among  900 
babies,  and  Kehrer  asserts  that  in  his  statistics  it  was  present  in  75  per  cent. 
The  last  of  these  estimates  is  much  too  high  a  proportion  for  private  prac- 
tice. Hofmeier  and  others  believe  that  it  is  hsematogenous  in  origin,  and 
results  from  the  destruction,  shortly  after  birth,  of  a  large  number  of  red  blood 
cells.  On  the  other  hand  it  not  rarely  happens  that  the  urine  is  slightly  bile- 
stained,  and  the  stools  are  lacking  in  bile,  which  would  indicate  disordered 
hepatic  action.  In  some  instances  the  portal  vein  may  have  been  overdis- 
tended  in  birth,  and  in  this  way  the  finer  bile-ducts  may  have  been  obstructed. 
Whatever  the  cause,  in  its  simple  form  the  condition  possesses  no  evil  import 
whatever. 

A  severe  and  rare  form  of  icterus  of  the  newborn  may,  however,  develop 
and  cause  the  death  of  the  child.  It  is  due  to  sepsis  following  infection  of  the 
umbilical  vein,  with  phlebitis,  to  congenital  syphilis  of  the  liver,  or  to  con- 
genital atresia  of  the  biliary  ducts,  so  that  the  bile  cannot  escape  into  the 
bowel. 


PANCREATITIS  687 

DISEASES  OF  THE  PANCREAS. 

PANCREATITIS. 

Definition. — Pancreatitis,  as  its  name  implies,  is  an  inflammation  of  the 
pancreas.  It  occurs  in  three  forms,  although  it  must  be  understood  that  no 
hard  and  fast  lines  separate  these  conditions  one  from  the  other.  These 
three  forms  are  the  acute,  the  subacute,  and  the  chronic. 

Acute  Pancreatitis.  History.— As  long  ago  as  1672  Tulpius  described 
an  acute  abscess  of  the  pancreas  due  to  pyaemia.  In  1799  Baillie  studied 
what  was  evidently  a  case  of  chronic  interstitial  pancreatitis.  In  1804  Portal 
recorded  an  instance  of  acute  suppurative  pancreatitis,  as  did  Percival  in 
1818.  In  1879  Balzer  reported  a  case  of  acute  pancreatitis,  with  fat-necrosis 
but  it  was  not  till  the  epoch-making  paper  of  Fitz  appeared  in  1889  that  the 
profession  recognized  the  frequency  and  importance  of  lesions  of  this  gland, 
although  in  1886  another  American  practitioner,  Senn,  had  written  a  paper 
upon  its  surgery.  Von  Mering  and  Minkowski  made  valuable  contributions 
in  1889  and  1890. 

Chronic  pancreatitis  was  not  recognized  till  Birch-Hirschfeld  described  it 
in  1895.  Since  that  time  the  literature  on  pancreatitis  has  become  quite  vol- 
uminous, and  a  number  of  studies  have  appeared,  of  which  the  most  notable, 
from  the  surgical  standpoint,  ha^  e  been  those  of  Robson  and  Moynihan,  of 
Leeds,  and,  from  the  pathological  standpoint,  one  by  Opie,  of  Baltimore,who 
has  done  more  than  anyone  else  to  throw  light  on  diseases  of  this  organ. 

Etiology. — By  far  the  more  common  cause  of  pancreatitis  is  infection  of  the 
gland  by  way  of  its  duct.  This  results  usually  from  the  presence  of  a  gall- 
stone in  the  ampulla  of  Vater,  which  prevents  the  flow  of  bile  into  the 
bowel,  but  does  not  occlude  the  opening  of  the  pancreatic  duct.  Again, 
the  presence  of  a  gallstone  is  prone  to  result  in  the  development  of  a  septic 
process  in  the  surrounding  mucous  membrane,  and  this  results  in  infection 
of  the  bile,  which  fluid  passes  along  the  duct  of  "Wirsung  and  so  enters  the 
pancreas.  This  is  particularly  apt  to  occur  if  the  gall-bladder  is  so 
shrunken  by  disease  that  it  cannot  readily  expand  when  the  bile  is  dammed 
back  into  the  ducts.  Further  than  this,  bile  alone  entering  the  pancreas, 
even  if  it  be  free  from  micro-organisms,  may  cause  hemorrhagic  pancrea- 
titis and  fat-necrosis. 

It  has  been  argued  that  if  these  causes  are  active  in  the  production  of  pan- 
creatitis, this  state  would  be  met  with  much  more  frequently.  The  explana- 
tion of  the  fact  that  so  many  cases  suffer  from  gallstones  and  gall-bladder 
infections  without  pancreatitis  lies  in  the  fact  that  in  a  certain  proportion  of 
individuals  the  bile-duct  and  pancreatic  duct  do  not  enter  the  bowel  by  one 
opening,  but  through  separate  openings.  In  a  few  cases  the  chief  secretion  of 
the  pancreas  escapes  by  way  of  the  duct  of  Santorini.     (See  Fig.  93.) 

Acute  pancreatitis  may  result  from  several  other  causes,  such  as  one  of  the 
acute  infectious  diseases,  or,  again,  in  the  course  of  septicaemia.     Another 


688 


DISEASES  OF   THE  PANCREAS 


cause  is  infection  from  a  neighboring  lesion,  as  in  direct  extension  from 
a  gastric  ulcer  or  cancer,  or  a  subphrenic  abscess.  Still  another  cause  is 
injury  by  blows  or  by  surgical  procedure. 

Pathology  and  Morbid  Anatomy. — ^Acute  pancreatitis  is  characterized  not 
only  by  a  primary  hypereemia  of  the  gland,  but  in  some  cases  by  the 
escape  of  its  ferments  into  its  own  tissues,  and  adjacent  tissues  as  well.  As  a 
result  of  this  accident,  a  condition  of  "fat-necrosis"  develops  in  the  fatty 
tissues  in  the  immediate  region  of  the  pancreas,  and  often  in  other  parts  of 
the  body  to  which  the  pancreatic  ferment  may  escape  in  the  lymph.  The  fat 
is  split  up  into  glycerin  and  fatty  acids.  The  glycerin  is  absorbed;  the  acids, 
being  insoluble,  are  not  eliminated,  but  combine  with  calcium  salts,  and  with 


Fig.  93 


Portion  of  human  pancreas  and  duodenum  from  a  person  who  had  been  executed  (after  Claude  Bernard 
Physiologic  Exp^rimentale,  1856,  tome  ii.  p.  185),  showing  a  condition  in  which  pancreatic  juice  may 
enter  the  intestine,  although  the  gall-duct  is  obstructed  :  A,  duodenum  showing  the  projections  formed 
by  Brunner's  gland;  B,  B,  the  large  pancreatic  duct ;  C,  C,  anastomoses  between  the  small  pancreatic 
duct  and  the  large  pancreatic  duct;  D.  opening  of  the  superior  pancreatic  duct  into  the  intestine ; 
E,  opening  of  the  small  inferior  pancreatic  duct  into  the  bile-duct. 


the  necrotic  fat  form  yellowish-white  patches  in  the  retroperitoneal  fat,  and 
in  the  fat  of  the  omentum,  mesentery,  abdominal  wall,  and  it  may  be  in  other 
parts. 

In  a  certain  number  of  cases  of  acute  pancreatitis,  but  not  in  all  cases, 
hemorrhage  into  the  body  of  the  gland  occurs,  forming  what  is  known  as 
acute  hemorrhagic  pancreatitis.  (See  also  Hemorrhage  into  the  Pancreas.) 
Whether  this  hemorrhage  is  the  result  of  the  action  of  the  ferment  of  the 
gland  upon  its  own  vessels  is  not  known. 

Acute  pancreatitis  may  proceed  to  suppuration  (suppurative  pancreatitis) 


PANCREATITIS  ggg 

or  to  gangrene  (gangrenous  pancreatitis).  The  suppurative  form  may  be 
circumscribed  or  diffuse.  In  some  cases  the  pus  may  be  confined  to  the 
pancreas  or  peripancreatic  structures,  but  the  lesser  peritoneum,  or  even  the 
general  peritoneum,  may  be  involved. 

Symptoms. — In  acute  pancreatitis  the  patient  is  suddenly  seized  by  a 
severe  fain  in  the  epigastric  region,  vi^hich  is  associated  with  faintness,  or 
even  collapse,  and  it  may  be  active  vomiting.  Inquiry  reveals  the  fact  that 
constipation  is  present,  and  so  the  physician  may  be  misled  into  a  diag- 
nosis of  intestinal  obstruction,  but  doubt  is  throv^n  upon  this  belief  by  the 
fact  that  gas  can  be  passed  by  the  anus.  The  pain  may  be  paroxysmal  in 
type,  and  there  is  great  tenderness  in  the  epigastrium  upon  pressure.  This 
area  becomes  swollen  and  tense,  and  as  the  case  progresses  the  entire  abdo- 
men may  become  distended.  The  face  is  pinched  and  anxious-looking,  and 
the  upper  lip  drawn  as  in  acute  peritonitis.  The  vomit  may  become  hlack 
and  tarry  from  the  presence  of  altered  blood. 

If  the  patient  survives  more  than  a  few  hours,  a  more  or  less  marked  jaun- 
dice develops,  provided  that  the  bile  is  prevented  from  escaping  into  the 
bowel  by  swelling  of  the  mucous  membrane  or  the  presence  of  a  stone. 
Hiccough  may  be  an  annoying  symptom,  and  the  pulse  is  rapid  and  running. 
The  temperature  may  be  febrile,  normal,  or  subnormal.  The  urine  may 
contain  casts  and  albumin.  Death  in  collapse  with  profound  asthenia 
usually  occurs  by  the  second  to  the  sixth  day,  but  recovery  may  occur  in 
mild  cases,  and  it  sometimes  happens  that  these  acute  symptoms  gradually 
merge  into  the  subacute  type  of  the  malady. 

Subacute  pancreatitis  cannot,  of  course,  be  sharply  separated  from  the 
acute  form,  yet  cases  occur  in  which  the  symptoms  are  sufficiently  modified 
to  indicate  that  another  form  of  pancreatitis  is  present.  The  malady  is  not 
so  sudden  in  its  onset,  the  pain  is  not  so  excruciating,  and  the  epigastric 
swelling  is  neither  so  great  nor  so  rapid  in  its  development.  The  pulse  is  less 
rapid,  and  the  constipation  is  more  prone  to  give  place  to  diarrhoea,  the  stools 
containing  pus,  tarry  blood,  and  undigested  food.  Chills  also  occur,  and 
after  a  few  days  a  swelling,  due  to  abscess,  may  be  felt.  This  abscess  may 
burj-ow  in  such  a  way  as  to  form  a  perirenal  abscess,  a  psoas  abscess,  or  a 
subphrenic  abscess,  or  it  may  burst  into  the  stomach  or  bowel.  The  symp- 
toms of  sepsis  are,  of  course,  present  in  such  a  case,  and  if  surgical  relief  is 
not  given  death  is  due  to  this  cause  or  to  profound  asthenia.  Such  a  case 
must  be  separated  from  perforation  of  a  gastric  ulcer,  from  abscess  due  to 
caries  of  the  spine,  from  suppurating  cholecystitis,  and  from  perirenal 
abscess. 

Diagnosis. — Fitz  gives  the  following  rule  for  the  diagnosis  of  this  state: 
"Acute  pancreatitis  is  to  be  suspected  when  a  previously  healthy  person,  or 
a  sufferer  from  occasional  attacks  of  indigestion,  is  suddenly  seized  with 
violent  pain  in  the  epigastrium,  followed  by  vomiting  and  collapse,  and  in 
the  course  of  twenty-four  hours  by  a  circumscribed  epigastric  swelling, 
tympanitic  or  resistant,  with  slight  rise  of  temperature."  These  symptoms 
are  still  more  indicative  if  there  is  a  history  of  gallstone  colic. 

Acute  pancreatitis  must  be  separated  from  intestinal  obstruction,  per- 
foration of  the  duodenum,  and  the  perforation  of  a  gastric  ulcer.     It  must 
44 


690  DISEASES  OF   THE  PANCREAS 

not  be  confused  with  rupture  of  the  gall-bladder,  suppurative  cholecystitis, 
and  fulminating  appendicitis.  The  differential  diagnosis  from  intestinal 
obstruction  has  already  been  touched  upon.  If  doubt  exists  an  operation 
will  reveal  the  true  cause  of  the  symptoms,  for  in  pancreatitis  fat-necrosis 
may  be  evident  as  soon  as  the  belly  is  opened.  The  operation  is  justified, 
because  it  ought  to  be  performed  in  either  instance  to  save  life.  When  per- 
foration of  the  stomach  or  duodenum  is  considered,  the  history  of  an  old 
gastric  ulcer  or  of  hemorrhage  from  the  bowel,  in  which  dark,  tarry  blood  is 
passed,  will  be  of  importance,  and  here,  again,  an  operation  to  save  life  is 
necessary,  whether  the  condition  be  pancreatic  disease  or  perforation. 

When  suppurative  cholecystitis  is  suspected,  it  may  be  confirmed  by  the 
discovery  that  the  early  swelling  is  in  the  neighborhood  of  the  gall-bladder, 
and  a  history  of  typhoid  fever  or  of  gallstones  will  be  presented.  However, 
this  latter  history  may  be  equally  suggestive  of  secondary  pancreatic  disease. 
Here,  again,  an  operation  primarily  for  diagnosis  and  secondarily  for  relief 
is  indicated. 

Perhaps  the  most  important  differential  diagnosis  lies  between  acute 
pancreatitis  and  fulminating  appendicitis,  because  appendicitis  is  a  common 
disease,  because  the  pain  accompanying  it  is  often  referred  to  the  epigas- 
trium, and  because  an  incision  in  the  pancreatic  region  is  far  removed  from 
that  required  for  appendectomy. 

Palpation  of  the  appendix  will  usually  elicit  pain  over  its  site,  and,  perhaps, 
localized  swelling.  Examination  by  the  rectum  may  reveal  marked  iliac 
tenderness  and  a  history  of  repeated  attacks  of  appendicitis  may  be  found. 

A  valuable  aid  to  diagnosis  in  these  cases  is  the  examination  of  the  urine 
for  leucin  and  tyrosin,  which  are  not  present  in  healthy  urine,  although  they 
may  be  present  in  other  conditions  than  pancreatitis.  The  urine  is  pre- 
cipitated with  basic  lead  acetate  and  filtered.  The  filtrate  from  which  the 
excess  of  lead  has  been  removed  by  hydrogen  sulphide  is  now  evaporated 
almost  to  dryness  and  allowed  to  stand  for  crystallization  to  take  place,  when 
crystals  of  leucin  and  tyrosin  may  be  found.  (For  a  valuable  article  on  the 
chemistry  of  the  urine  in  disease  of  the  pancreas  see  Cammidge,  British 
Medical  Journal,  April  2,  1904.) 

Opie  has  described  a  test  for  lypolytic  substances  in  the  urine,  and 
Cammidge  has  advocated  a  test  for  glycerin  derivatives  in  the  urine  as 
aids  to  diagnosis;  but  neither  of  these  methods  is  readily  employed  by 
the  general  practitioner. 

Prognosis. — Acute  pancreatitis  is  always  an  exceedingly  grave  state.  Death 
ensues  in  the  majority  of  cases.  Recovery  occurs  in  the  very  mild  cases,  as 
has  been  proved  by  instances  in  which  a  subsequent  operation  has  revealed 
the  evidences  of  the  disease. 

Treatment. — ^The  treatment  of  acute  pancreatitis  consists  in  the  prompt 
institution  of  surgical  proceedings  as  soon  as  the  shock  of  the  onset  of  the 
disease  has  been  overcome.  Robson  insists  that  the  surgeon  should  not  wait 
until  collapse  passes  off,  as  the  collapse  may  be  due  to  septic  absorption, 
which  only  an  operation  can  relieve.  By  the  relief  of  pressure,  the  pro- 
viding of  drainage,  and  the  removal  of  the  cause  of  the  attack,  if  it  exists 
in  the  gall-duct,  relief  may  be  given  the  patient  and  the  process  arrested 


PANCREATITIS  691 

before  it  has  proceeded  too  far.  In  a  certain  proportion  of  cases,  however, 
the  state  of  the  patient  from  the  onset  is  too  grave  to  permit  of  surgical  inter- 
vention. Excessive  pain  is  to  be  reUeved  by  morphine  given  hypodermically, 
and  collapse  is  to  be  treated  by  the  employment  of  strychnine  and  atropine. 

The  treatment  of  the  subacute  form  of  the  disease  consists  in  supporting 
the  nutrition  of  the  patient  by  the  use  of  predigested  foods  and  stimulants, 
and  by  surgical  intervention  for  the  relief  of  tension  and  removal  of  pus  as 
soon  as  the  diagnosis  is  made  and  the  patient  is  strong  enough  to  stand 
operative  procedures. 

Chronic  Pancreatitis. — This  form  of  pancreatitis  has  been  in  the  past 
considered  quite  rare,  but  it  would  seem  probable  that  it  exists  more  com- 
monly than  is  generally  thought.  It  is  usually  developed  as  a  result  of 
chronic  catarrh  of  the  duct  of  Wirsiing,  which,  in  turn,  is  caused  by  chronic 
gastroduodenal  catarrh  or  by  cholelithiasis,  pancreatic  lithiasis,  or  by  gastric 
ulcer. 

Of  chronic  pancreatitis,  Opie,  of  Baltimore,  thinks  there  are  two  types. 
One  is  an  interlobular  pancreatitis,  with  increase  in  the  connective  tissue 
between  the  lobules ;  the  intralobular  tissues  being  unaffected  and  the  islands 
of  Langerhans  escaping  until  very  late  in  the  pathological  process.  This  is 
the  type  of  chronic  pancreatitis  which  follows  blocking  of  the  pancreatic  duct 
by  a  morbid  growth  or  by  pancreatic  or  biliary  calculi.  Glycosuria  is  rarely 
present,  because  the  islands  escape.  This  is  the  common  form.  In  the 
second  form  there  is  an  interacinar  pancreatitis,  that  is,  new  connective- 
tissue  formation  in  the  lobules  themselves.  The  islands  of  Langerhans  are 
seriously  affected  in  this  type,  and  hence  glycosuria  is  usually  present.  This 
form  is  not  due  to  obstruction  of  the  ducts. 

These  pathological  facts  show  why  it  is  that  glycosuria  does  not  appear 
as  a  sign  of  pancreatic  disease  in  most  cases  in  which,  as  the  result  of  gall- 
stone disease  or  other  sources  of  infection  or  obstruction,  we  suspect  the 
presence  of  pancreatitis.  For  a  recent  and  exhaustive  consideration  of  the 
Relation  of  the  Islands  of  Langerhans  to  Morbid  Conditions  of  the  Pan- 
creas and  Diabetes  Mellitus  see  Finney's  article  in  the  Medical  Chronicle 
for  June,  1903. 

The  interstitial  type,  like  the  more  acute  forms,  may  be  diffuse  or  local- 
ized. When  localized  a  single  area  may  manifest  the  change.  A  somewhat 
subacute  form  is  also  recognized,  and  in  some  of  these  cases  there  is 
a  conspicuous  enlargement  of  the  area  involved,  so  that  the  head  of 
the  pancreas  when  affected  may  be  mistaken  for  a  neoplasm.  Presum- 
ably this  enlargement  represents  a  cellular  infiltration,  which  later  passes 
on  to  a  fibrosis.  The  typical  fibroid  pancreas  is  small,  dense,  resists  incision , 
and  may  creak  when  under  the  knife.  Fatty  infiltration  is  usually  also 
present,  and  evidences  of  a  primary  acute  process  may  be  manifest.  On 
microscopic  examination  there  is  a  notable  increase  in  the  fibrous  tissue, 
which,  as  already  stated,  may  be  perilobular  or  interlobular,  or  it  may  be 
interacinar.  In  the  latter  form  the  islands  of  Langerhans  show  hyaline  or 
fibrohyaline  transformation,  or  they  may  be  absent  from  certain  areas,  or, 
perhaps,  cannot  be  demonstrated  in  any  part  of  the  organ.  The  ducts 
may  show  dilatation,  and  in  some  instances  be  stained  with  bile. 


692 


DISEASES  OF   THE  PANCREAS 


Symptoms. — Chronic  pancreatitis  may  be  divided  into  those  cases  in  which 
the  s}Tnptoms  are  mild  and  those  in  which  they  are  severe.  In  one  case 
there  may  be  Uttle  if  any  pain,  but  there  is  present  persistent  loss  of  flesh, 
and  in  the  epigastrium,  near  the  gall-bladder,  may  be  found  a  hard  mass 
which  may  be  mistaken  for  a  malignant  growth  in  the  stomach  or  gall- 
bladder. The  patient  complains  of  epigastric  distress,  such  as  that  which 
follows  taking  food  which  is  difficult  of  digestion,  and  attacks  of  vomiting 
may  occur.  Sometimes  jaundice  appears.  Fever  may  be  present  if.  the 
infection  of  the  ducts  is  marked. 

In  the  more  severe  form  of  chronic  pancreatitis,  the  symptoms  are  in 
close  accord  with  those  of  the  subacute  form,  in  that  the  symptoms  may 
begin  with  severe  pain  in  the  epigastrium,  as  if  the  patient  had  gallstone 
colic.  There  is  tenderness  in  the  midepigastrium.  Chills  and  fever  may  be 
well  developed. 

Diagnosis. — Chronic  pancreatitis  is  to  be  separated  from  gallstones  in  the 
ductus  communis  choledochus,  from  cancer  of  the  head  of  the  pancreas, 
from  cancer  of  the  gall-bladder  and  of  the  liver,  and  from  subphrenic  abscess. 
From  impacted  gallstones  in  the  common  duct  the  differentiation  is  prac- 
tically impossible.  Tenderness  on  deep  pressure  will  usually  be  found 
over  the  gall-bladder  in  the  case  of  gallstones  and  over  the  epigastrium^  in 
pancreatic  disease,  and  etherization  may  permit  sufficiently  deep  palpation 
to  feel  the  enlarged  head  of  the  pancreas  if  chronic  pancreatitis  is  present. 
The  distribution  of  the  pain  may  be  of  value  in  the  differentiation.  In 
gallstone  cases  the  pain  is  in  the  gall-bladder  area  and  radiates  around  to 
the  right  scapular  region;  whereas,  in  pancreatic  disease  it  is  central  and 
travels  directly  backward  to  a  space  between  the  ends  of  the  scapula. 

Cancer  of  the  head  of  the  pancreas  is  a  disease  of  advanced  life;  its  onset 
is  usually  painless,  and  the  jaundice  that  may  ensue  is  gradual  in  onset  and 
persistent,  because  the  growth  primarily,  or  secondarily,  presses  continually 
on  the  gall-ducts.  The  presence  of  great  swelling  of  the  gall-bladder  in  asso- 
ciation with  jaundice  and  with  the  other  symptoms  of  pancreatic  disease 
already  named  indicates  cancer.  Sometimes  in  these  cases  secondary  can- 
cerous nodules  are  to  be  found  in  the  liver  and  in  other  organs.  The  liver 
may  be  much  enlarged  from  the  damming  back  of  bile  and  from  second- 
ary growths.  Robson  and  Mpynihan  lay  stress  on  the  fact  that  the  absence 
of  pancreatic  secretion  from  the  stools  causes  them  to  be  clay-colored,  even 
when  bile  is  present,  and  this  may  aid  in  diagnosis.  If  on  testing  the  stools 
bile  is  found,  and  the  feces  are,  nevertheless,  light  in  hue,  it  is  a  fair  sup- 
position that  pancreatic  secretion  is  absent.  The  test  of  the  urine  for  leucin 
and  tyrosin,  already  described,  should  also  be  used. 

There  are  two  other  facts  which,  if  present,  will  decide  the  diagnosis  posi- 
tively, namely,  fatty  stools  due  to  the  lack  of  pancreatic  juice  in  the  bowel 
and  the  presence  of  glycosuria  due  to  the  invasion  of  the  islands  of  Langer- 
hans  in  the  pancreas  by  the  pathological  process.  Both  of  these  signs  are 
often  absent,  but  if  they  are  present  they  are  pathognomonic  of  pancreatic 
disease.     (See  Diabetes  Mellitus.) 

Prognosis. — Patients  suffering  from  chronic  pancreatitis  in  moderate  degree 
may  live  for  months  or  even  for  years.    If  glycosuria  develops  the  prognosis 


PANCREATIC  CALCULUS  693 

becomes  very  grave,  not  only  because  this  symptom  is  grave  in  itself,  but 
because  the  glycosuria  indicates  that  the  involvement  of  the  gland  in  the  dis- 
ease process  is  well-nigh  universal,  for  as  long  as  but  a  few  islands  of  Langer- 
hans  exist  glycosuria  does  not  ensue.  Great  emaciation,  marked  jaundice, 
and  the  development  of  a  tendency  to  have  multiple  hemorrhages  are  evil 
signs. 

It  is  in  this  form  of  pancreatitis  that  surgery  has  given  its  most  valuable 
results,  often  producing  perfect  recovery. 

Treatment. — ^The  treatment  of  the  mild  form  of  chronic  pancreatitis 
depending  upon  catarrh  of  the  biliary  and  pancreatic  ducts  may  be  medi- 
cinal for  a  time  in  the  hope  that  the  condition  may  be  relieved.  The 
measures  instituted  are  practically  identical  with  those  advised  in  cases  of 
chronic  cholangitis  (which  see).  It  is,  however,  a  vital  mistake  to  permit 
these  cases  to  drift  along  in  a  state  of  chronic  ill  health,  because  the  condi- 
tion is  one  which  will  eventually  lead  to  pancrea'tic  cirrhosis,  and  this  in 
turn  results  in  great  emaciation  and  the  development  of  glycosuria,  which 
causes  death.  In  other  words,  if  the  patient  does  not  improve  surgical 
measures  should  be  adopted  to  give  relief. 

The  treatment  of  chronic  pancreatitis  of  the  severe  type  is  wholly  surgical, 
for  it  is  cured  in  the  majority  of  instances  by  abdominal  section  and  drainage 
of  the  pancreatic  and  gall-ducts.  Robson  gives  the  mortality  of  operations 
in  chronic  pancreatitis  as  12.9  per  cent,  in  62  cases.  Operations  in  all  cases 
of  jaundice  are  of  a  grave  character,  because  persistent  oozing  hemorrhage 
is  prone  to  follow.  Robson  and  Moynihan  are  firmly  convinced  that  the 
danger  from  oozing  hemorrhage  after  operation  in  cases  of  jaundice  without 
pancreatic  lesions  is  less  than  in  those  cases  in  which  the  pancreas  is  affected. 
They  strongly  advise  the  use  of  full  doses  of  calcium  chloride  in  all  these 
cases  prior  to  operation,  to  increase  coagulability  of  the  blood.  They  advise 
20  to  60  grain  doses  three  times  a  day  for  one  or  two  days.  It  is  not  to 
be  forgotten  that  the  persistent  use  of  this  salt  finally  decreases  the  coagu- 
lability of  the  blood. 

To  sum  up  the  subject  of  treatment,  it  may  be  said  that  all  forms  of  pan- 
creatitis should  be  operated  upon  if  the  condition  is  such  than  an  operative 
procedure  can  be  supported.  While  in  acute  pancreatitis  the  operation  can 
do  little  good  directly,  it  permits  drainage  and  it  may  remove  some  provok- 
ing cause,  and  so  lead  to  recovery.  In  any  case  it  is  the  patient's  only  chance. 
In  the  hemorrhagic  or  suppurative  cases,  the  relief  of  pressure  or  of  pus  is, 
of  course,  advantageous. 

PANCREATIC  CALCULUS. 

Pancreatic  calculus  is  an  exceedingly  rare  condition.  The  stones  are 
composed  of  phosphates  and  carbonates.  They  vary  in  size  from  two  and 
a  half  inches  in  length  to  fine  sand,  and  they  may  be  single  or  multiple. 
As  many  as  300  have  been  reported  in  one  case. 

Symptoms. — There  are  no  pathognomonic  signs  of  the  presence  of  pan- 
creatic calculus.  Pain  in  the  upper  zone  of  the  abdomen  near  the  middle 
line  or,  as  in  Minnich's  case,  near  the  left  costal  border  may  be  present.    It 


694  DISEASES  OF  THE  PANCREAS 

is  often  colicky  in  character,  and  with  the  pain  there  may  be  vomiting,  sweat- 
ing, and  collapse,  as  in  gallstone  colic.  Fatty  stools  from  the  absence  of 
pancreatic  juice  may  be  present,  and  glycosuria  may  occur.  Occasionally 
pieces  of  the  stone  or  small  stones  can  be  found  in  the  stools. 

Treatment. — The  treatment  consists  in  removal  of  the  stones  from  the 
duct  by  operation.  Hypodermic  injections  of  pilocarpine  have  been  advised 
to  increase  the  flow  of  the  pancreatic  fluid,  but  this,  of  course,  cannot 
remove  the  stone  if  it  is  embedded. 


PANCREATIC  CYSTS. 

These  occur  in  four  forms,  namely,  as  retention  cysts,  proliferation  cysts, 
hydatid  cysts,  and  pseudocysts.  Such  cysts  are,  however,  exceedingly  rare. 
Hale  White  states  that  in  6000  autopsies  at  Guy's  Hospital  cysts  of  the  pan- 
creas were  found  only  4  times. 

Retention  cysts  arise  from  blocking  of  the  flow  of  secretion  by  calculi  or 
by  a  single  calculus,  by  the  formation  of  cicatricial  tissue,  which  narrows  the 
duct,  and  by  pressure  from  neighboring  morbid  growths.  If  no  infection 
accompanies  the  retention  of  the  fluid  a  cyst  results  instead  of  pancreatitis. 

Proliferation  cysts  occur  as  cystadenoma,  or  multilocular  tumors,  with  a 
lining  of  cylindrical  epithelium,  and  as  cystic  epithelioma.  Hydatid  cysts  of 
the  pancreas  are  very  rare  indeed,  particularly  in  the  United  States  and 
England;  Hale  White  has  reported  one  in  England. 

Hemorrhagic  cyst  results  from  the  occurrence  of  a  hemorrhage  into  the 
gland  tissue.     Its  existence  is  doubted  by  many  pathologists. 

Pseudocysts  are  not  real  cysts  of  the  pancreas,  but  small  cystic  accumula- 
tions of  fluid  in  adjacent  tissues.  Sometimes  a  pancreatic  pseudo-cyst  is  due 
to  effusion  into  the  lesser  peritoneal  cavity.  They  are  thought  to  follow  some 
injury  to  the  epigastrium. 

Pancreatic  cysts  occur  at  all  ages  from  infancy  to  old  age,  and  are  met  with 
more  frequently  in  men  than  in  women,  but  the  difference  in  the  two  sexes 
is  very  slight.  The  fluid  varies  very  greatly  in  appearance.  It  may  be  as 
clear  as  water,  or  it  may  be  opaque,  or  yellow,  or  coffee-colored,  and  even 
green  or  black.  Its  specific  gravity  is  from  1.010  to  1.020,  and  it  contains 
albumin.  Sometimes  it  contains  all  the  digestive  ferments  of  the  pancreas. 
The  presence  of  any  of  them  is  of  value  in  diagnosis,  but  their  absence  does 
not  negative  the  pancreatic  origin  of  the  fluid.  Nor  does  their  presence 
prove  that  the  cysts  arose  from  the  pancreas.  Pressure  upon  the  pancreas 
and  secondary  changes  in  a  cyst  wall  may  cause  communication  with  the 
pancreas  and  admit  its  secretion  to  the  cyst  cavity. 

Symptoms. — The  s}Tnptoms  of  pancreatic  cyst  are  dependent  upon  the 
pressure  which  is  produced,  and,  therefore,  more  or  less  discomfort  may  be 
the  only  sign  of  its  existence.  If  the  pressure  is  great  pain  is  present.  If 
the  cyst  be  large  enough  to  palpate  it  will  be  found  to  fluctuate,  to  be  flat 
on  percussion,  and  to  transmit  an  impulse  as  in  ordinary  hallottement. 
Puncture  with  a  fine  aspirating  needle  may  reveal  the  character  of  the 
fluid. 


HEMORRHAGES  INTO  THE  PANCREAS  695 

Diagnosis. — Pancreatic  cysts  must  be  separated  from  cystic  kidney,  horse- 
shoe kidney,  ovarian  cysts,  cysts  of  the  hver,  hydrops  of  the  gall-bladder,  and 
cysts  of  the  suprarenal  capsules.  It  must  also  be  separated  from  mesenteric 
cysts,  omental  cysts,  and  retroperitoneal  cysts. 

Prognosis. — Pancreatic  cyst  may  last  for  years  without  causing  discom- 
fort or  death.  On  the  other  hand,  cases  occur  in  which  the  cyst  ruptures 
into  the  peritoneal  cavity  or  into  the  bowel  or  stomach,  and  when  this  hap- 
pens death  ensues,  preceded  by  vomiting  and  diarrhoea.  Rarely  hemorrhage 
takes  place  into  the  cyst,  and  this  is  accompanied  by  sudden  increase  in 
its  size,  and  by  faintness  and  collapse. 

Treatment. — ^The  treatment  consists  in  aspiration,  evacuation  and  drainage, 
or  complete  extirpation  of  the  cyst  wall.  The  second  procedure  is  usually 
that  of  election 


PANCREATIC  TUMORS. 

These  growths  are  exceedingly  rare.  Park  states  that  in  53,000  autopsies 
only  226  showed  primary  malignant  disease  of  this  gland.  Tumors  of  the 
pancreas  consist  in  carcinoma,  sarcoma,  adenoma,  and  gumma.  The  infre- 
quency  of  carcinoma  is  shown  by  the  fact  that  in  23,581  autopsies  made  in 
various  parts  of  the  world,  in  only  29  instances  was  pancreatic  carcinoma 
present.  The  relative  frequency  of  these  growths  is  scirrhus,  encephaloid 
and  colloid. 

Carcinoma  is  the  most  frequent  primary  growth,  according  to  Osier,  and 
sarcoma  is  a  more  common  secondary  tumor  because  of  involvement  of 
the  retroperitoneal  glands  by  this  disease. 

As  nearly  all  cases  of  pancreatic  malignant  growth  are  secondary  to  disease 
of  the  gall-bladder,  a  tumor  in  the  region  of  that  viscus  will  usually  be  found 
to  confirm  the  diagnosis. 

The  prognosis  in  the  case  of  malignant  tumors  is,  of  course,  hopeless.  In 
benign  tumors  the  outlook  depends  upon  the  pressure  S}inptoms.  If  a 
gumma  is  present,  antisyphilitic  treatment  is,  of  course,  indicated. 

HEMORRHAGES  INTO  THE  PANCREAS. 

This  condition  is  to  be  distinctly  separated  in  the  physician's  mind  from 
"  acute  hemorrhagic  pancreatitis."  Local  hemorrhages  may  take  place  into 
the  pancreas  without  any  injury  being  received  and  without  the  patient  being 
a  sufferer  from  hemorrhages  elsewhere.  The  hemorrhage  may  occur  in  a 
person  who  has  seemingly  been  in  excellent  health  without  any  other  symp- 
toms than  collapse,  with  a  feeble  pulse  and  evidences  of  shock.  Sometimes 
hemorrhage  into  the  pancreas  occurs  as  the  result  of  aneurysm  of  nearby 
vessels,  or  of  cancer  of  the  head  of  the  gland.  When  hemorrhage  into  the 
pancreas  occurs,  it  may  be  a  limited  extravasation  of  blood  into  the  gland, 
from  which  the  patient  may  recover,  or  it  may  be  so  profuse  as  to  flood  the 
retroperitoneal  space,  extending  back  to  the  kidneys  and  up  to  the  posterior 
insertion  of  the  diaphragm. 


696  DISEASES  OF   THE  KIDNEYS 

The  differentiation  between  the  symptoms  produced  by  hemorrhage  into 
the  pancreas  and  acute  pancreatitis  is  practically  impossible  if  there  is  no 
previous  history  of  hepatic  and  duodenal  disorder.  If  the  condition  is  due 
to  hemorrhage,  an  operation  to  relieve  local  tension  is  indicated,  as  death  is 
due  rather  to  this  cause  than  to  the  loss  of  blood. 


DISEASES  OF  THE  KIDNEYS. 

MALFORMATIONS  OF  THE  KIDNEY. 

It  happens  not  very  rarely  that  one  kidney  is  absent,  its  place  being 
occupied  by  a  little  fibrous  tissue  or  by  atrophied  renal  tissue  and  fat.  In 
order  that  the  blood  may  be  relieved  of  effete  materials  the  other  kidney  is 
often  very  large,  and,  as  it  is  usually  lower  down  in  the  loin  for  this  reason, 
it  may  be  mistaken  for  a  dislocated  or  cystic  kidney,  and  removed,  which 
means  death  to  the  patient.  Not  uncommonly  one  kidney  is  larger  than  the 
other,  even  if  both  are  functionally  active.  In  other  cases  one  kidney  has  two 
pelves  and  two  ureters.  Perhaps  the  most  common  of  these  malformations 
is  the  so-called  "horseshoe  kidney,''  in  which  the  two  kidneys  are  joined 
across  the  vertebral  column  by  a  mass  of  renal  or  connective  tissue.  Some- 
times this  horseshoe  kidney  is  displaced  into  the  pelvis,  or  it  may  be  altogether 
on  one  side  of  the  vertebral  column. 

Again,  the  kidneys  may  be  fused  into  a  single  mass,  usually  occupying  a 
median  position  much  below  the  normal  level,  or  even  in  the  pelvis. 

MOVABLE  KIDNEY. 

Definition. — Aside  from  the  renal  malpositions  incident  to  malformation, 
and,  therefore,  essentially  of  congenital  origin,  the  kidney  may  wander  from 
its  normal  position.     Several  forms  of  such  displacement  are  recognized. 

The  movable  kidney  lies  behind  the  peritoneum,  and  usually  can  be  made 
to  assume  its  normal  position,  but  descends  during  the  erect  posture;  its  mal- 
position may  be  parallel  to  the  axis  of  the  body,  or  it  may  show  a  lateral 
movement,  or  the  two  may  be  combined — the  "cinder-sifting"  kidney.  The 
organ  may  be  pushed  from  its  place  and  anchored  in  its  new  position — the 
"  incarcerated  kidney.'' 

When  the  kidney  falls  forward  and  develops  a  pedicle,  consisting  of  the 
ureter,  vessels^  and  peritoneum,  the  last  also  covering  the  organ,  it  then 
becomes  a  "floating  kidney,"  the  pedicle  forming  the  so-called  mesone- 
phron. 

Kidneys  enlarged  from  any  cause  are  prone  to  displacement,  and  displaced 
kidneys,  on  account  of  obstruction  of  the  ureters  and  veins,  are  frequently 
subject  to  enlargement. 


MOVABLE  KIDNEY  697 

Movable  kidney  is  far  more  frequent  in  women  than  in  men,  in  the  pro- 
portion of  about  7  to  1.  Again,  the  right  kidney  is  the  one  at  fault  in  the 
majority  of  cases,  or  in  the  proportion  of  about  7  to  1.  Sometimes  both  kid- 
neys are  movable. 

Etiology. — The  most  important  etiological  factor  is  undoubtedly  bodily 
configuration.  Women  of  the  lean,  lank  type  with  floating  ribs  that  slope 
markedly  downward  and  who  are  hollow  in  the  flank,  like  a  hunting  dog  in 
training,  are  the  most  frequent  subjects.  Their  muscles  are  usually  poorly 
developed,  and,  if  they  have  been  pregnant,  as  a  rule,  the  abdominal  wall 
is  relaxed.  If  to  the  natural  configuration  and  these  other  causes  is 
added  the  effect  of  a  tight  corset  and  a  sudden  effort  or  fall,  the  needful 
etiological  factors  are  all  present,  and  a  sharp  pain  in  the  side  may  be  the 
sign  that  the  kidney  has  made  its  maiden  movement  from  its  natural  site. 
In  one  case  the  woman  says  she  has  had  a  fall  and  has  wrenched  her  side  in 
falling;  in  another  she  has  reached  high  above  her  head,  as  in  playing  tennis; 
and  in  a  third  case  a  blow  or  jar  in  a  railway  accident  may  have  been  the 
needed  trauma. 

Symptoms. — Many  patients  have  no  symptoms  of  this  condition  for  years. 
If  on  examining  the  belly  in  the  region  of  the  gall-bladder  a  floating  kidney 
is  found  in  a  person  ignorant  of  its  existence,  and  anything  is  said  of  it,  the 
patient  not  rarely  becomes  a  hypochondriac  on  this  subject,  and  goes  from 
physician  to  surgeon,  insisting  on  relief  of  symptoms  which  are  often 
not  really  in  existence.  As  the  condition  is,  to  a  large  extent,  harmless,  it 
should  be  ignored,  unless  it  is  causing  symptoms. 

When  symptoms  are  present  they  vary  over  a  wide  degree  of  severity.  In 
some  they  consist  of  a  sensation  of  dragging  in  the  back  and  side,  in  others 
they  amount  to  keen  suffering,  and  in  still  others  they  may  consist  in  attacks 
of  agony  due  to  twisting  or  angulation  of  the  ureter  by  the  kidney  becoming 
rotated  on  its  axis  or  bent  by  great  displacement.  These  paroxysms  of  pain 
have  been  called  ^'Dietl's  crises."  Nausea,  vomiting,  chills,  and  collapse 
are  present,  and  after  the  attack  the  urine  is  found  loaded  with  urates  and 
perhaps  pus  and  blood  cells.  Sometimes  even  free  hcemaiuria  may  be  present. 
When  by  postural  change  or  manipulation  the  kidney  assumes  its  normal 
position,  a  distinct  renal  pelvis  may  suddenly  be  emptied  and  a  gush  of  urine 
overdistends  the  bladder  and  escapes  by  the  urethra. 

Diagnosis. — ^There  are  several  states  that  resemble  the  pain  of  floating  kid- 
ney. Violent  pain  in  the  epigastrium  may  be  due  to  this  cause  or  to  appen- 
dicitis, or  gastric  ulcer.  I  have  seen  a  "Dietl's  crisis"  closely  resemble  a  severe 
attack  of  acute  appendicitis.  It  also  may  resemble  gallstone  or  renal  colic, 
or  the  symptoms  produced  by  abdominal  aneurysm.  The  presence  of  the 
mass  in  the  abdominal  cavity  may  lead  to  a  diagnosis  of  malignant  growth 
or  of  impacted  feces. 

The  dislocated  kidney  may  be  felt  on  careful  palpation  in  thin  women 
just  below  the  border  of  the  ribs  and  back  of  the  area  in  which  the  tip 
of  the  gall-bladder  can  be  felt  when  that  viscus  is  enlarged,  but  gentle 
pressure  often  causes  it  to  disappear.  A  floating  kidney  may,  however,  be 
found  almost  anywhere  in  the  abdominal  cavity,  and  has  even  been  dis- 
covered in  the  pelvis.     When  found  in  the  belly  it  is  usually  so  movable 


698  DISEASES  OF   THE  KIDNEYS 

as  to  be  easily  pushed  about,  and  it  is  so  free  and  slippery  that  it  is  often 
elusive,  being  found  one  moment  and  lost  the  next.  Not  rarely  some  move- 
ment of  the  patient  may  cause  it  to  slip  into  its  normal  position.  This  fact 
often  leads  the  physician  to  overlook  its  presence,  and  only  when  the  patient 
is  repeatedly  examined  is  the  kidney  found  "  away  from  home."  In  other 
words,  inability  to  find  a  floating  kidney  at  one  examination  does  not  prove 
that  the  patient  is  not  a  sufferer  from  this  state. 

Pressure  upon  the  kidney  gives  rise  to  a  sickening  sensation,  which  causes 
the  patient  to  wince. 

To  examine  the  patient  properly  the  woman  should  be  placed  on  her  back 
with  the  knees  drawn  up  so  that  the  belly  wall  is  relaxed.  If  the  right  side 
is  being  examined  the  left  hand  of  the  physician  is  so  placed  that  the  tissues 
of  the  right  side  can  be  grasped  close  to  the  last  rib,  between  the  thumb  in 
front  and  the  fingers  behind.  The  patient  is  then  told  to  take  a  deep  breath, 
when  the  kidney  may  be  felt  to  slip  out  between  the  fingers  and  thumb,  as  a 
watermelon  seed  slips  when  pressed  upon  in  this  way.  The  left  hand  remain- 
ing in  situ  to  block  the  pathway  of  return,  the  fingers  of  the  right  hand  can 
now  feel  the  smooth,  rounded  surface  of  the  organ  below  the  area  grasped  by 
the  left  hand.  If  the  pressure  by  the  left  hand  be  relaxed  and  pressure 
upward  is  produced  by  the  right  hand,  the  kidney  may  be  felt  to  slip  back 
into  its  place.  AVhile  the  kidney  is  wandering  deep  palpation  in  the  flank 
may  reveal  a  lack  of  resistance  due  to  absence  of  the  kidney.  When  the  left 
kidney  is  examined  the  same  process  is  followed,  save  that  the  right  hand 
takes  the  place  of  the  left. 

Treatment. — No  treatment  is  needed  unless  the  kidney  really  causes  pain. 
If  it  does  it  can  usually  be  kept  in  place  by  the  avoidance  of  tight  lacing  and 
of  severe  exercise,  or  by  wearing  a  properly  adjusted  pad  and  bandage  to  sup- 
port the  tissues  just  below  the  floating  ribs.  Operative  interference,  with  the 
object  of  stitching  the  kidney  in  place,  is  needed  in  bad  cases,  but  the  diffi- 
culty is  that  the  relief  obtained  by  operation  is  not  permanent  in  all  cases, 
the  kidney  wandering  away  from  where  it  is  sutured.  Further  than  this,  the 
operation  is  not  entirely  devoid  of  danger.  My  colleague,  Dr.  Keen,  has 
placed  the  mortality  at  2  to  3  per  cent.  Out  of  137  cases  which  were 
operated  upon  and  collected  by  Watson  there  were  5  deaths,  but  4  were  not 
the  result  of  the  operation.  In  neurasthenic  patients  operation  should  be 
avoided,  at  least  until  a  rest  cure  is  instituted,  when  not  rarely  all  signs  of 
renal  tenderness  may  disappear.  Even  in  those  cases  which  have  had  one 
attack  of  severe  pain  (Dietl's  crisis)  the  kidney  may  give  no  further  trouble 
if  a  belt  and  pad  are  worn. 


CIRCULATORY  DISTURBANCES  IN  THE  KIDNEY. 

Changes  in  the  circulation  in  the  kidneys  produce  very  great  alterations 
in  the  urinary  flow,  both  as  to  its  quantity  and  quality.  If  the  vessels  of  the 
kidney,  and  particularly  those  of  the  Malpighian  tufts,  are  poorly  supplied 
with  blood,  the  urinary  secretion  is  scanty,  even  though  the  amount  of  solids 
in  the  urine  may  be  fairly  large.    On  the  other  hand,  any  cause  which  sends 


CIRCULATORY  DISTURBANCES  IN   THE  KIDNEY  QQQ 

a  large  amount  of  rapidly  flowing  blood  to  the  kidneys  results  in  free  diuresis. 
Thus,  chilling  the  surface  of  the  body  often  causes  a  profuse  urinary  flow, 
and  nitroglycerin,  by  dilating  the  renal  vessels,  may  do  likewise. 

Any  substance  which  acts  deleteriously  upon  the  delicate  cells  of  the 
Malpighian  tufts  causes  them  to  permit  not  only  the  transudation  of  fluid, 
but  of  albumin  as  well. 

Acute  HyperaBmia. — An  acute  hypersemia  of  the  kidneys  may  follow 
exposure  to  cold,  or  the  ingestion  and  attempted  elimination  of  irritating 
substances,  such  as  cantharides,  turpentine,  and  a  host  of  other  drugs 
capable  of  damaging  the  kidney  epithelium.  It  is  also  generally  accepted 
that  a  similar  state  of  these  organs  may  exist  in  the  course  of  acute 
infectious  diseases,  like  scarlet  fever,  but  it  is  exceedingly  doubtful  if  this  is 
the  case  even  in  a  modified  form. 

Treatment. — The  treatment  of  this  state  consists  in  the  use  of  a  few  dry 
cups  on  the  back  over  the  kidneys  and  in  the  liberal  administration  of  some 
water,  like  Poland  water,  to  flush  these  organs.  Rest  in  bed  is,  of  course, 
essential.  An  old-fashioned  and  useful  remedy  is  watermelon-seed  tea  or  the 
infusion  of  flaxseed.  Often  the  use  of  an  alkaline  diuretic,  such  as  2  drachms 
of  liquor  potassii  citratis,  with  1  drachm  of  sweet  spirit  of  nitre,  is  valuable, 
if  given  every  three  hours. 

Chronic  Hypersemia. — Chronic  hypersemia  is  a  very  much  more  common 
condition,  and  occurs  in  nearly  every  case  in  which  the  circulation  becomes 
sluggish  by  reason  of  cardiac  weakness,  as  in  valvular  disease  with  rupture 
of  compensation,  in  cases  of  ascites  with  pressure  on  the  kidneys,  and  when 
tumors  produce  a  mechanical  interference  with  the  flow  of  blood  in  these 
organs. 

Symptoms. — Albuminuria  is  a  prominent  symptom  of  this  state,  and 
hyaline  casts  and  tube  casts  containing  blood  cells  may  be  found.  The 
amount  of  urine  passed  in  each  twenty-four  hours  is  often  very  scanty. 
If  such  kidneys  are  seen  at  autopsy,  they  will  be  found  to  be  cyanotic 
in  the  early  stages,  somewhat  enlarged  and  heavier  than  normal,  but  the 
capsule  is  not  adherent  and  the  surface  of  the  kidney  is  not  roughened. 
Later  the  connective  tissue  increases,  and  when  the  kidney  is  incised  it  is 
found  to  be  firm  and  tough,  due  to  overgrowth  of  interstitial  tissue.  The 
pyramids  are  dark  and  purple  in  appearance.  A  more  minute  examination 
will  reveal  the  fact  that  the  capillaries  forming  the  Malpighian  tufts  are 
greatly  engorged,  their  walls  thickened,  and  that  the  vasa  recta,  the  inter- 
lobular veins,  and  the  stellate  veins  of  the  cortex  are  also  in  a  similar 
state. 

Diagnosis. — Such  kidneys  may  lead  the  physician  to  a  diagnosis  of  neph- 
ritis complicating  cardiac  disease,  but  the  renal  symptoms  often  disappear 
entirely  under  rest  and  proper  cardiac  treatment,  although  developed  fibroid 
changes  in  the  organ  are,  of  course,  irremediable. 

Treatment. — ^The  treatment  consists  in  giving  the  patient  digitalis  in  full 
doses  if  the  heart  is  feeble,  and  in  applying  a  hot  compress  over  the  kidneys; 
or  in  the  use  of  dry  cups  over  these  organs,  and  in  the  employment  of  gin  and 
digitalis  as  an  alcoholic  stimulant  to  the  heart  and  kidneys.  Rest  in  bed 
for  the  tired  heart  and  for  the  congested  kidneys  is  essential.     Another  very 


700  DISEASES  OF  THE  KIDNEYS 

useful  remedy  is  fluid  extract  of  apocynum  cannabinum  in  the  dose  of  5  to 
10  minims  twice  or  thrice  a  day.     (See  Valvular  Disease  of  the  Heart.) 


ACUTE  BRIGHT'S  DISEASE. 

Definition.— By  acute  Bright's  disease  is  meant  a  state  in  which  the  tissues 
of  the  kidney  are  involved  in  an  acute  inflammatory  process,  that  is  to  say, 
it  is  an  acute  diffuse  nephritis.  The  condition  is  not  far  removed  from  that 
of  acute  hypersemia  already  described. 

Etiology. — ^The  causes  of  acute  diffuse  nephritis  are  the  acute  infectious 
diseases,  particularly  scarlet  fever,  and  also  diphtheria,  croupous  pneumonia, 
and  septicaemia.  Sometimes  typhoid  fever  or  malaria  act  as  exciting  causes. 
In  other  cases  an  acute  infection  gains  access  to  the  body  through  the  tonsils, 
and  it  is  remarkable  how  often  evidences  of  renal  irritation  follow  the  onset 
of  tonsillitis.  Still  another  cause  is  exposure  to  cold,  particularly  if  the  circu- 
lation is  disturbed  by  violent  exercise,  and  if  the  kidneys  are  irritated  by  the 
process  of  eliminating  alcohol  and  other  waste  products  after  a  Bacchanalian 
revel.  So,  too,  the  ingestion  and  elimination  of  irritant  poisons  may  cause  it. 
Severe  burns  or  scalds  may  also  produce  acute  nephritis. 

Acute  and  subacute  nephritis  are  exceedingly  rare  in  children,  unless 
produced  by  one  of  the  acute  infections,  and  by  this  term  is  included  not 
only  the  eruptive  fevers,  but  infections  such  as  bronchopneumonia  and  the 
various  forms  of  severe  summer  diarrhoea,  in  all  of  which  nephritis  is  by  no 
rjieans  unusual.  Thus,  in  70  cases  of  gastrointestinal  disorder  Morse  found 
signs  of  renal  inflammation  in  no  less  than  15  per  cent.,  and  Holt  states  that 
in  every  case  in  which  these  conditions  become  severe  the  kidneys  suffer. 

Pathology  and  Morbid  Anatomy. — As  with  all  acute  inflammatory  processes, 
great  variations  as  to  the  severity  of  the  alterations  in  the  kidney  are  met 
with  in  different  cases.  In  mild  cases  the  organ  may  show  no  gross  changes. 
The  essential  point  to  be  remembered  is  that  the  texture  of  the  kidney  is 
inflamed  through  and  through,  although  not  uniformly  so.  The  glomeruli, 
the  tubules,  the  connective  tissue,  and  the  bloodvessels  all  share  in  the 
process.  In  typical  cases,  for  this  reason,  the  kidney  is  more  or  less  congested, 
enlarged  and  oedematous,  pitting  on  pressure,  and  if  it  is  cut  it  oozes  free 
blood  in  excess.  The  capsule  strips  readily  and  is  often  less  firmly  attached 
than  normal.  As  a  rule,  the  more  oedematous  the  organ  the  less  adherent  is 
the  capsule.  Often  the  pyramids  are  red  and  engorged,  while  the  broadened 
cortex  is  comparatively  pallid. 

In  some  instances  (glomerular  nephritis)  the  glomeruli  appear  to  bear  the 
brunt  of  the  process.  Under  the  microscope  the  vessels  forming  the  tuft  are 
seen  to  be  distended  and  contain  leukocytes  and  larger  cells  having  large 
nuclei,  which  are  probably  endothelial  in  origin.  Degeneration  of  these 
cells  ensues,  and  as  this  change  progresses  they  are  shed  into  Bowman's 
capsule  with  large  mononuclear  leukocytes,  which  fill  it  so  completely  that 
the  vessels  of  the  tuft  are  compressed.  The  epithelium  lining  the  capsule 
may  escape,  although  it  usually  undergoes  proliferation,  degeneration,  and 
exfoliation.     Added  to   these  different  sets  of  cells  we  find  an  albuminous 


ACUTE  BRIGHT'S  DISEASE  701 

exudate,  due  to  the  acute  inflammatory  state  of  the  surrounding  tissues, 
mixed  with  both  red  and  white  blood  cells. 

In  the  tubules  there  is  also  degeneration  and  necrosis  of  the  epithelium 
lining  their  walls,  so  that  the  cells  become  albuminous  or  fatty,  and 
desquamate.  In  this  way  the  tubules  are  more  or  less  distended,  not 
only  with  these  cells,  but  with  red  and  white  cells  and  granular  detritus. 
Fusion  of  these  materials  results  in  the  formation  of  casts  of  the  tubules, 
which  appear  in  the  urine  as  blood  casts,  and  as  casts  of  desquamated 
epithelium. 

As  with  inflammations  elsewhere,  there  is  an  extravasation  of  fluid  into 
the  tissues,  and  when  this  occurs  the  interstitial  portions  of  the  kidney 
become  oedematous,  filled  with  outwandering  leukocytes,  and,  in  addition, 
a  considerable  number  of  small  spheroidal  cells,  many  of  which,  in 
some  cases,  as  shown  by  Councilman,  are  of  the  plasma-cell  type.  If  the 
inflammation  is  very  severe,  there  is  an  actual  hemorrhage  into  the  tissues — 
"hemorrhagic  nephritis."  When  the  extravasation  of  serum  and  leukocytes 
is  particularly  copious,  Delafield  calls  the  condition  "exudative  nephritis." 
This  is  the  form  prone  to  occur  during  or  after  scarlet  fever. 

Symptoms. — ^The  symptoms  of  acute  diffuse  nephritis  are  usually  rather 
sudden  in  onset.  A  child  convalescing  from  scarlet  fever,  or  a  man  suffering 
from  an  acute  infection,  or  after  exposure,  suddenly  suffers  from  scanty 
urinary  flow,  and  almost  before  the  scantiness  is  noticed  the  face  may  be 
seen  to  be  cedematous  and  the  ankles  swollen.  The  patient  may  go  to  sleep 
with  a  normal  visage  and  awaken  with  a  puffy  one,  the  puffiness  being  par- 
ticularly marked  on  the  pendent  side.  In  children,  if  the  nephritic  irrita- 
tion be  severe,  a  convulsion  may  develop  as  one  of  the  early  signs.  Fever 
may  or  may  not  be  present. 

It  is  an  interesting  fact  that  severe  anr^mia  develops  with  extraordinary 
speed,  so  that  the  swollen  face  becomes  pallid  and  white  in  appearance  as 
soon  as  it  is  puffy.  Nausea  and  vomiting  are  often  early  symptoms,  and 
are  to  be  regarded  with  some  alarm,  as  they  are  indicative  of  toxaemia. 

The  scanty  urine  is  heavily  loaded  with  solids,  and  if  examined  micro- 
scopically it  shows  red  blood  cells,  epithelial  cells  from  the  uriniferous 
tubules,  and  tube  casts  composed  of  blood  cells,  epithelial  cells,  and 
hyaline  material.  When  the  heat  and  nitric  acid  test  is  applied  to  the 
urine,  the  amount  of  albumin  present  is  found  to  be  very  large,  forming  a 
thick  and  heavy,  curd-like  mass,  which,  in  the  heat  test,  gradually  settles  to 
the  bottom  of  the  tube.  The  fulse  is  usually  hard  and  the  tension  high,  but 
sometimes  the  high  tension  is  more  apparent  than  real,  the  pulse  being  full, 
but  gaseous  in  resistance. 

Auscultation  will  reveal,  in  the  cases  which  have  a  high  arterial  tension, 
an  accentuated  aortic  second  sound,  and  a  comparatively  feeble  first  sound 
at  the  apex.  Sometimes  acute  cardiac  dilatation  develops,  and  secondary 
'pulmonary  congestion  aids  in  the  destruction  of  the  patient.  In  other  cases 
in  which  oedema  is  particularly  marked  a  rapid  effusion  of  fluid  takes  place 
into  the  pleural  spaces  and  into  the  peritoneal  cavity,  and  pulmonary  oedema 
develops  with  remarkable  rapidity.  The  only  vessels  which  do  not  leak 
freely  are  those  of  the  skin,  the  kidneys,  and  the  bowels.     The  shin  is 


702  DISEASES  OF  THE  KIDNEYS 

dry  and  harsh,  the  urine  scanty  or  suppressed,  and  the  bowels  are  usually 
constipated. 

These  are  the  symptoms  of  what  may  be  called  a  severe  attack  of  the 
disease,  but  it  is  important  to  bear  in  mind  that  very  often  no  oedema  is 
present,  and  that  in  others  the  urinary  flow  is  not  greatly  diminished.  Often 
anaemia  and  pallor  may  be  the  first  sign  during  convalescence  from  an  acute 
infectious  malady,  to  show  that  all  is  not  well  with  the  kidneys.  In  other 
cases  some  giddiness  may  be  present,  and,  if  the  patient  is  an  adult,  ursemic 
symptoms  are  more  prone  to  develop  than  if  he  is  a  child. 

The  urine  of  persons  suffering  from  the  infectious  diseases  should  be 
examined  repeatedly,  in  order  that  the  earliest  signs  of  renal  involvement  may 
be  recognized.  There  is  no  excuse  for  letting  the  condition  run  on  unrecog- 
nized until  it  is  forced  upon  the  physician  by  marked  objective  symptoms. 

Diagnosis. — It  is  evident  that  this  state  does  not  present  signs  or  S}Tnptoms 
which  are  often  presented  by  other  maladies,  but,  on  the  other  hand,  it  is 
important  for  the  physician  to  recall  the  fact  that  certain  prominent  symptoms 
may  be  absent  without  casting  doubt  on  the  diagnosis.  Thus  the  amount 
of  albumin  in  the  urine  may  be  small,  the  degree  of  oedema  slight,  and  the 
urinary  flow  may  not  be  greatly  decreased.  Again,  the  mere  presence  of 
large  amounts  of  albumin  is  not  alone  indicative,  because,  as  already 
pointed  out  in  the  article  on  circulatory  disorders  of  the  kidneys,  it  often 
happens  that  scanty  urine  and  a  large  amount  of  albumin  are  present  in 
renal  congestion. 

Prognosis. — ^The  outlook  in  cases  of  acute  diffuse  nephritis,  if  the  patient 
has  previously  had  healthy  kidneys,  is  favorable,  particularly  if  his  habits 
of  life  have  been  satisfactory.  This  statement  holds  true  of  the  acute  condi- 
tion following  exposure  in  young  adults  rather  than  in  children  and  in  young 
adults  who  have  nephritis  from  acute  infectious  maladies,  particularly  scarlet 
fever.  The  younger  the  child  the  more  grave  the  danger  in  scarlet  fever. 
(See  Scarlet  Fever.)  Evil  symptoms  are  drowsiness  from  toxaemia,  a  tendency 
to  pulmonary  oedema,  a  feeble  heart,  and  a  free  transudation  into  the  subcu- 
taneous tissues.    Suppression  of  urine  is,  of  course,  a  most  serious  symptom. 

The  renal  lesions  in  those  who  survive  the  acute  stage  of  the  inflammation 
vary  greatly  in  their  persistency.  In  some  cases  all  signs  of  renal  trouble 
clear  up  in  a  fortnight,  but  in  others  albuminuria  in  some  degree  persists  for 
months  and  returns  whenever  the  patient  is  chilled  or  takes  excessive  exercise. 
When  anaemia  is  persistent  and  resists  fresh  air  and  tonics,  even  if  the  albu- 
minuria is  scanty,  suspicion  of  subacute  or  chronic  lesions  following  the  acute 
stage  is  aroused.  In  other  cases  the  acute  nephritis  is  but  an  exacerbation  of 
a  hitherto  unrecognized  chronic  parenchymatous  nephritis,  in  which  case 
the  outlook  is  most  grave.  Sometimes,  just  as  the  most  encouraging  progress 
is  being  made,  a  terminal  pneumonia  occurs,  and  death  ensues. 

Treatment. — ^The  treatment  of  acute  diffuse  nephritis  consists  in  putting 
the  patient  to  bed  at  absolute  rest  and  in  the  ordering  of  a  liquid  diet  con- 
taining nothing  which  can  irritate  the  kidneys,  such  as  condiments  like 
pepper  or  mustard.  Counterirritation  over  the  kidneys  in  the  shape  of  fre- 
quently renewed  hot  compresses  are  of  value,  but,  as  a  rule,  it  is  unwise  to 
add  any  irritating  drug  to  these  compresses,  for  it  may  be  absorbed  and  cause 


CHROMC  BRIGHTS  DISEASE  703 

renal  irritation.  If  the  pulse  is  quick,  small  doses  of  tincture  of  aconite 
(1  minim  every  one  or  two  hours)  may  be  given,  with  a  teaspoonful  of  sweet 
spirit  of  nitre  in  cool  water. 

During  convalescence  tincture  of  the  chloride  of  iron  and  tincture  of  nux 
vomica  may  be  used  as  tonics  and  to  combat  anaemia.  Great  care  should 
be  taken  that  the  patient  is  not  exposed  to  cold  and  dampness,  and  that 
woollen  garments  are  worn  next  the  skin  to  protect  it  from  being  chilled, 
since  chilling  of  the  surface  may  produce  secondary  renal  congestion. 


CHRONIC  BRIGHT'S  DISEASE. 

Definition. — ^The  term  "chronic  Bright's  disease"  is  applied  to  several 
types  of  slow,  persistent,  inflammatory  process  in  the  kidney  which  result 
in  very  definite  alterations  from  the  normal  in  these  organs.  Each  type  is 
also  so  distinct  from  the  other  in  its  rapidity  of  progress  and  results  that  it  is 
difiicult  to  regard  them  as  related  in  any  way,  yet  in  each  instance  we  find 
inflammation  and  degeneration  forming  the  chief  pathological  change. 

The  two  chief  forms  of  chronic  Bright's  disease  are  called  "  chronic  paren- 
chymatous nephritis"  and  "chronic  interstitial  nephritis,"  because  in  the  first 
the  pathological  process  is  chiefly  concerned  with  the  parenchyma  of  the 
organ,  and  in  the  second  form  the  conspicuous  changes  are  in  the  connective 
tissue. 

There  are  also  cases  in  which  these  two  forms  of  nephritis  exist  simultane- 
ously, that  is,  the  kidneys  present  the  changes  found  in  both  types.  Indeed, 
these  cases  are  much  more  numerous  than  is  generally  thought,  because 
physicians,  having  been  taught  in  student  days  that  nephritis  is  capable  of 
being  divided  into  two  forms,  are  continually  trying  to  force  cases  that  come 
to  them  into  one  of  these  categories,  it  being  forgotten  that  while  classification 
and  division  are  artificial  methods  devised  for  teaching  purposes,  nature  does 
not  adhere  to  any  such  boundaries,  but  presents  cases  which  may  partake  of 
more  than  one  type  at  the  same  time.  It  is  perhaps  well,  then,  to  consider 
that  chronic  Bright's  disease  is  a  chronic  diffuse  nephritis,  although  some- 
times the  parenchyma  and  sometimes  the  interstitial  tissues  suffer  chiefly. 

On  the  other  hand,  the  clinical  pictures  afforded  by  the  two  classes  of 
cases  constitute  adequate  grounds  for  recognizing  chronic  parenchymatous 
nephritis  as  different  from  the  chronic  interstitial  form.  There  can  be  no 
doubt  that  we  have  been  laying  too  much  stress  on  the  results  obtained 
from  an  examination  of  the  urine  in  differentiating  the  two  conditions. 
Sometimes  a  urinary  examination  at  once  settles  the  diagnosis,  but  Cabot 
is  clearly  right  in  his  contention  that  the  urine,  in  many  cases,  offers  no 
information  as  to  the  exact  type  of  change  going  on  in  the  renal  cortex. 
Differentiation,  when  possible,  must  rest  upon  symptoms  considered  with  the 
results  of  urinary  examination. 

Etiology. — Chronic  nephritis  may  follow  acute  nephritis,  but  this  is 
very  rarely  the  case.  Its  most  common  causes  are  alcoholism  and  exposure, 
and  in  the  upper  classes  alcoholism  and  overfeeding,  with  lack  of  exercise. 
Gout  and  syphilis,  chronic  lead  poisoning,  and  chronic  digestive  disorders 


704  DISEASES   OF  THE  KIDNEYS 

are  also  causes,  in  all  probability.  \\'Tiile  the  latter  are  not  as  yet  proved 
to  be  definite  causes,  there  is  good  reason  to  believe  that  the  continued 
absorption  of  toxic  materials  from  the  bowels  for  long  periods  of  time  may 
cause  renal  lesions  in  the  effort  of  these  organs  to  eliminate  the  noxious  sub- 
stances. A  very  important  cause,  in  all  probability  very  closely  allied  to  those 
just  named,  is  arteriosclerosis,  it  being  considered  that  the  changes  in  the 
bloodvessels  are  responsible  for  renal  changes,  although,  on  the  other  hand, 
the  renal  lesions  are  often  the  cause  of  the  vascular  degeneration.  In 
many  cases  it  is  probable  that  the  same  causes  produce  both  the  arterial  and 
the  renal  changes  simultaneously.  In  some  cases,  indeed,  it  may  be  said  in 
the  majority,  the  exciting  cause  of  the  renal  changes  is  undiscoverable,  and 
perhaps  may  depend  upon  some  congenital  defect,  which  as  yet  we  do  not 
understand.  This  defect  may  be  localized  in  the  kidneys,  or  lie  in  other 
organs  whose  imperfectly  performed  labor  results  indirectly  in  renal  dis- 
ease. 

Chronic  parenchymatous  nephritis  is  a  disease  of  early  and  middle  life, 
while  chronic  interstitial  nephritis  is  observed  in  patients  of  more  advanced 
years,  but  exceptions  to  this  rule,  of  course,  occur. 

Frequency. — Chronic  renal  disease  is  one  of  the  most  common  maladies 
affecting  man,  a  large  proportion  of  the  deaths  of  all  persons  over  thirty 
years  of  age  being  due  to  this  cause.  Not  only  do  the  mortality  statistics 
prove  the  correctness  of  this  statement,  but  it  is  now  becoming  a  well-recog- 
nized fact  that  many  cases  which  die  of  acute  pneumonia  are  in  reality  cases 
of  chronic  nephritis,  in  which  the  pneumonia  acts  as  a  terminal  infection  and 
destroys  the  patient  when  his  powers  of  resistance  have  diminished  as  a  result 
of  his  renal  state.  The  United  States  census  for  1900  shows  that  disease  of 
the  kidneys  stands  sixth  in  the  list  of  diseases  causing  death,  pneumonia, 
tuberculosis,  heart  disease,  diarrhoeal  affections,  and  unknown  causes  only 
leading  it. 

Of  41,924  medical  cases  treated  in  five  large  Philadelphia  hospitals,  1395, 
or  3.32  per  cent.,  were  affected  with  nephritis,  and  of  24,624  medical  cases 
treated  in  four  large  Philadelphia  hospitals  in  which  the  form  of  the  lesion 
was  stated,  797,  or  3.23  per  cent.,  were  affected  with  chronic  nep'hritis.  On 
the  other  hand,  of  228,232  cases  treated  in  the  medical  dispensaries  of  four 
large  Philadelphia  hospitals,  only  1902,  or  0.9  per  cent.,  were  affected  with 
some  form  of  nephritis.  This  remarkable  difference  in  frequency  in  the 
wards  and  in  the  out-patient  departments  is  probably  due  chiefly  to  the  fact 
that  most  of  the  cases  of  renal  disease  presenting  themselves  for  treatment 
were  so  ill  that  they  became  in-patients,  and  are  so  recorded. 

From  this  point  on  it  will  be  best  to  consider  the  two  chief  forms  of  chronic 
renal  disease  separately. 

Chronic  Parenchymatous  Nephritis. — Chronic  parenchymatous  nephritis 
is  sometimes  called  "  chronic  desquamative  nephritis,"  because  of  the  des- 
quamation of  the  epithelial  cells  lining  the  tubules;  "chronic  tubular 
nephritis,"  because  the  uriniferous  tubules  are  involved,  or  in  certain 
cases,  "  chronic  glomerulonephritis,"  because  the  glomeruli  of  the  kidney 
are  chiefly  affected  in  this  malady.  It  is  also  called  "  chronic  diffuse 
nephritis." 


CHRONIC  BRIGHT'S   DISEASE  705 

Pathology  and  Morbid  Anatomy. — In  typical  cases  the  kidney  is  found  to 
be  large,  pale,  its  subcapsular  veins  conspicuous,  and  the  capsule  easily 
detached.  The  organ  offers  little  resistance  to  incision,  and  inspection  of  the 
incised  surfaces  shows  that  the  marked  enlargement  of  the  organ  is  due  to 
broadening  of  the  cortex.  The  medullary  pyramids,  while  often  lighter  in  color 
than  normal,  never  attain  the  pale  yellowish  hue  of  the  cortex,  and  may  be 
dark  from  associated  congestion.  In  this  form  the  microscope  shows  the 
epithelium,  especially  that  of  the  convoluted  tubules,  granular  or  even  fatty, 
desquamating,  and  coalescing  to  form  casts,  which  may  readily  be  recognized 
in  position,  or,  having  been  passed,  these  casts  leave  tubules  w  hich  are  imper- 
fectly lined  by  epithelial  cells.  There  is  a  less  conspicuous,  but  fairly  con- 
stant, change  of  a  similar  character  involving  the  glomerular  epithelium,  and 
also  the  epithelial  cells  of  some  of  the  pyramidal  tubes.  Hemorrhages  in  the 
interstitial  tissue  are  sometimes  present.  This  is  the  form  called  "  large  white 
kidney." 

In  some  cases  the  interstitial  tissue  is  but  slightly  involved,  but  in  others  it 
is  notably  increased  and  irregularly  distributed,  with  unequal  contractions, 
giving  rise  to  a  more  or  less  bossed  or  granular  surface,  not  unlike  that 
seen  in  typical  interstitial  nephritis.  In  this  form  (small  white  kidney)  the 
organ  may  not  be  enlarged,  and  may  be  even  smaller  than  normal.  It  resists 
incision,  due  to  the  increase  in  fibrous  tissue,  which,  with  the  unaided  eye, 
may  be  seen  as  grayish  patches  in  the  yellow  cortex.  Hemorrhages  may  be 
present,  mottling  the  incised  surface  with  reddish  or  reddish-brown  areas. 

Microscopically,  the  changes  in  the  epithelium  are  similar  to  those  seen 
in  the  large  white  kidney,  but  the  increase  in  fibrous  tissue  constitutes  a  con- 
spicuous difference.  It  has  not  been  definitely  decided  whether  the  small 
white  kidney  is  a  later  stage  of  large  white  kidney,  an  independent  affection, 
or  a  form  of  nephritis  which  having  been  primarily  interstitial  has  had 
parenchymatous  disease  superimposed. 

The  cardiovascular  changes  of  chronic  parenchymatous  nephritis  are 
similar  in  kind,  but  do  not  approach  in  degree  those  found  in  chronic 
interstitial  nephritis.  With  the  small  white  kidney,  cardiac  hypertrophy 
and  slight  arteriosclerotic  changes  are  not  of  infrequent  occurrence.  There 
is  usually  an  excess  of  fluid  in  the  serous  cavities,  a  varying  quantity  of 
oedema  in  the  subcutaneous  fat,  and  also  in  the  lungs  and  meninges. 
Retinal  hemorrhages  are  occasionally  observed. 

Symptoms. — When  chronic  diffuse  nephritis  of  the  "large  white  type"  is 
well  developed  there  are  few  clinical  pictures  which  are  so  typical.  The  more 
or  less  sivollen  visage;  the  greasy,  'pallid  shin;  the  stupid  jades,  and  the 
dyspnoea  on  exertion  strike  the  eye  at  once.  Not  rarely  the  partly  buttoned 
waistcoat  and  the  loosely  laced  shoes  show  that  sufficient  anasarca  exists  to 
cause  the  patient  some  discomfort. 

If  the  pretibial  tissues  are  pressed  upon,  they  pit  on  pressure.  Percussion 
may  show  the  presence  of  fluid  in  the  pleural  and  peritoneal  cavities,  although 
large  effusions  are  not  commonly  met  with  in  these  cases. 

If  the  heart  is  examined,  its  sounds  are  found  to  be  altered,  so  that  the 
first  sound  lacks  good  quality,  and  the  second  sound  is  usually  accentuated. 
The  pulse  is  rapid,  and  the  arterial  tension  higher  than  normal.  The 
45 


706  DISEASES  OF  THE  KIDNEYS 

patient  is  prone  to  be  sleepy  during  the  day  and  restless  at  night,  and  may 
be  dyspnoeic  on  lying  down.  The  urine  is  scanty  and  heavily  laden  with 
solids,  and  under  the  microscope  shows  a  large  number  of  fatty,  granular, 
hyaline,  and  epithelial  casts,  leukocytes,  and  even  red  blood  corpuscles.  Occa- 
sionally the  granular  casts  are  particularly  opaque  to  light,  forming  the  "  big 
black,  granular  casts,"  which  are  so  significant  of  severe  parenchymatous 
nephritis.  Tested  with  heat  or  nitric  acid,  the  urine  is  found  to  contain  an 
excessive  amount  of  albumin,  so  that  the  coagulum  may  equal  half  the  urine. 
The  specific  gravity  of  the  urine  is  high — about  1.025.  With  the  advent  of 
marked  interstitial  fibrosis,  the  quantity  of  urine  increases  and  may  equal  or 
even  exceed  the  normal  amount.  At  this  time  the  albumin  diminishes,  the 
casts  often  lessen  in  number,  and  cardiovascular  changes  occur,  the  chief 
sign  of  which  is  increased  arterial  tension. 

When  the  function  of  the  kidneys  is  seriously  disturbed,  apathy,  stupor, 
and  finally  coma  may  ensue  from  uroemia,  and  in  some  cases  convulsions 
occur.  These  may  vary  from  a  slight  twitch  followed  by  stupor  to  a  severe 
general  convulsion,  in  which  all  the  voluntary  muscles  are  involved.  Some- 
times a  fleeting  monoplegia,  aphasia,  or  hemiplegia  comes  on  as  the  result 
of  the  ursemic  poisoning  and  without  any  connection  with  an  actual  apoplexy. 
(See  Ursemia.) 

Patients  suffering  from  chronic  parenchymatous  nephritis  are  sometimes 
seized  by  a  severe  serous  diarrhoea,  which  is  an  effort  at  elimination  on 
the  part  of  the  economy,  and  should  be  cautiously  checked  only  when  it 
becomes  severe  enough  to  be  dangerous  in  itself. 

Comparatively  rarely  in  the  course  of  chronic  parenchymatous  nephritis 
an  albuminuric  retinitis  develops,  but  when  the  nephritis  complicates  preg- 
nancy this  ocular  symptom  is  very  common. 

The  combinations  of  symptoms  just  recited  are  met  with  in  the  well- 
developed  cases  which  present  characteristic  manifestations  of  the  disease. 
It  is  to  be  distinctly  recollected  that  in  many  cases  few  or  none  of  these  signs 
develop  until  the  patient  is  suddenly  overwhelmed  by  the  climax  of  his 
malady,  and  that  of  all  the  chronic  and  grave  maladies  which  affect  man 
none  advance  and  develop  as  insidiously  as  does  chronic  parenchymatous 
nephritis  in  many  cases.  In  one  instance  a  persistent  indigestion  which  fails 
to  yield  to  appropriate  digestive  remedies  is  found  to  be  due  to  renal  disease; 
in  another  anaemia  fails  to  yield  to  ordinary  chalybeates  and  is  found  to  be 
renal  in  origin ;  in  still  another  a  persistent  failure  of  health  without  appar- 
ent cause  has  its  origin  in  bad  kidneys.  In  yet  another  group  of  cases  a 
persistent  bronchitis  is  founded  on  this  cause.  If  consulting  physicians  could 
be  polled,  I  feel  confident  that  they  would  universally  state  that  the  average 
case  of  grave  ill-health  seen  by  them  in  consultation,  when  the  diagnosis  is 
obscure,  is  not  really  difficult  of  diagnosis  if  the  state  of  the  kidneys  is 
carefully  studied.  It  is  not  sufficient  to  examine  the  urine  once.  It  should 
be  done  repeatedly  before  deciding  that  it  throws  no  light  on  the  case. 

An  important  clinical  fact  to  bear  in  mind  is  that  a  latent  chronic  parenchy- 
matous nephritis  may  exist  for  a  long  time,  and  finally  be  recognized  by  the 
sudden  development  of  ursemia  due  to  an  acute  congestive  nephritis  coming 
on  as  a  complication. 


CHRONIC  BRIGHT'S  DISEASE  'JQ'J 

Diagnosis. — The  diagnosis  of  chronic  parenchymatous  nephritis  is  reached 
by  the  following  symptoms  and  tests :  The  face  is  puffy  and  pallid ;  there  is 
often  dyspnoea,  even  without  exertion,  and  the  second  sound  of  the  heart  is 
usually  accentuated.  If  the  case  is  well  developed,  general  anasarca  may 
be  manifest.  The  chief  diagnostic  factor,  however,  is  the  state  of  the 
urine.  It  is  less  than  normal  in  quantity,  of  high  specific  gravity,  and 
contains  very  considerable  quantities  of  albumin.  (See  Albuminuria.)  A 
microscopic  examination  of  its  sediment  reveals  fatty,  granular,  and  hyaline 
casts,  red  blood  cells,  and  large  amounts  of  desquamated  epithelium  from  the 
uriniferous  tubules.  The  gravity  of  the  disease  is  usually  in  direct  propor- 
tion to  the  quantity  and  quality  of  the  casts,  the  large,  dark,  granular  casts 
being  indicative  of  grave  disease.  Quantitative  analysis  reveals  marked 
decrease  in  the  total  elimination  of  urea  in  each  twenty-four  hours. 

Prognosis. — ^The  prognosis  of  chronic  parenchymatous  nephritis  is  inevi- 
tably fatal,  and  the  patient's  life  is  rarely  prolonged  over  a  few  months,  when 
once  the  disease  is  well  developed.  In  those  cases  of  chronic  parenchymatous 
nephritis  characterized  by  early  dropsy  which  rapidly  develops  into  general 
anasarca,  Senator  states  that  the  duration  of  life  varies  from  a  few  months  to 
a  year.  In  those  cases  in  which  the  development  of  dropsy  is  gradual  and 
irregular,  varying  in  degree  from  time  to  time,  he  says  that  death  ensues  in 
from  one  to  two  years  after  the  beginning  of  the  malady.  Striimpell  gives 
the  average  duration  of  life  in  chronic  parenchymatous  nephritis  as  from  one- 
half  to  one  and  one-half  years.  Every  clinician  of  experience  will,  however, 
agree  with  Senator  in  recognizing  another  class  of  cases  which  extend  over 
several  years,  and  which  are  characterized  by  mildness  of  symptoms.  In  these 
cases  there  is  not  much  albumin  in  the  urine,  but  slight  headache,  and  little 
swelling  of  the  lower  extremities  or  of  the  face.  Gradually  these  patients 
become  worse,  until  they  finally  fall  into  one  of  the  well-defined  classes 
already  described.  They  are  probably  representative  of  that  form  of  the 
disease  characterized  by  moderate  changes  in  the  parenchyma  of  the  kidney 
with  associated  interstitial  disease. 

Treatment. — It  has  been  generally  held  that  diet  is  a  very  important  factor 
in  the  treatment  of  this  form  of  renal  disease.  While  it  is  somewhat  icono- 
clastic to  say  that  this  general  belief  is  untrue,  it  is,  nevertheless,  a  fact  that  a 
generous  diet  which  does  not  strain  the  digestion  and  the  eliminating  organs 
can  usually  be  allowed  in  most  cases.  We  have  before  us  a  patient  who  is 
bound  to  die  within  a  few  months,  and  the  question  arises  as  to  whether  we 
can  so  regulate  the  diet  that  we  will  obtain  results  which  compensate  for 
the  discomforts  and  unhappiness  of  the  rigid  milk  diet,  which  is  usually 
ordered,  or  one  which  causes  the  patient  to  regard  his  food  with  loathing 
and  which  is  a  constant  reminder  that  he  is  ill. 

Although  skimmed  milk  is  theoretically  capable  of  maintaining  nutrition, 
it  is  practically  incapable,  because  such  enormous  quantities  must  be 
consumed,  to  provide  an  adult  with  a  sufficient  amount  of  nutriment. 
Again,  milk  lacks  the  quantity  of  iron  which  ordinary  food  contains.  It  pre- 
sents to  the  patient  the  same  quantities  of  calcium,  magnesium,  potassium, 
and  phosphorus  as  is  found  in  the  ash  of  newborn  animals,  but  it  contains 
six  times  less  iron ;  this  lack  of  iron  being  made  up  in  the  young  by  the 


708  DISEASES  OF   THE  KIDNEYS 

storage  of  this  metal  in  the  hver,  and  possibly  in  other  organs  during 
intrauterine  life.  Again,  the  quantity  of  proteid  which  is  present  in  milk 
is  excessive.  A  normal  adult  requires  approximately  3000  calories  a  day 
to  maintain  full  nutrition.  One  quart  of  milk  has  a  caloric  value  of  about 
700,  and  therefore  it  takes  about  four  to  four  and  a  half  quarts  of  cows'  milk 
to  present  sufficient  nourishment.  This  large  quantity  of  milk  contains 
nearly  170  grams  of  proteid,  whereas  the  normal  average  quantity  of  proteid 
ingested  by  a  healthy  adult  does  not  exceed  100  grams  a  day.  A  milk  diet, 
if  taken  in  the  quantities  which  are  necessary  for  the  maintenance  of  nutri- 
tion, forces  the  kidneys  to  eliminate  enormous  quantities  of  liquid,  which 
they  are  illy  prepared  to  do  when  suffering  from  disease,  and  if  the  patient 
does  not  take  these  quantities  his  vitality  is  impaired  by  nephritis  and 
starvation  combined.  Again,  such  a  diet  causes  the  kidneys  to  eliminate 
large  quantities  of  urea  and  much  phosphates,  and  so,  again,  kidneys  which 
are  impaired  in  function  because  of  disease  are  forced  to  perform  an  ex- 
cessive amount  of  work. 

It  is  entirely  possible  to  arrange  a  suitable  diet  for  cases  of  nephritis  with- 
out in  any  way  throwing  undue  stress  on  any  of  the  organs  of  digestion  or 
elimination,  and  at  the  same  time  maintain  the  nutrition  of  the  body.  Un- 
skimmed milk  —  that  is,  milk  containing  cream — is  useful,  since  the  fats 
add  a  very  considerable  number  of  calories  to  the  milk,  and  by  the  use 
of  starchy  food  an  additional  number  of  calories  can  be  provided  the 
patient,  who,  at  the  same  time,  does  not  receive  an  excess  of  fluid.  As 
Croftan  well  says,  one  litre  and  a  half  of  milk,  plus  a  quarter  of  a  litre  of 
cream,  for  instance,  contains  approximately  50  grams  of  proteids  (equal  to 
225  calories),  75  grams  of  carbohydrates  (equal  to  337  calories),  and  150  grams 
of  fat  (equal  to  1350  calories),  or  a  sum  total  of  about  1912  calories.  In  order 
to  make  up  the  difference  of  1088  calories,  a  little  meat,  eggs,  sugar,  butter, 
toast,  zweiback,  rice,  fresh  vegetables,  etc.,  may  be  allowed  with  impunity, 
care  being  taken  that  the  caloric  value  of  3000  is  not  greatly  exceeded, 
and  that  all  articles  of  diet  that  lead  to  the  formation  of  irritating  urinary 
end-products,  and  spices,  condiments,  etc.,  are  avoided.  These  views  are 
in  accord  with  opinions  expressed  by  Robin,  of  Paris,  Bradford,  and  Hale 
White,  of  London,  and  other  clinicians  of  experience. 

The  fact  having  been  established  by  several  investigators  that  in  many 
cases  of  parenchymatous  nephritis  with  oedema  there  is  a  retention  of 
sodium  chloride  in  the  tissues,  it  has  been  suggested  that  this  salt  be 
temporarily  removed  from  the  diet.  The  ground  for  this  is  that  the  excess 
of  salt  in  the  tissues  requires  an  excess  of  fluid  to  keep  it  in  the  normal 
molecular  concentration,  ^^^len  the  patient  is  deprived  of  salt  increased 
diuresis  takes  place  and  the  dropsy  often  diminishes. 

Much  discussion  has  occurred  among  physicians  as  to  the  quantity  of  water 
which  should  be  allowed  patients  suffering  from  Bright's  disease.  Some 
believe  that  the  amount  should  be  as  small  as  possible,  on  the  ground  that 
copious  draughts  of  water  engorge  the  vessels  and  increase  the  labor  of  the 
heart.  That  this  cardiac  influence  is  an  important  one  we  doubt,  but  as 
Edsall  and  others  have  shown  that  excessive  water-drinking  increases  nitrog- 
enous metabolism,  and  as  the  kidneys  in  Bright's  disease  are  unable  to  fully 


CHRONIC  BRIGHT'S  DISEASE  709 

deal  with  the  products  of  normal  metabolism,  it  would  seem  evident  that 
excessive  quantities  of  water  must  be  harmful.  On  the  other  hand,  there 
can  certainly  be  no  good  results  from  depriving  the  patient  of  water  to  the 
extent  of  making  him  suffer. 

The  remedial  measures  other  than  diet  consist  in  the  use  on  each  alter- 
nate day,  if  the  heart  is  strong  enough,  of  a  moderate  Turkish  bath,  in  order 
that  the  skin  may  aid  the  kidneys  in  eliminating  fluids  and  solids  from  the 
body.  Fresh  air  and  sunlight  are  essential,  and  severe  exercise  is  to  be 
prohibited. 

Drugs  are  of  little  value,  except  to  relieve  symptoms  which  may  be  annoy- 
ing. It  has  been  the  custom  of  physicians  for  many  years  to  prescribe  iron, 
usually  in  the  form  of  Basham's  mixture,  for  the  purpose  of  combating  the 
anaemia  of  chronic  parenchymatous  nephritis.  This  method  of  treatment 
does  not  possess  the  advantages  with  which  it  has  been  credited.  The 
anaemia  depends  upon  the  toxgemia  of  the  disease,  and  this,  of  course,  is  not 
removed  by  the  administration  of  iron.  Further  than  this,  iron  has  a  tendency 
to  produce  constipation,  and  constipation  is  prone  to  increase  anaemia,  and, 
again,  constipation  is  a  particularly  undesirable  condition  in  Bright's  dis- 
ease, since  it  prevents  the  bowels  from  aiding  the  kidneys  in  eliminating 
impurities. 

The  administration  of  very  large  doses  of  Basham's  mixture  is,  therefore, 
unwise.  It  should  be  borne  in  mind  that  iron  has  no  curative  effect  upon 
the  renal  condition,  and  therefore  it  is  useless  to  administer  more  than 
the  system  can  utilize  for  the  relief  of  the  secondary  anaemia  in  the  blood. 
Small  doses  of  Basham's  mixture  are,  therefore,  as  useful  as  large  ones,  so  far 
as  the  anaemia  is  concerned.  If  the  effect  of  Basham's  mixture  as  a  diuretic 
is  desired,  the  liquor  ammonii  acetatis  of  the  United  States  Pharmacopma 
may  be  added  to  a  teaspoonful  of  Basham's  mixture  and  given  three  or  four 
times  a  day,  as  in  this  way  the  diuretic  effect  is  obtained  without  an  excess  of 
iron  being  given. 

Should  evidence  of  cardiac  dilatation  develop  digitalis  is  indicated,  and 
may  be  given  in  the  dose  of  5  or  10  minims  of  the  tincture  three  times  a  day 
until  some  evidence  of  its  physiological  effect  is  obtained,  when  the  dose 
should  be  cut  down  one-half.  While  the  infusion  of  digitalis  has  the  repu- 
tation of  being  more  diuretic  than  the  tincture,  it  is  so  much  more  prone  to 
disorder  the  stomach  that  the  tincture  is  usually  preferable. 

A  useful  formula  in  place  of  digitalis  will  be  found  on  page  519. 

If  uraemic  symptoms  develop,  the  patient  should  be  given  a  hot  pack,  and 
if  there  is  any  reason  to  believe  that  pulmonary  oedema  is  threatened,  or  that 
the  heart  is  too  feeble  to  endure  the  hot  pack,  a  hypodermic  injection  of 
strychnine,  ^  of  a  grain,  should  be  given  before  the  pack  is  begun.  Some- 
times a  cup  of  strong  black  coffee  is  also  useful  at  this  time.  Pilocarpine 
should  not  be  employed,  as  it  is  too  depressant  and  prone  to  produce  pul- 
monary oedema. 

The  question  as  to  whether  the  bowels  should  be  thoroughly  purged 
by  one  of  the  hydragogue  cathartics  is  debatable.  On  the  one  hand,  it  is 
claimed  that  by  this  means  the  intestines  are  unloaded  and  a  large  quantity 
of  liquid  and  toxic  material  is  removed  from  the  body,  and,  on  the  other. 


710  DISEASES  OF  THE  KIDNEYS 

that  the  purging  may  cause  concentration  of  the  blood,  and  so  increase 
toxsemia.  Probably  the  best  rule  to  follow  is  to  administer  a  hydragogue 
cathartic  only  when  there  is  reason  to  believe  that  the  bowels  are  con- 
fined and  are  consequently  loaded  with  fecal  matter,  Hypodermoclysis, 
which  is  so  useful  in  the  uraemia  of  chronic  contracted  kidney,  is  worse  than 
useless  in  chronic  parenchymatous  nephritis,  owing  to  the  presence  of 
oedema. 

A  valuable  drug  for  the  purpose  of  diminishing  arterial  tension  and  so 
decreasing  the  work  of  the  heart,  and  also  because  it  diminishes  the  loss  of 
albumin  through  the  kidneys,  is  nitroglycerin,  which  should  be  given  in  the 
dose  of  Y^  of  a  grain  three  or  four  times  a  day.  This  drug  often  increases 
the  urinary  flow  when  it  is  scanty. 

In  regard  to  the  treatment  of  ursemic  convulsions,  it  is  commonly  held 
that  the  administration  of  morphine  hypodermically  for  this  purpose  is 
dangerous,  although  there  are  some  active  practitioners  who  believe  that 
it  is  a  useful  drug.  It  is  probably  more  dangerous  in  the  parenchy- 
matous than  in  the  interstitial  form  of  the  disease.  If  the  convulsion  is 
severe  chloroform  or  nitrite  of  amyl  should  be  given  by  inhalation.  (See 
Uraemia.) 

Comparatively  recently  it  has  been  suggested  that  cases  of  chronic  renal 
disease  should  be  treated  by  decapsulation  of  the  kidney.  This  plan  of  treat- 
ment is  more  indicative  of  surgical  enthusiasm  than  of  a  clear  conception  of 
the  pathology  of  the  disease.  A  knowledge  of  the  pathology  and  the  results  of 
experiments  on  animals  show  its  futility,  if  not  its  danger.  These  views  will 
be  found  in  detail  in  the  editorial  columns  of  the  Therapeutic  Gazette  for 
January,  1904,  and  June  15,  1904. 

Chronic  Interstitial  Nephritis. — To  this  form  of  chronic  renal  disease 
the  terms  "contracted  kidney,"  "granular  kidney,"  "cirrhosis  of  the 
kidney,"  and  "sclerotic  kidney"  are  applied. 

Pathology. — Chronic  interstitial  nephritis  is  usually  a  primary  process, 
although  the  small  white  kidney  is  really  a  combination  of  the  fibroid  and 
the  chronic  parenchymatous  form.  In  this  type  the  overgrowth  of  the  con- 
nective tissue  of  the  kidney  is  the  dominant  part  of  the  pathological  process, 
and  the  degeneration  of  the  parenchyma,  as  represented  by  the  glomeruli 
and  the  tubules,  plays  a  secondary  role. 

^Vhen  kidneys  affected  by  this  state  are  examined,  it  is  found  that  they 
contain  large  masses  of  fibrous  tissue  extending  through  the  organ,  which 
by  contraction  cause  a  shrinkage  in  size  and  a  puckering  of  the  surface. 
The  capsule  becomes  thickened  and  exceedingly  adherent,  and  the 
tissues  beneath  it  are  torn  if  it  is  stripped  off.  The  surface  of  the  cortex 
is  roughened  by  rounded  granules  of  varying  size  and  cysts  may  appear 
at  various  points  on  its  surface  (Fig.  94).  When  an  attempt  is  made  to 
cut  through  the  kidney,  it  is  found  to  be  tough  and  difficult  to  incise. 
After  the  organ  is  split  open  it  is  seen  that  the  cortical  portion  is  very 
much  wasted. 

When  the  renal  tissues  are  placed  under  the  microscope,  they  show 
an  irregularly  distributed  increase  in  the  connective  tissue,  involving  in 
particular  the  cortex  and  the  interlobular  vessels.     There  is  also  an  asso- 


CHRONIC  BRIGHT' S  DISEASE 


711 


dated  atrophy  of  the  epithehum  hning  the  uriniferous  tubules.  Casts  are 
seen  in  the  tubules,  but  not  to  the  degree  in  which  they  are  met  with  in 
the  parenchymatous  form  of  nephritis.  The  glomeruli  in  advanced  cases 
may  be  converted  into  thick,  fibrous  bulbs;  the  walls  of  the  bloodvessels 
forming  the  tuft  may  be  thickened,  and  the  capsule  is  seen  to  be  dense 
and  fibrous.  Nor  does  the  fibroid  process  affect  the  finer  bloodvessels  and 
the  connective  tissue  alone.  It  extends  to  the  large  bloodvessels,  and  even 
to  the  renal  arteries  and  veins. 


Fig.  94 


2  cm 


Kidney  of  chronic  interstitial  nephritis.  The  surface  is  granulated  and  irregular,  and  contains 
numerous  cysts.  The  contraction  is  quite  marked,  the  organ  being  but  little  more  than  half  the 
normal  size. 

It  is  also  a  noteworthy  fact  that  while  cardiac  hypertrophy  and  arterio- 
sclerosis are  often  met  with  to  some  degree  in  parenchymatous  nephritis, 
they  are  constantly  found  in  a  well-developed  degree  in  the  interstitial  type  of 
the  disease.  This  cardiac  hypertrophy  is  not  limited  to  the  left  ventricle, 
as  it  is  in  the  parenchymatous  form.  It  affects  the  whole  heart  and 
it  is  often  very  great.  The  cause  for  the  hypertrophy  has  been  the  sub- 
ject of  much  debate,  but  the  conditions  present  in  the  bloodvessels  seem  to 
offer  an  adequate  explanation  of  the  state.  These  vessels  are  always  fibroid 
and  lacking  in  normal  elasticity,  and  this,  of  course,  offers  greater  resistance 


712  DISEASES  OF  THE  KIDNEYS 

to  the  flow  of  blood  through  them  and  into  the  capillary  networks.  As  the 
process  is  a  gradual  one,  there  is  a  gradual  increase  in  the  demands  made 
upon  the  heart,  and  this  is  met  by  an  increasing  hypertrophy.  The  difficulty 
in  forcing  blood  through  the  renal  vessels  also  aids  in  producing  this  effect, 
but  such  influence  has  no  doubt  been  overestimated. 

This  is  not  the  place  to  dilate  upon  the  relationship  of  these  vascular 
changes  to  the  renal  lesions.  Many  persons  think  that  the  renal  changes 
are  the  cause  of  the  vascular  lesions,  and  others  hold  that  the  vascular 
degeneration  causes  the  renal  state.  A  most  striking  illustration  of  the 
relation  between  arterial  disease  and  contracted  kidney  was  shown  by 
Welch  at  the  meeting  of  the  American  Medical  Association  in  1904.  He 
presented  a  specimen  which  consisted  of  a  kidney  supplied  by  two  renal 
arteries,  one  of  which  was  sclerotic.  The  area  of  the  kidney  supplied  by 
this  vessel  was  typically  fibroid,  while  the  other  pole  of  the  organ  nourished 
by  the  uninvolved  trunk  was  but  slightly  changed. 

Again,  it  is  held  by  many  that  the  overgrowth  of  connective  tissue  takes 
place  to  fill  gaps  made  by  the  atrophy  of  the  parenchyma,  and  by  others  the 
view  is  taken  that  the  overgrovd;h  of  the  connective  tissue  destroys  the  paren- 
chyma by  pressure.  The  latter  view  seems  the  more  probable,  but  the  former 
opinion  is  adhered  to  by  many  pathologists,  who  believe  the  primary  change 
is  in  the  parenchyma. 

Symptoms. — ^This  is  the  type  of  renal  disease  which  is  found  in  the  iron- 
master or  stock  broker  who  boasts  that  he  has  never  had  a  sick  day  in  his 
life,  and  who  begins  to  find  himself,  at  forty  or  fifty,  lacking  in  initiative, 
and  who  suffers  from  vertigo  or  dizziness,  which  he  thinks  are  due  to  a  club 
dinner  or  a  strong  cigar.  This  is  the  disease  of  the  hard-working,  "  high-ner- 
vous-tension "  individual  who  has  lived  hurriedly,  and  perhaps  quieted  him- 
self between  periods  of  great  exertion  by  a  drink  or  two  of  whiskey,  repeated 
it  may  be  many  times.  Often  it  develops  in  those  who  have  not  used 
alcohol,  but  given  a  man  who  takes  little  exercise,  some  whiskey,  and  who  is 
managing  one  or  more  large  business  interests,  and  he  is  the  individual  who 
is  paving  the  way  for  or  has  already  developed  chronic  contracted  kidney. 
Very  rarely,  indeed,  the  disease  develops  in  early  life,  but  cases  have  been 
reported  by  a  number  of  clinicians  in  children  as  young  as  from  two  to 
seven  years.  Most  of  the  instances  have  occurred  about  puberty.  Suther- 
land and  Walker  have  reported  2  cases,  aged  eight  and  sixteen  months, 
respectively,  who  had  contracted  kidney  due  to  congenital  syphilis. 

The  symptoms  of  contracted  kidney  are,  in  a  large  proportion  of  cases, 
absent  until  the  disease  progresses  so  far  that  grave  secondary  changes  take 
place.  Indeed,  it  not  rarely  happens  that  the  patient  continues  in  what  he 
considers  good  health  until  an  acute  attack  of  urcsmia  or  cardiac  failure  sends 
him  to  the  hands  of  the  physician,  who  may  be  misled  into  the  diagnosis  of 
acute  syncope,  due  to  overexertion,  by  the  fact  that  the  heart  seems  to  be 
feeble,  and  because  the  urine  shows  little  or  no  albumin.  The  number  of 
diagnoses  that  have  been  wrecked  upon  the  shoal  of  "no  albumin"  is  a 
multitude,  because  it  is  a  peculiarity  of  chronic  contracted  kidney  that 
albumin  is  often  absent  for  brief  periods,  or  present  in  such  minute  amounts 
that  it  is  overlooked.     It  is  only  when  the  heart  begins  to  fail  so  that  some 


CHRONIC  BRIGHTS  DISEASE  713 

congestion  of  the  kidney  develops  that  the  albumin  becomes  more  copious. 
The  albuminuria  of  contracted  kidney  is,  as  a  rule,  as  scanty  as  it  is  profuse 
in  the  parenchymatous  form.  Again,  the  scanty  urine  of  the  parenchymatous 
type  is  replaced  by  a  profuse  flow  in  the  contracted  type,  and  the  patient  in 
consequence  is  disturbed  in  his  sleep  by  having  to  get  up  at  night  to  empty 
the  bladder.  The  specific  gravity  of  the  urine  is  low,  about  1.005  to  1.012,  and 
it  is  clear  and  lacks  color.  If  the  urea  is  estimated  this  ingredient  is  usually 
much  reduced,  not  only  relatively,  but  actually,  so  that  the  patient  in  many 
cases  does  not  excrete  half  the  normal  output  per  day.  Casts  may  not  be 
found  and  rarely  are  abundant,  and  often  the  centrifuge  has  to  be  employed 
to  reveal  them.  Further,  these  casts  are  readily  overlooked,  for  they  are 
chiefly  hyaline  and  so  transparent  that  if  careful  focusing  and  illumination 
are  not  resorted  to  they  are  not  seen.  In  some  cases  granular  casts  are 
only  periodically  demonstrable. 

The  circulatory  symptoms  of  contracted  kidney  are  as  important  in  reach- 
ing a  diagnosis  as  the  renal  signs.  The  pulse  is  hard  and  tense,  and  so  high 
is  the  blood  pressure  that  it  may  be  almost  impossible  to  occlude  the  vessel  by 
pressing  upon  it.  If  the  radial  artery  is  rolled  under  the  fingers,  it  feels  like 
a  piece  of  thick  rubber  tubing,  and  it  is  easily  recognized  as  being  distinctly 
fibrous  when  it  is  palpated  carefully.  In  other  words,  the  blood  tension 
is  high  and  the  vessel  is  thick.  If  the  heart  is  examined,  there  is  found,  as 
a  very  constant  symptom,  a  sharply  accentuated  aortic  second  sound  at  the 
second  right  costal  cartilage,  which  is  due  to  the  high  arterial  tension.  On 
inspection  the  apex  of  the  heart  is  found  to  be  displaced  downward  and  out- 
ward because  of  the  cardiac  hypertrophy.  At  the  apex  a  more  or  less  dis- 
tinct systolic  murmur  is  heard  in  many  cases,  due,  as  a  rule,  to  stretching  of 
the  mitral  orifice  under  the  stress  of  high  pressure  in  the  ventricle,  resulting 
from  great  arterial  tension.  When  compensation  fails,  either  because  the 
heart  becomes  exhausted  or  because  of  fibroid  or  other  myocardial  degen- 
eration, these  symptoms  may  be  replaced  by  weak  heart  sounds  and  by  a 
feeble  pulse.  It  is  only  while  the  heart  has  vigor  that  high  tension  can 
exist. 

The  respiratory  system  does  not  offer  much  that  is  characteristic,  but  com- 
plicating lesions  often  develop  in  these  parts.  One  of  the  most  common  is 
pneumonia,  which  finds  a  fair  field  for  its  development  in  all  cases  of  renal 
I  disease.  Indeed,  in  every  case  of  acute  pneumonia  the  physician  should 
'  study  the  renal  condition.  Often  the  routine  examination  of  the  vessels 
and  of  the  urine  in  a  case  of  pneumonia  is  the  first  evidence  that  chronic  con- 
tracted kidney  is  present.  Perhaps  the  most  common  respiratory  manifesta- 
tion is  difficult  breathing  resembling  asthma,  which,  coming  on  in  persons 
not  previously  asthmatic,  should  always  raise  the  suspicion  of  renal  disease. 
Effusions  into  the  lung  or  pleural  spaces  may  occur  with  suddenness  and  cause 
death.  When  the  toxaemia  is  well  marked,  Cheyne-Stokes  breathing  may 
develop. 

The  cerebral  symptoms  consist  in  vertiginous  attacks,  migraine-like  seizures, 
and  persistent,  dull,  or  throbbing  headache.  Apoplexy  due  to  the  degener- 
ative arterial  changes  may  take  place. 

It  is  a  most  interesting  fact  that  oedema  is  as  rare  in  contracted  kidney  as 


714 


DISEASES  OF  THE  KIDNEYS 


When  it  occurs  it  is  not  renal  in 
The  skin  in  this  type  of  renal  dis- 


it  is  common  in  the  large  white  kidney, 
origin,  but  due  to  the  failure  of  the  heart, 
ease  is  usually  dry,  and  is  chalky  in  hue 

Next  in  importance  to  the  examinations  of  the  urine  and  the  study  of  the 
peripheral  circulation  in  these  cases  is  the  observation  of  the  state  of  the 
retinal  vessels.    They  very  commonly  reveal  the  renal  condition. 


Fig.  95 


Retina  showing  Hirschberg's  vessels.     The  high  tension  in  the  arteries  can  be  seen  to  be  narrowing 
the  veins  by  pressure,      (de  Schweinitz.) 

Different  observers  give  varying  percentages  of  occurrence  of  retinal  lesions. 
Out  of  935  cases  of  renal  disease,  Groenouw  found  retinal  lesions  in  209, 
or  22.4  per  cent.  The  age  at  which  they  most  frequently  are  met  with  is  from 
fifty  to  sixty  years,  but  they  have  been  seen  in  adolescents. 

Five  types  of  these  lesions  are  recognized  by  ophthalmologists :  (a)  typical 
albuminuric  retinitis;  (h)  degenerative  albuminuric  retinitis;  (c)  hemorrhagic 
albuminuric  retinitis;  {d)   albuminuric  neuroretinitis,  and   (e)   albuminuric 


CHRONIC  BRIGHT'S  DISEASE 


715 


'papillitis.  In  the  first  form  irregularly  shaped  white  dots  or  spots  appear  in 
and  around  the  macula,  and  may  take  a  stellate  form.  When  the  condition 
is  well  developed  a  zone  of  whitish-yellow  may  surround  the  head  of  the 
optic  nerve.  Flame-like  hemorrhages  may  also  appear.  The  condition  is  at 
first  one  of  hypememia,  then  of  degeneration,  and  finally  one  of  atrophy.  In 
the  second  form  the  white  spots  are  small,  and  hemorrhages  are  more  limited, 
and  the  white  zone  about  the  nerve  head  is  not  well  developed.  The 
third  form,  as  its  name  indicates,  is  chiefly  hemorrhagic  in  type,  and  the 
hemorrhages  are  large  or  profuse,  while  the  other  changes  are  insignificant. 
Only  when  the  hemorrhages  are  absorbed  do  these  areas  become  whitish. 
The  fifth  form  shows  that  the  process  has  been  confined  to  the  optic  nerve, 
so  that  a  papillitis  or  choked  disk  is  present,  the  retina  being  but  little 
involved. 

Fig.  96 


Albuminuric  retinitis.     Granular  kidney.     Note  hard-edged  "asterisk"  exudation  and  the  silver-wire 
condition  of  the  arteries,  and  the  punctate  and  linear  hemorrhages. 


In  some  cases  detachment  of  the  retina  or  hemorrhagic  glaucoma  develop  as 
complications. 

Of  even  greater  importance  than  the  states  just  described  in  the  early 
diagnosis  of  renal  and  cardiovascular  disease  is  the  tortuosity  of  the  retinal 
veins  and  their  narrowing  by  the  pressure  of  the  retinal  arteries  wherever 
these  vessels  cross  the  veins — the  so-called  "  Hirschberg's  vessels"  (Fig.  95). 

Because  of  the  fact  that  the  symptoms  of  chronic  contracted  kidney  are 
so  often  insidious  in  their  development,  the  ophthalmologist  is  often  the 
first  to  recognize  the  existence  of  the  disease,  because  a  man  who  considers 
himself  in  perfect  health  asks  for  glasses  for  failing  vision  or  seeks  relief  for 


716  DISEASES  OF  THE  KIDNEYS 

blindness  in  one  eye.    Not  rarely  these  patients  have  repeated  attacks  of  rup- 
ture of  subconjunctival  vessels,  as  well  as  hemorrhages  into  the  retina. 

Flexner  states  that  the  terminal  dysentery  of  Bright's  disease  is  often  due 
to  the  Bacillus  dysenterioB. 

Prognosis. — Here,  again,  chronic  contracted  kidney  presents  a  widely  differ- 
ent aspect  from  that  of  the  parenchymatous  form,  for,  while  in  the  latter 
lesion  death,  as  a  rule,  occurs  inside  of  eighteen  months  at  best,  these  cases 
often  live  for  many  years,  if  the  process  is  not  already  far  advanced  when  the 
case  is  first  seen.  The  points  governing  prognosis  are  the  state  of  the  heart 
and  the  vessels,  the  ability  of  the  kidneys  to  approximate  the  nonnal  daily 
task,  and  the  life  which  the  patient  can  or  will  lead.  It  is  manifest,  from 
what  has  been  said  as  to  its  pathology,  that  the  affection  is  incurable,  but 
patients  often  live  as  long  as  ten  or  fifteen  years  after  undoubted  signs  of  the 
malady  are  present.  The  development  of  signs  of  uraemia,  of  feeble  heart, 
or  of  pulmonary  congestion,  oedema,  or  pneumonia  is,  of  course,  alarming. 

By  far  the  most  important  factor  in  determining  the  probable  duration  of 
life  is  the  state  of  the  retinal  vessels  already  named.  De  Schweinitz  has 
studied  this  matter  most  carefully  from  the  standpoint  of  the  ophthalmologist, 
and  we  have  followed  a  number  of  cases  together. 

These  facts  are  well  emphasized  by  the  following  figures,  which  illus- 
trate the  duration  of  life  in  chronic  interstitial  nephritis  after  the  occur- 
rence of  retinal  changes:  Belt  collected  419  cases,  of  which  72  per  cent, 
died  within  one  year  and  90  per  cent,  within  two  years.  The  cases 
reported  from  Haab's  practice  by  Possauer  showed  that  none  of  the  men 
applying  to  the  clinic  for  treatment  lived  more  than  two  years;  of  the 
women,  68  per  cent,  died  within  the  same  period  of  time.  Of  private 
patients  who  could  live  comfortably,  only  59  per  cent,  of  the  men  and  53  per 
cent,  of  the  women  had  died  at  the  end  of  two  years.  Gruening  collected 
100  cases,  none  of  which  survived  more  than  two  years  after  retinal  changes 
began,  and  Bull  found  that  69  out  of  103  cases  died  within  two  years.  Of 
the  remaining  34,  17  died  after  a  longer  period,  and  17  were  alive  at  the  time 
his  paper  was  published.  Harlan  analyzed  40  cases  with  the  following 
results:  33  ended  fatally  at  various  periods,  averaging  four  months;  3  lived 
a  year  after  the  discovery  of  retinal  changes;  3  recovered,  and  1  regained  his 
eyesight,  although  the  urine  was  albuminous  at  the  end  of  two  years.  Miley 
traced  45  cases,  and  found  the  average  duration  of  life  to  be  less  than  four 
months  from  the  time  eye  changes  were  first  observed.  One  of  his  patients 
lived  eighteen  months  and  two  fourteen  months,  but  all  the  others  died  within 
a  year.  Webster  mentions  the  case  of  a  clergyman  suffering  from  chronic 
interstitial  nephritis,  in  whom  retinal  changes  had  been  recognized  ten  to 
fifteen  years  before,  and  "  who  is  still  living,"  and  Wert  had  a  woman  under 
observation  in  whom  retinal  changes  had  been  noticed  more  than  four  years 
before  he  reported  the  case.  Her  general  condition  was  much  the  same  as 
when  she  came  under  his  charge.  I  ha.ve  under  my  care  at  this  time  a  man 
who  has  been  under  observation  four  years,  during  which  retinal  hemor- 
rhages have  repeatedly  occurred,  and  whose  arterial  tension  is  astonishingly 
high.  He  is  now  taking  j  a  grain  of  nitroglycerin  a  day  with  the  iodides, 
to  lower  his  blood  pressure  and  relieve  his  heart.    Such  a  result  is  most  rare. 


CHRONIC  BRIGHT S  DISEASE  717 

Most  of  these  cases  with  very  high  tension  and  retinal  changes  die  from 
apoplexy  or  an  acute  myocardial  failure  soon  after  retinal  changes  develop, 
the  patient  often  dropping  dead  without  warning  symptoms.  These  extreme 
instances  are  interesting,  but  they  are  rare  in  the  history  of  the  malady. 

Treatment. — There  are  few  diseases  of  an  incurable  character  in  which  the 
patient  can  be  so  greatly  benefited  by  treatment. 

The  question  of  diet  in  cases  of  chronic  contracted  kidney  is  to  be  decided 
along  pretty  much  the  same  lines  as  those  which  have  been  drawn  in  the  article 
upon  the  treatment  of  chronic  parenchymatous  nephritis.  W.  Hale  White 
has  expressed  the  belief,  in  which  we  coincide,  that,  as  a  rule,  this  disease 
is  treated  too  zealously,  and  that  in  the  desire  to  spare  the  kidneys  the  patient  is 
starved,  with  the  result  that  the  only  means  by  which  the  degenerative  process 
can  be  retarded,  namely,  the  maintenance  of  general  good  health,  is  impaired. 

As  we  do  not  know  of  any  articles  of  ordinary  diet  which  can  be  con- 
sidered really  harmful  in  granular  kidney,  it  is  best  to  give  the  patient 
ordinary  plain  digestible  foods  containing  the  normal  proportions  of  pro- 
teids,  fats,  carbohydrates,  and  salts,  just  as  it  is  necessary  to  give  a  person 
in  health  a  similar  mixed  diet.  It  need  hardly  be  stated  that  highly  seasoned 
foods,  or  foods  which  are  difficult  of  digestion,  should  be  interdicted.  Again, 
we  are  glad  to  note  that  Dr.  White  is  in  accord  with  us  in  believing  that  the 
limitation  of  these  patients  to  a  diet  of  chicken  and  fish  without  any  red  meat 
is  entirely  unnecessary.  Not  only  does  such  a  limitation  do  no  good,  but  it 
is  often  harmful  in  the  sense  that  it  makes  the  patient  consider  himself 
seriously  ill,  and  also  diminishes  his  appetite.  Patients  with  interstitial 
nephritis,  however,  should  especially  eschew  all  forms  of  alcohol,  since  it  is 
imperfectly  oxidized  in  these  cases,  and  tends  to  increase  arterial  tension. 

It  is  of  vital  importance  in  chronic  contracted  kidney  that  arterial  tension 
should  be  kept  at  a  point  as  near  the  normal  level  as  possible,  since  by  this 
means  danger  of  rupture  of  a  cerebral  vessel  is  diminished  and  the  work  of 
the  heart  is  decreased.  A  sufficient  quantity  of  nitroglycerin  to  accomplish 
this  result  should  always  be  administered.  It  is  not  a  question  of  the  size  of 
the  dose,  but  of  the  quantity  required.  It  is  also  to  be  remembered  that 
patients  rapidly  become  accustomed  to  nitroglycerin,  so  that  ascending  doses 
are  nearly  always  necessary.  Very  large  doses  may  be  taken  by  many  of 
these  patients  without  any  disagreeable  symptoms  of  the  full  action  of  the 
drug.  Beginning  with  yut  grain  three  times  a  day,  I  have  seen  as  much 
as  ^  grain  a  day  taken  with  no  other  than  excellent  results. 

Another  valuable  drug  in  chronic  contracted  kidney,  both  from  the  stand- 
point of  arterial  tension  and  of  the  fibroid  changes  in  the  arteries,  is  the 
iodide  of  potassium.  There  can  be  no  doubt  that  this  salt  diminishes  arterial 
tension,  and  if  any  remedy  exercises  an  influence  for  good  in  arresting  the 
pathological  changes  in  the  kidneys  and  in  the  bloodvessels,  that  remedy  is 
certainly  one  of  the  iodides.  Usually  doses  of  from  10  to  20  grains,  three  or 
four  times  a  day,  are  quite  sufficient.  A  useful  substitute  for  the  potassium 
salt  is  the  sodium  or  strontium  salts  or  the  syrup  of  hydriodic  acid  given  in 
ascending  doses,  beginning  with  30  drops  three  times  a  day.  It  goes  without 
saying  that  the  iodides  have  not  as  powerful  an  influence  in  decreasing 
arterial  tension  as  have  the  nitrites. 


718  DISEASES  OF   THE  KIDNEYS 

Digitalis  is  rarely  needed  in  chronic  interstitial  nephritis,  as  the  cardiac 
hypertrophy  is  usually  adequate,  and  digitalis  tends  to  raise  tension  in  the 
vessels  which  is  undesirable,  but  in  some  cases  there  comes  a  time  when 
the  blood  pressure  falls  largely  because  the  advancing  myocardial  degenera- 
tion and  cardiac  fatigue  prevent  the  heart  from  pumping  the  blood  with 
normal  energy.  In  such  cases  digitalis  and  strophanthus  do  good,  and 
nitroglycerin  may  do  harm.     (See  Arteriosclerosis.) 

Ursemia  is  to  be  treated  by  the  use  of  the  hot  pack,  if  the  patient's  heart 
is  strong;  by  the  employment  of  hypodermoclysis,  and  if  the  patient  is  fairly 
full-blooded  by  venesection  as  well.  (See  Uraemia.)  Cups  may  be  placed 
over  the  kidneys,  if  there  is  any  condition  of  renal  congestion,  and  three  or 
four  cups  should  be  placed  over  the  base  of  each  lung,  if  any  signs  of  pul- 
monary oedema  develop.  When  evidences  of  pulmonary  difficulty  arise,  full 
hypodermic  doses  of  strychnine  are  advisable,  and  if  any  tendency  to  urinary 
suppression  occurs,  ^  to  ^  of  a  grain  of  cocaine  may  be  given  hypodermically 
every  four  to  six  hours  for  several  doses. 

Many  practitioners  have  thought  it  wise  to  employ  full  doses  of  morphine 
hypodermically  in  the  treatment  of  ursemic  convulsions.  I  have  recently 
made  a  collected  investigation  in  regard  to  this  matter,  and  have  obtained 
the  opinion  of  physicians  of  experience  in  both  this  country  and  in  England. 
This  opinion  is  almost  universally  adverse  to  this  use  of  morphine. 

The  convulsions  should  be  controlled  by  nitrite  of  amyl  and  by  chloroform 
given  by  inhalation.     (See  Uraemia.) 

The  question  of  renal  decapsulation  has  already  been  discussed  under 
Chronic  Parenchymatous  Nephritis. 

If  the  progress  of  the  disease  is  slow,  it  is  advisable  to  send  the  patient  to 
some  warm  climate  during  the  winter  months,  if  his  home  is  in  a  northern 
latitude.  The  object  is  to  avoid  rapid  changes  in  temperature  in  the  atmos- 
phere and  consequent  chilling  of  the  surface,  with  secondary  congestion  of 
the  kidneys  and  decrease  in  the  activity  of  the  sldn. 

The  best  climate  is  to  be  found  in  the  neighborhood  of  San  Diego,  Cali- 
fornia, or  in  Egypt. 


AMYLOID  DISEASE  OF  THE  KIDNEYS. 

Definition. — Amyloid  disease  of  the  kidneys  is  part  of  a  general  process 
affecting  many  organs.  The  renal  manifestation  is  characterized  by  the 
deposit  of  lardacein  in  the  subintimal  stratum  of  the  bloodvessels,  in  the 
glomeruli,  and,  to  a  lesser  degree,  in  the  connective  tissue  of  the  tubules. 

Etiology. — Amyloid  disease  of  the  kidney  is  usually  the  result  of  a  pro- 
longed suppurative  process,  such  as  hip-joint  disease,  chronic  pulmonary 
tuberculosis  with  cavity,  or  any  cause  whereby  the  system  is  simultaneously 
sapped  by  suppuration  and  poisoned  by  the  absorption  of  toxic  substances. 
It  may  also  be  a  sequence  of  one  of  the  prolonged  fevers  or  occur  as  an 
associated  change  with  chronic  diffuse  nephritis  of  the  parenchymatous  type. 
Syphilis  is  a  common  cause,  and  malaria  may  be  the  only  demonstrable 
antecedent. 


AMYLOID  DISEASE  OF  THE  KIDNEYS  719 

Pathology. — ^The  kidneys  are  usually  enlarged,  and  when  incised  the  cut 
surface  is  shining  or  polished  in  appearance.  When  the  condition  is  com- 
bined with  interstitial  nephritis  these  organs  may  be  small.  The  surface  of 
the  organ  is  paler  than  normal,  particularly  in  the  cortex,  but  the  pyramids 
are  deep  red  in  hue,  and  the  glomeruli  are  readily  seen. 

If  an  aqueous  solution  of  iodine  is  painted  over  the  cut  surface  of  such  a 
kidney,  the  areas  most  affected  by  the  amyloid  change  stain  a  deep  mahogany 
brown,  and  if  to  these  areas  is  applied  a  dilute  aqueous  solution  of  sulphuric 
acid,  the  brown  hue  is  changed  to  blue. 

Microscopically  the  kidney  structure  when  examined  reveals  the  fact  that 
the  capillary  vessels  forming  the  tufts  in  the  capsules  are  parts  of  the  paren- 
chyma most  affected,  the  tuft  being  transformed  into  a  waxy  mass.  The 
disease  process  also  involves  the  afferent  and  efferent  bloodvessels  of  the 
tuft  and  the  straight  or  direct  vessels  of  the  kidney.  In  marked  cases  the 
connective  tissue  of  the  tubules  is  infiltrated,  the  interstitial  tissue  increased, 
and  the  epithelial  cells  may  be  granular  or  fatty,  as  in  parenchymatous  neph- 
ritis.   In  some  instances  all  these  types  occur  together. 

Symptoms. — There  are  no  symptoms  which,  taken  by  themselves,  may  be 
considered  indicative  of  amyloid  disease  of  the  kidneys.  It  is  only  when  cer- 
tain urinary  signs  develop  in  a  case  which  is  the  subject  of  those  maladies 
which  predispose  to  amyloid  change  that  we  can  say  that  a  diagnosis  is 
assured.  The  patient  is  usually  pallid,  may  be  well  covered  by  unhealthy 
waxy  fat,  and  the  heart  is  not  rarely  somewhat  enlarged,  although  no  less 
an  authority  than  Dickinson  contradicts  this  view.  The  urine  is  passed  more 
freely  than  is  normal.  It  is  clear  and  has  a  low  specific  gravity,  about  1005 
to  1010.  The  quantity  of  albumin  which  it  contains  varies,  but  it  is  usually 
present  in  considerable  quantity.  There  is  a  distinct  increase  in  the  quantity 
of  serum  globulin  in  the  urine.  Under  the  microscope  the  tube  casts  are 
found  to  be  hyaline,  fatty,  or  waxy.  Occasionally  the  amyloid  reaction 
already  named  may  be  demonstrated  in  the  urine.  The  degree  of  oedema  and 
the  state  of  the  bloodvessels  and  heart  depend  more  upon  the  presence  of 
associated  nephritis  than  upon  the  amyloid  change  itself.  If  nephritis  is 
well  developed,  anasarca  and  high  arterial  tension  may  be  present  as  an 
associated  state. 

Prognosis. — ^The  prognosis  depends  upon  the  gravity  of  the  causative 
process  and  the  degree  to  which  the  secondary  change  in  the  kidneys  has 
progressed.  Then,  too,  it  must  be  remembered  that  amyloid  disease  is  not  a 
condition  limited  to  the  kidneys,  but  affects  such  organs  as  the  liver,  spleen, 
and  even  the  heart,  and,  therefore,  the  patient  is  peculiarly  handicapped  in 
his  struggle  for  health.  If  the  casts  are  fatty  or  waxy,  and  are  present  in 
large  numbers,  if  the  albuminuria  is  copious,  and  if  anemia  is  marked, 
the  outlook  is  bad.  Indeed,  in  every  case  it  is  anything  but  good,  and 
the  longer  the  suppurative  process  continues  the  worse  the  outlook  be- 
comes. 

Treatment. — This  consists  in  the  same  measures  as  have  been  recommended 
for  chronic  parenchymatous  nephritis,  such  as  iron,  arsenic,  cod-liver  oil, 
and  fresh  air  and  sunlight  to  combat  the  underlying  cause.  If  possible,  the 
suppurative  process,  if  such  is  the  cause,  should  be  removed. 


720  DISEASES  OF  THE  KIDNEYS 


UREMIA. 


Definition. — Uraemia  is  a  condition  in  which  as  the  result  of  faulty  activity 
of  the  kidneys  a  patient  develops  a  series  of  symptoms  of  which  the  most 
notable  are  stupor,  coma,  convulsions,  or  paralysis,  or  in  other  instances 
gastrointestinal  disorders. 

Etiology  and  Pathology. — ^The  causes  of  uraemia  are  not  clearly  under- 
stood. It  is  well  known,  and  universally  recognized,  that  the  condition  is 
due  to  perverted  renal  activity,  both  as  to  the  elimination  of  the  ordinary 
products  of  metabolism  and  the  effects  of  renal  disease  upon  the  tissues  of 
the  body,  but  beyond  this  the  actual  cause  is  as  yet  undetermined. 

At  one  time,  under  the  leadership  of  Traube,  the  idea  prevailed  that  the 
symptoms  of  uraemia  were  dependent  upon  changes  in  the  circulation  in  the 
brain  produced  by  the  constriction  of  its  arteries  by  the  vascular  changes 
associated  with  nephritis  or  by  cerebral  oedema.  In  other  words,  that 
cerebral  anaemia  due  to  arterial  constriction  was  the  cause  of  the  symptoms. 
This  view  has  been  cast  aside  because  it  has  been  shown  that  ligature  of 
the  carotid  arteries  does  not  cause  uraemic  symptoms,  because  it  has  been 
proved  that  the  high  arterial  tension  of  renal  disease  results  in  dilatation 
of  the  cerebral  vessels,  since  they  are  poorly  endowed  with  muscular  fibres, 
and  finally  because  it  is  impossible  to  cause  active  contraction  of  the  cerebral 
vessels  by  any  drug  or  measure  used  for  raising  arterial  tension. 

The  theory,  that  uraemia  is  due  to  the  retention  of  the  ordinary  effete 
materials  of  the  body  owing  to  renal  disease,  also  cannot  be  accepted  as  a 
complete  explanation  of  the  condition,  because  it  has  been  found  that  liga- 
tion of  the  renal  arteries  in  animals  and  ligation  of  the  ureters  fail  to  produce 
uraemia,  although  the  function  of  the  kidney  is  by  these  means  completely 
arrested.  Again,  suppression  of  urinary  secretion  by  the  presence  of  stone 
in  both  kidneys,  and  even  by  necrosis  of  the  cortex  of  both  kidneys  in  man, 
does  not  cause  typical  uraemia.  Further  than  this  the  injection  of  urea 
and  even  of  healthy  urine  into  the  blood  does  not  cause  any  symptoms 
of  true  uraemia.  Again,  in  certain  cases  of  renal  disease,  as  in  chronic 
contracted  kidney  of  the  aged,  when  the  renal  excretion  is  seriously  impaired, 
uraemia  is  rare.  All  forms  of  deficient  renal  activity  do  not,  therefore, 
cause  uraemia. 

A  third  theory  is  that  as  a  result  of  the  renal  disease  peculiar  poisons  are 
made  in  the  body  which  when  they  accumulate  cause  uraemia,  or  that  the 
condition  of  the  system  in  renal  disease  permits  certain  micro-organisms  to 
grow  and  produce  a  toxic  substance. 

A  fourth  opinion  is  that  the  kidney  secretes  when  in  health  an  "internal 
secretion "  which  governs  metabolism  and  so  prevents  the  formation  of  cer- 
tain poisons.  The  last  theory  falls  to  the  ground  because  ligation  of  the 
renal  vessels  does  not  result  in  uraemia,  as  it  would  do  if  these  symptoms 
were  caused  by  the  lack  of  some  internal  secretion. 

We  are  left,  therefore,  with  the  fact  that  uraemia  is  due  to  the  presence 
in  the  body  of  peculiar  poisons  arising  in  Bright's  disease,  either  as  the 
result  of   the  growth  of   micro-organisms  or  perverted  metabolism,  and 


URyEMIA  721 

with  the  knowledge  that  the  kidneys  are  unable  by  reason  of  disease 
to  be  active  in  the  elimination  of  any  poisons.  It  would  seem  probable 
that  this  combination  of  extra  poisons  and  deficient  renal  activity  are  the 
two  factors  necessary  to  the  development  of  uraemia.  This  is  further  sup- 
ported by  the  fact  that  if  the  labor  of  the  kidneys  is  increased  by  gastro- 
intestinal fermentation  or  putrefaction,  an  attack  of  uraemia  is  very  prone 
to  occur.  Finally,  there  is  additional  proof  of  the  development  of  extra 
poisons  in  the  body  in  renal  disease.  This  is  found  in  the  marked  loss  of 
weight  in  patients  suifering  from  nephritis,  the  wasting  showing  that  metab- 
olism is  seriously  impaired  and  that  tissue  breakdown  is  marked.  Mani- 
fest loss  of  weight  may  not  be  present  because  of  dropsy,  but, if  this  is  removed 
by  purging,  the  wasting  is  manifest.    The  toxicity  of  the  urine  is  increased. 

Symptoms. — Uraemia  occurs  in  several  forms.  The  most  common  mani- 
festation of  uraemia  is  that  in  which  the  patient  passes  into  coma,  which 
may  be  preceded  by  delirium  and  drowsiness.  In  certain  cases  there  is 
associated  with  the  development  of  the  comatose  state  twitchings  and  con- 
tractions of  widely  separated  muscles,  and  particularly  the  extensors  and 
flexors  of  the  forearms. 

The  most  startling,  but  by  no  means  the  most  frequent,  form  is  the 
convulsive  type.  In  this  condition  the  patient,  with  or  without  any  pre- 
liminary indications  of  nervous  disturbance,  is  seized  with  a  more  or  less 
severe  epileptoid  attack,  which  usually  involves  the  muscles  of  the  face  and 
hands,  and  then  spreads  rapidly  to  the  whole  body.  No  sooner  is  one  seizure 
over  than  another  comes  on,  and  with  the  repetition  of  the  attacks,  or  it 
may  be  with  the  development  of  the  first  fit,  the  patient  becomes  uncon- 
scious, or  has  very  distinct  mental  impairment.  The  body  temperature 
usually  falls  unless  the  convulsions  are  so  severe  as  to  temporarily  cause 
a  slight  rise.  The  knee-jerks  are  usually  markedly  exaggerated  and  the 
pupils  are  contracted.  Because  these  symptoms  are  so  extraordinary, 
the  idea  has  gained  ground  that  convulsive  seizures  in  uraemia  are  commonly 
met  with.  This  is  incorrect,  as  they  are  not  common  except  in  that  pecu- 
liar form  of  eclamptic  convulsion  due  to  toxaemia  which  is  encountered 
in  pregnancy. 

A  third  form  is  that  in  which  there  is  marked  respiratory  disorder  of  a 
dyspnoeic  type.  The  patient  finds  it  exceedingly  difficult  to  breathe,  and 
feels  as  if  suffocated.  Not  only  is  the  respiration  wheezing,  as  it  is  in  asthma, 
but  it  is  peculiar  in  that  it  is  accompanied  by  a  hissing  sound,  the  patient 
very  frequently  ending  each  expiration  with  a  puffing  hiss.  Associated 
with  these  symptoms  there  may  be  some  duskiness  of  the  skin,  but  cyanosis 
is  not  marked.  The  patient's  mind  is  usually  clear,  and  he  not  infrequently 
complains  of  his  great  difficulty  in  getting  sufficient  air.  As  this  condition 
proceeds,  the  respirations  may  become  "Cheyne-Stokes"  in  type.  Although 
it  is  generally  held  that  the  development  of  Cheyne-Stokes  respirations 
under  any  circumstances  is  indicative  of  a  fatal  result,  it  not  infrequently 
happens  that  patients  with  this  symptom  arising  during  the  course  of  uraemia 
recover  from  that  particular  attack.  Sometimes  the  Cheyne-Stokes  breath- 
ing occurs  only  during  sleep,  and  it  may  be  the  only  manifestation  of 
uraemia,  the  mind  remaining  clear. 
46 


722  DISEASES  OF  THE  KIDNEYS 

There  is  still  a  fourth  form  in  which  the  patient  develops  mania  or  acute 
insanity.  He  is  restless,  very  excited,  and  may  be  extremely  violent.  As  a 
rule,  after  these  symptoms  have  lasted  for  a  short  time,  the  mental  excitation 
is  followed  by  gradually  increasing  drowsiness  which  finally  passes  into 
coma. 

In  the  so-called  paralytic  form  of  uraemia,  either  hemiplegia  or  mono- 
plegia may  come  on  suddenly,  as  does  hemiplegia  in  cases  of  cerebral  hemor- 
rhage. But  the  paralysis  is  not  due  to  rupture  of  a  bloodvessel,  to  a  forma- 
tion of  a  thrombus,  or  the  plugging  of  a  vessel  by  an  embolus.  So  far  as  is 
known,  it  depends  upon  intoxication  of  the  nervous  centres  controlling  the 
parts  involved  in  the  paralysis.  It  is  of  course  possible  for  cerebral  apoplexy 
to  complicate  uraemia,  and  for  this  reason  it  may  be  difficult  to  immediately 
make  a  differential  diagnosis  between  the  hemiplegia  of  uraemia  and  the 
complicating  hemiplegia  of  cerebral  rupture. 

There  is  still  another  form  of  uraemia  which  manifests  itself  in  persistent 
insomnia  with  muscular  irritability  or  cramps  and  hiccoughs. 

In  some  cases  of  uraemia  violent  gastrointestinal  disorders  suddenly 
assert  themselves,  vomiting  may  be  persistent  and  severe,  and  nausea  intense. 
Not  rarely  profuse  serous  purging  comes  on,  which  may  be  an  effort  on 
the  part  of  the  body  at  elimination. 

In  some  cases  uroemic  amaurosis  develops.  This  consists  in  sudden, 
bilateral,  and  complete  blindness.  Rarely  one  eye  suffers  before  the  other, 
and  in  some  cases  the  perception  of  light  may  be  preserved,  although  ordinary 
vision  is  destroyed.  In  the  greater  number  of  these  cases  the  ophthalmo- 
scope reveals  no  changes  in  the  retina,  although  it  may  be  found  to  be  oedem- 
atous  and  there  may  be  an  appearance  of  the  optic  nerve  like  that  of  choked 
disk.  This  condition  develops  more  commonly  in  those  cases  of  acute 
nephritis  associated  with  the  eruptive  fevers,  as  scarlet  fever,  than  in  ordinary 
chronic  nephritis.  The  amaurosis  lasts  for  a  few  hours  to  a  day  or  even 
longer  than  this,  and  vision  often  returns  as  suddenly  as  it  was  lost.  The 
prognosis  is  favorable  as  to  vision. 

All  of  these  forms  of  uraemia  differ  very  materially  from  that  type  which 
has  been  called  "latent  uraemia"  by  the  late  Sir  William  Roberts,  and  of 
which  mention  may  be  found  in  connection  with  the  article  upon  Nephro- 
lithiasis. In  these  patients  life  is  maintained  for  periods  varying  from  one 
to  two  weeks  in  the  presence  of  total  urinary  suppression.  They  remain 
conscious  almost  to  the  moment  of  death,  and  the  uraemic  symptoms  just 
described  in  their  various  forms  are  never  present.  There  may  be  some 
headache  and  nausea  and  weakness  and  drowsiness.  The  temperature  is 
subnormal  and  the  pupils  are  contracted.  In  some  instances  vomiting 
is  a  prominent  symptom  in  this  type  of  uraemia.  It  is  unfortunate  that  the 
term  "latent  uraemia"  should  be  applied  to  this  condition,  as  the  condition 
is  really  not  one  of  latency  nor  of  uraemia  as  that  term  is  generally  under- 
stood. 

A  very  important  symptom  of  uraemia  is  the  peculiar  odor  about  the 
patient,  which  is  quite  characteristic  and  which  may  be  due  in  part  to  urea 
which  is  being  eliminated  by  the  skin  or  to  the  presence  of  some  toxic  sub- 
stance as  yet  not  isolated. 


UREMIA  723 

Diagnosis. — The  presence  of  albuminuria  with  casts  of  the  uriniferous 
tubules,  of  somewhat  thickened  bloodvessels,  and  of  an  accentuated  aortic 
second  sound  in  association  with  the  development  of  any  of  the  symptoms 
which  have  just  been  described,  makes  the  diagnosis  of  uraemia  practically 
certain.  If  the  patient  is  bled  for  the  purpose  of  relieving  symptoms  of 
venous  engorgement,  it  is  wise,  if  opportunity  offers,  to  make  a  determina- 
tion of  the  urea  in  the  blood  if  the  physician  is  sufficiently  skilful  to  perform 
the  necessary  manipulations.  The  most  difficult  differentiation  lies  between 
ursemic  monoplegia  and  hemiplegia  due  to  rupture  of  a  bloodvessel,  or  to  an 
embolus,  or  thrombus.  In  some  cases  such  a  differentiation  is  impossible 
because  these  vascular  lesions  may  be  present  as  a  complication  of  the 
ursemic  state.  The  presence  of  the  urinary  changes  just  described  and 
of  the  other  signs  and  symptoms  mentioned  in  the  article  upon  Bright's 
Disease  will  serve  to  aid  in  the  differentiation  to  some  extent. 

At  times,  if  the  ursemic  poisoning  is  not  of  such  a  character  as  to  produce 
convulsions,  but  merely  semi-consciousness,  the  patient  may  live  in  a  state 
of  stupefaction  for  several  days  or  weeks,  and  because  of  the  mental  condi- 
tion, of  the  feeble  pulse,  of  the  slight  fever,  of  the  coated  tongue,  be  con- 
sidered a  case  of  typhoid  fever  or  general  tuberculosis. 

Opium  poisoning  is  to  be  separated  from  uraemia  by  the  presence  of  an 
odor  of  laudanum  on  the  breath  if  laudanum  has  been  used  instead  of 
morphine,  by  the  fact  that  the  pupils  are  contracted  to  a  pinpoint,  and  by 
the  examination  of  the  urine.  From  alcoholism  uraemia  is  separated  by  the 
examination  of  the  urine,  by  the  odor  of  alcohol  in  the  breath,  and  by  the 
history  of  the  patient.  But  it  must  not  be  forgotten  that  many  alcoholics 
have  chronic  renal  disease  and  that  the  ingestion  of  considerable  quantities 
of  alcohol  may  precipitate  an  attack  of  uraemia,  and  so  an  alcoholic  history 
may  be  present  which  will  mislead  the  physician. 

As  a  rule,  sudden  fulminating  urtemic  symptoms  develop  in  patients  with 
chronic  interstitial  nephritis,  whereas  the  types  of  uraemia  with  headache, 
vertigo,  and  other  warnings  of  toxaemia  are  seen  most  frequently  in  the 
parenchymatous  form. 

In  hot  weather,  when  men  are  exposed  to  great  heat  in  rolling  mills  and 
furnaces,  the  distinction  between  heatstroke  and  uraemia  may  be  difficult, 
since  in  both  conditions  violent  convulsions  with  cyanosis  may  be  present. 
In  heatstroke,  however,  the  temperature  is  usually  much  higher  than  in 
uraemia  and  the  cyanosis  is  usually  more  intense.  It  is,  however,  quite 
possible  for  heatstroke  to  complicate  nephritis. 

Prognosis. — The  prognosis  is  always  grave,  but  not  necessarily  fatal 
by  any  means.  A  professor  in  one  of  the  medical  schools  of  Philadel- 
phia had  a  moderate  ursemic  seizure  after  nearly  every  lecture  for  a 
whole  winter  course  of  lectures  before  a  final  fatal  seizure  came  on.  In 
uraemia  due  to  acute  nephritis  the  prognosis  is  good  if  the  patient  can  but 
survive  the  attacks  long  enough  for  the  kidneys  to  regain  their  function. 
In  the  cases  due  to  chronic  renal  disease  the  outlook  depends  to  some  extent 
upon  the  general  state  of  the  patient  and  particularly  the  condition  of  the 
lungs.  If  any  tendency  to  pulmonary  oedema  or  congestion  is  present,  the 
outlook  is  much  more  serious. 


724  DISEASES  OF   THE  KIDNEYS 

Treatment. — The  treatment  of  uraemia  depends  to  some  extent  upon  the 
variety  of  nephritis  which  has  produced  it  and  the  pecuKarities  of  the  indi- 
vidual who  is  suffering  from  the  attack.  When  ursemia  comes  on  as  a  com- 
pHcation  of  acute  nephritis,  such  as  that  compUcating  scarlet  fever,  the 
patient  should  have  hot  compresses  placed  across  the  small  of  the  back, 
and,  if  diarrhoea  is  not  already  present,  one  of  the  saline  purgatives,  such 
as  the  citrate  of  magnesium  or  the  sulphate  of  magnesium,  should  be  given 
in  sufficiently  concentrated  form  to  produce  several  watery  movements. 
After  this  has  been  accomplished  5  to  10  grains  of  the  citrate  of  potassium 
dissolved  in  Poland  water  should  be  given  three  or  four  times  a  day. 

If  the  symptoms  of  uraemia  persist,  it  will  be  necessary  to  place  the  patient 
in  a  warm  pack.  This  may  be  given  in  one  of  two  forms,  the  choice  of  the 
form  depending  upon  the  condition  of  the  patient's  skin  and  the  presence 
of  an  eruption  resulting  from  the  disease.  The  choice  also  depends  to  some 
extent  upon  the  temperature  of  the  patient.  If  the  rash  has  to  some  extent 
disappeared,  the  skin  is  dry  and  hot,  and  the  temperature  high,  it  is  well  to 
wrap  the  patient  in  a  sheet  wrung  out  of  water  at  70°  or  (S0°,  and  then  to 
immediately  surround  him  with  a  dry  blanket.  The  primary  effect  of  this 
cold  sheet  is  to  aid  in  the  dissipation  of  heat  over  the  body,  but  it  very  rapidly 
becomes  warmed  by  the  heat  of  the  body  so  that  the  patient  at  first  is  under 
the  influence  of  cold,  and  very  shortly  afterward  is  surrounded  by  a  warm 
pack.  The  primary  cold  drives  the  blood  from  the  surface,  and  the  secondary 
heating  fills  the  peripheral  capillaries  so  that  the  temperature  is  lowered 
by  an  improved  peripheral  circulation,  and  the  skin  is  thoroughly  supplied 
with  blood  so  that  it  has  a  better  opportunity  to  eliminate  poisons.  If  no 
fever  is  present,  and  the  rash  has  not  faded,  or  if  for  any  reason  it  is  con- 
sidered inadvisable  to  use  cold  primarily,  the  hot  pack  may  be  given,  the 
patient  being  quickly  wrapped  up  in  a  blanket  which  has  been  wrung  out 
of  water  as  hot  as  the  skin  can  bear.  Outside  of  this  is  placed  a  dry  blanket 
and  on  the  patient's  head  is  placed  an  ice-bag  to  prevent  cerebral  congestion. 
Every  few  moments  the  patient  is  given  a  few  sips  of  cold  water  to  drive 
the  blood  from  the  internal  portions  of  the  body  to  the  skin,  the  object 
being  to  flush  the  peripheral  circulation,  and  to  cause  a  sweat  which  will 
relieve  internal  congestion  and  eliminate  impurities  from  the  body.  If  the 
arterial  tension  is  high,  nitroglycerin  may  be  given  in  the  dose  of  -^^-^  of  a 
jjrain  to  a  child,  or  y^^  to  a  man,  every  three  or  four  hours;  or,  in  its  place 
for  a  child  ^  drachm  to  a  drachm  of  the  sweet  spirit  of  nitre  may  be  given. 

In  the  uraemia  of  chronic  parenchymatous  nephritis  a  plan  of  treatment 
identical  with  that  which  has  just  been  described  for  that  of  acute  nephritis 
may  be  carried  out.  As  a  rule,  the  patient  is  already  too  anaemic  to  permit 
of  bleeding,  and  his  tissues  are  so  oedematous  that  hypodermoclysis  is  im- 
possible. 

In  the  uraemia  of  chronic  contracted  kidney  with  high  arterial  tension, 
the  measures  already  indicated  for  the  uraemia  of  acute  nephritis  may  be 
instituted,  the  nitroglycerin  being  particularly  useful,  and  being  given 
hypodermically  in  order  that  it  may  act  promptly.  It  also  has  a  beneficial 
effect  in  that  it  relaxes  the  spasm  of  the  renal  bloodvessels  and  so  produces 
diuresis.    If  there  is  much  engorgement  of  the  venous  system,  venesection  is 


PYELONEPHRITIS  AND  PYELITIS  725 

exceedingly  useful,  particularly  if  it  is  accompanied  by  free  hypodermoclysis, 
or,  in  urgent  cases,  by  an  intravenous  injection  of  normal  saline  solution. 
Sometimes  in  these  cases  if  the  heart  seems  strong,  small  doses  of  pilocar- 
pine, ^  of  a  grain,  may  be  given  hypodermically  to  aid  in  producing  the 
sweat  which  is  caused  by  the  hot  pack,  and,  with  the  object  of  preventing 
cardiac  depression,  it  is  usually  wise  to  combine  with  it  -^-q  of  a  grain  of 
strychnine.  The  lungs  and  the  heart  should  be  carefully  watched,  and  if 
any  signs  of  pulmonary  oedema  or  cardiac  failure  develop,  strychnine  should 
be  given  freely,  and  1  or  2  drachms  of  Hoffmann's  anodyne  should  be  admin- 
istered as  a  rapidly  acting  diffusible  stimulant.  In  some  cases  in  which 
there  is  a  tendency  to  suppression  of  urine,  not  only  nitroglycerin  but  cocaine 
in  the  dose  of  |-  to  |  of  a  grain  may  be  given  hypodermically  twice  or  thrice 
a  day.  Should  convulsions  occur,  they  should  be  controlled  by  chloroform, 
if  they  are  exceedingly  severe,  and  by  the  use  of  a  drachm  of  bromide  of 
sodium  and  20  grains  of  chloral  by  the  rectum.  Morphine,  which  has  been 
largely  used  to  control  ursemic  convulsions,  is  not  regarded  with  favor  by 
most  practitioners  at  the  present  time.  If  the  arterial  tension  is  exceedingly 
high,  full  doses  (5  to  10  minims)  of  the  tincture  of  veratrum  viride,  repeated 
every  half-hour  until  some  evidences  of  circulatory  depression  are  produced, 
may  be  advantageous. 


PYELONEPHRITIS  AND  PYELITIS. 

Definition. — Pyelonephritis  signifies  an  inflammatory  process  involving 
both  the  pelvis  of  the  kidney  and  the  kidney  texture  itself.  The  term  is 
usually  applied  to  that  form  in  which  the  condition  is  suppurative.  Some- 
times it  is  called  suppurative  pyelonephritis.  Pyelitis  is  an  inflammatory 
state  of  the  pelvis  of  the  kidney  without  involvement  of  the  kidney  proper. 
As  synonyms  to  pyelonephritis  we  may  use  the  terms  pyonephritis,  pyo- 
nephrosis, and  caseative  nephritis. 

Etiology. — ^These  conditions  are  nearly  always  the  result  of  infection  from 
below;  that  is,  they  are  secondary  to  infection  of  the  lower  urinary  tract, 
viz.,  the  bladder  or  urethra.  Very  rarely  infection  of  the  kidney  may  take 
place  through  the  blood,  but  this  is  only  when  the  vital  resistance  of  all  the 
tissues  is  greatly  impaired,  or  when  the  infection  is  very  virulent,  for  the 
healthy  kidney  quite  readily  eliminates  micro-organisms  brought  to  it  by 
the  blood  stream.  It  is  possible,  too,  in  cases  of  floating  kidney,  in  which 
the  ureter  becomes  twisted  or  obstructed  so  that  the  vital  resistance  of  the 
pelvis  is  impaired,  that  infection  through  the  blood  may  ensue.  Although 
stones  in  the  kidney  are  now  attributed  to  bacteria,  it  is  conceivable  that  a 
renal  calculus  by  damaging  the  pelvic  wall  may  prepare  the  way  for  infec- 
tion, so  acting  as  a  direct  cause  of  pyelitis.  Infected  emboli  may  also  produce 
this  state. 

The  micro-organisms  which  most  frequently  cause  pyelitis  and  pyelo- 
nephritis are  the  Bacillus  coli  communis,  the  Streptococcus  pyogenes,  the 
Staphylococcus  pyogenes  aureus,  the  tubercle  bacillus,  the  typhoid  bacillus, 
the  gonococcus,  and  the  Bacillus  proteus  vulgaris.    Brown  has  shown  that 


726 


DISEASES  OF  THE  KIDNEYS 


the  Bacillus  coli  communis  is  the  most  frequent  cause  in  women,  probably 
because  of  the  near  relationship  of  the  anus  and  the  meatus  urinarius.  Brown 
also  asserts  that,  whereas  some  devitalizing  cause  is  usually  necessary  to 
permit  infection,  a  constantly  ammoniacal  urine  is  sufficient  cause  in  many 
cases. 

Pathology  and  Morbid  Anatomy. — Pyelonephritis  may  be  catarrhal,  pseudo- 
membranous, gangrenous,  or  suppurative.     The  first  two  forms  usually 


Fig.  97 


Brewis' case  of   pyonephrotic  kidney.     Girth,  forty-eight  inches;  weight,  forty-five  pounds. 

depend  upon,  and  are  overshadowed  by,  associated  diseases  such  as  typhoid 
fever,  and  rapidly  assume  the  suppurative  type.  In  pyelonephritis  the  mucous 
membrane  lining  the  pelvis  of  the  kidney  is  thickened  and  coated  with  pus. 
A  fibrinous  exudate  may  also  be  present.  The  kidney  structure  may  be 
involved  in  two  ways :  either  small  abscesses  are  scattered  through  the  paren- 
chyma of  the  kidney  or  in  long  white  streaks  which  project  themselves 
along  the  tubules.    The  renal  tissue  in  and  near  these  areas  is,  of  course, 


PYELONEPHRITIS  AND  PYELITIS  727 

necrotic.  If  the  suppurative  process  proceeds,  the  calyces  of  the  kidney 
become  enlarged,  the  renal  tissues  waste  and  suppurate,  and  the  kidney 
structure  is  largely  replaced  by  a  large  single  or  multiple  abscess.  Finally, 
if  the  patient  survives  so  long,  the  liquid  drains  off  through  the  ureter,  and 
the  pus  becomes  inspissated  so  that  a  cheesy  mass  remains  which  may 
become  infiltrated  with  lime-salts.  This  process  may  extend  to  the  tissues 
surrounding  the  kidney  causing  paranephritis.  When  one  kidney  is  involved 
the  cause  is  nearly  always  primary  disease  in  the  bladder,  and  to  this  type 
the  term  "  surgical  kidney  "  is  given. 

Symptoms. — The  symptoms  of  pyelitis  and  pyelonephritis  may  be  in 
many  cases  so  masked  by  the  conditions  which  produce  this  disorder 
in  the  renal  pelvis  that  they  are  overlooked.  Thus  the  urinary  picture 
is  commonly  obscured  by  an  associated  cystitis,  which  may  either  pre- 
cede or  follow  the  renal  lesion.  The  most  definite  symptoms  are  pain 
and  tenderness  in  the  back  over  the  kidneys,  with  or  without  frequent 
urination.  The  pain  is  increased  by  jarring  the  body  or  by  coughing,  and 
it  is  often  felt  in  the  testicle  or  inside  of  the  thigh  on  the  affected  side. 
The  quantity  of  urine  passed  is  usually  scanty  in  acute  pyelitis  but  profuse 
in  the  chronic  form.  With  the  development  of  suppuration  septic  fever 
develops,  vomiting  may  come  on,  and  occasionally  a  profuse  septic  sweat 
follows  a  chill  and  fever.  The  urine  is  acid  and  contains  pus,  blood  cells, 
and  degenerated  epithelium.  At  times  the  urine  may  appear  perfectly  nor- 
mal, but  soon  returns  to  its  earher  state.  This  variation  is  due  to  the  ureter 
becoming  blocked  by  a  plug  of  putty-like  pus,  so  that  for  several  hours 
only  one  kidney,  and  that  the  healthy  one,  drains  into  the  bladder.  Such 
a  variation  in  the  urine  therefore  proves  the  difficulty  to  be  unilateral. 
This  plugging  of  a  ureter  may  give  rise  to  attacks  of  pain,  somewhat  like 
those  due  to  a  renal  calculus  becoming  engaged  in  the  ureter,  but  the  pain 
is  rarely  so  severe. 

Diagnosis. — Pyelonephritis  is  sometimes  taken  for  malarial  fever,  as  are 
other  septic  processes,  because  of  the  chills,  fevers,  and  sweats.  An  exami- 
nation of  the  patient  and  of  his  blood  and  urine  readily  excludes  malaria  and 
reveals  the  renal  disease. 

In  other  cases  the  dry  tongue,  loss  of  weight,  diarrhoea,  and  abdominal 
tympany  may  mislead  one  into  a  diagnosis  of  typhoid  fever. 

From  suppurative  cystitis  the  condition  is  to  be  differentiated  by  the 
fact  that  the  pain  is  felt  chiefly  in  the  renal  region,  by  the  greater  quan- 
tity of  pus  in  the  latter  state,  by  the  greater  alkalinity  of  the  urine  in 
vesical  disease,  and  finally  by  the  use  of  the  cystoscope  and  the  ureteral 
catheter. 

Usually  there  is  more  albumin  in  the  urine  in  pyelonephritis  than  in 
cystitis,  and  more  discomfort  in  the  suprapubic  area  in  the  latter  condition 
than  in  the  former. 

From  perinephric  abscess  pyelonephritis  is  separated  by  the  greater  ten- 
derness over  the  kidney  in  the  former  condition,  by  the  fact  that  this  area 
is  not  bulging.  Most  important  of  all  is  the  absence  of  pus  in  the  urine 
in  the  first  condition  and  its  presence  in  the  second.  In  some  cases,  how- 
ever, of  pyelonephritis  very  distinct  bulging  over  the  kidney  is  manifested. 


728  DISEASES  OF   THE  KIDNEYS 

m 

A  valuable  sign  in  this  state  is  that  the  swelling  occasionally  disappears  or 
diminishes  as  the  pus  and  urine  escapes  through  the  ureter,  when  an  obstruc- 
tion is  removed.  A  bulging  or  swelling  in  the  renal  area  may  also  be  due 
to  hydronephrosis,  but  there  is  usually  no  fever  in  this  state. 

The  possibility  of  a  painful  swelling  in  the  region  of  the  kidney  being  due 
to  an  aneurysm  must  always  be  excluded  before  operation  is  resorted  to. 

Prognosis. — Prognosis  depends  largely  upon  the  cause  of  the  malady  and 
the  state  of  the  kidney.  If  the  condition  is  one  of  simple  pyelitis,  occurring 
during  the  course  of  one  of  the  infectious  diseases,  the  outlook  is  not  neces- 
sarily bad,  (See  Typhoid  Fever.)  If  the  suppuration  is  marked  the  prognosis 
is  not  good,  and  if  the  kidney  structure  is  involved  to  the  extent  of  pyo- 
nephrosis the  prognosis  is  bad,  and  death  may  come  from  the  exhaustion  of 
prolonged  septic  fever,  from  the  extension  of  suppuration  to  other  parts,  or 
because  of  amyloid  degeneration  in  other  organs. 

Treatment. — The  treatment  of  pyelitis  in  its  milder  phases  consists  in  the 
use  of  mild  diuretics  if  the  urine  is  concentrated,  of  counterirritation  by 
cups  or  heat  over  the  loins,  and  rest  in  bed.  No  highly  seasoned  foods  are 
permissible.  The  reaction  of  the  urine  must  be  determined.  If  the  urine  is 
acid,  alkaline  diuretics  and  salol  are  useful.  If  it  is  alkaline,  then  we  may 
give  5  grains  of  uritone  or  urotropin  three  or  four  times  a  day  in  a  glass  of 
sparkling  water.  The  diet  should  be  hearty  and  easily  digested.  Bitter 
tonics  and  iron  are  useful,  but  quinine  is  contraindicated  because  of  the 
state  of  the  bladder,  upon  which  it  acts  as  an  irritant.  When  hectic  fever 
is  developed  and  remains  persistent  the  patient  should  be  subjected  to 
nephrotomy  or  nephrectomy  before  he  becomes  exhausted  by  sepsis.  Opium 
or  morphine  may  be  needed  to  control  the  pain.  Recently  several  ob- 
servers have  reported  cases  in  which  benefit  was  derived  from  lavage  of 
the  renal  pelves,  by  means  of  ureteral  catheterization. 


HYDRONEPHROSIS. 

Definition. — Hydronephrosis  is  a  condition  in  which  because  of  obstruc- 
tion in  the  ureter  there  takes  place  in  the  pelvis  of  the  kidney  an  accumulation 
of  fluid  which  is  not  purulent.  This  fluid  as  it  increases  in  quantity  stretches 
and  dilates  the  pelvis  and  the  calyces  until  very  large  amounts  of  fluids  are 
retained  and  a  good-sized  cyst  is  formed. 

Etiology  and  Pathology, — Hydronephrosis  may  be  acquired  or  congenital, 
constant  or  intermittent.  It  arises  from  permanent  or  intermittent  closure 
of  the  ureter  so  that  the  urine  cannot  escape  into  the  bladder.  When  con- 
genital the  ureter  may  never  have  been  patulous  or  it  may  have  a  stricture 
or  be  abnormally  inserted  into  the  bladder  wall.  When  acquired  it  arises 
from  stricture  of  the  ureter,  or  from  plugging  by  a  clot  or  a  fragment  of  cal- 
culus. It  may  result  from  twisting  of  the  ureter  in  floating  kidney,  but  cal- 
culus is  the  most  common  cause  of  unilateral  hydronephrosis.  When  either 
of  these  causes  are  responsible  for  the  retention  of  fluid,  the  hydronephrosis 
may  be  intermittent,  because,  when  the  twist  is  undone,  or  when  the  calculus 
slips,  the  fluid  can  escape.    The  patient  may  remain  free  from  trouble  for 


HYDRONEPHROSIS  729 

years  unless  the  obstruction  forms  again.  The  obstruction  may  be  at  the 
bladder,  as  in  tumor  of  that  organ,  or  consist  in  a  paracystitis.  In  the  female 
pelvic  adhesions,  neoplasms,  and  cysts  may  press  upon  the  ureter  and  impede 
the  urinary  flow. 

The  secondary  effects  of  this  condition  upon  the  kidney  are  disastrous  if 
it  is  long  continued  and  severe.  The  pressure  acting  upon  the  renal  tissues 
causes  atrophy  and  wasting  so  that  finally  the  kidney  structure  largely 
disappears  and  in  its  place  only  a  large  collection  of  fluid,  surrounded 
by  fibrous  tissue  and  remnants  of  renal  tissue,  remain.  So  large  may 
the  tumor  grow  that  it  projects  downward  into  the  abdomen,  and  it  has 
even  been  mistaken  for  ascites.  The  other  kidney  may  be  similarly  affected, 
but  often  it  undergoes  hypertrophy  to  compensate  for  the  inability  of  its  mate. 

Symptoms. — The  presence  of  symptoms  depends  largely  upon  the  rapidity 
of  the  accumulation  of  fluid  and  the  size  of  the  renal  pelvis.  If  it  develops 
slowly  and  if  a  previous  attack  has  enlarged  the  pelvic  capacity,  much  fluid 
may  be  present  without  the  patient  presenting  any  symptoms.  If,  on  the 
other  hand,  the  fluid  rapidly  accumulates,  pain  may  be  very  severe.  When 
stricture  is  the  cause  the  accumulation  is  usually  slow,  but  when  a  twist  or 
a  calculus  closes  the  ureter  it  is  speedy  and  painful.  In  the  slow  cases  sharp 
pain  may  be  replaced  by  a  sense  of  weight  and  dragging.  A  very  charac- 
teristic sign  in  some  cases,  when  the  obstruction  is  suddenly  removed,  is  a 
profuse  flow  of  urine  which  fills  the  bladder  rapidly,  although  it  may  have 
been  emptied  but  a  short  time  before.  The  tumor  which  may  have  been 
present  in  such  a  case  disappears  with  the  flow. 

Diagnosis. — Palpation  of  the  abdomen  reveals  in  some  cases  a  mass  pro- 
jecting from  beneath  the  floating  ribs,  in  which  fluctuation  maybe  detected. 
When  the  history  of  the  causes  and  symptoms  is  as  clear  as  has  just  been 
detailed  the  diagnosis  is  not  difficult,  but  the  history  is  frequently  not  clear. 
In  children  such  a  mass  has  been  mistaken  for  an  enlarged  spleen  and  for 
a  sarcoma  of  the  kidney  or  of  the  retroperitoneal  glands.  (See  Tumors  of 
the  Kidney.)  In  other  cases,  if  the  kidney  is  fioating  and  hydronephrotic, 
the  tumor  may  be  taken  for  an  ovarian  cyst.  In  still  other  instances  the 
tumor  may  so  fill  the  abdomen  as  to  lead  to  a  diagnosis  of  ascites.  Thus, 
Sutton  has  recorded  a  case  in  which  the  cyst  held  no  less  than  thirty  gallons ! 
Aspiration  of  the  fluid  may  reveal  that  it  contains  some  urea  or  that  it  par- 
takes of  a  urinous  odor. 

Prognosis. — The  prognosis  depends  entirely  upon  the  cause  of  the  diffi- 
culty and  the  state  of  the  other  kidney.  When  the  closure  is  congenital 
and  complete,  death  ensues  in  a  few  days.  When  the  closure  is  due  to  a 
twist  of  the  ureter  or  to  a  calculus,  much  depends  upon  whether  the  flow  is 
entirely  stopped  and  how  long  it  is  arrested.  A  single  attack  followed  by 
sudden  relief  may  never  be  repeated.  When  the  disease  is  bilateral  the 
gradual  involvement  of  the  kidneys  may  result  in  uriemia,  or  if  infection  of 
the  kidneys  ensues  suppuration  may  develop. 

Treatment. — It  is  evident  that  no  medicinal  treatment  can  be  curative  in 
hydronephrosis.  Morphine  and  atropine  hypodermically  to  allay  pain  and 
relieve  spasm  may  be  useful  at  a  time  when  the  obstruction  is  complete  and 
the  accumulation  of  fluid  rapid.    If  the  condition  is  due  to  a  floating  kidney 


730  DISEASES  OF   THE  KIDNEYS 

with  twisting  of  the  ureter,  the  replacing  of  the  kidney  in  its  normal  position 
may  give  relief.  In  other  instances  the  temporary  assumption  of  the  knee- 
chest  position  is  curative.  If  the  attacks  occur  very  frequently,  it  may  be 
wise  to  suture  the  kidney  in  place. 

When  hydronephrosis  occurs  in  a  woman,  ureteral  catheterization  is  of 
value:  first,  because  it  withdraws  the  accumulated  fluid,  and,  second,  because 
if  a  stricture  is  present  a  catheter  may  dilate  the  stricture  and  so  exercise  a 
curative  influence.  But  catheterization  of  the  ureter  is  a  much  more  delicate 
procedure  than  catheterization  of  the  bladder,  and  there  is  greater  danger 
of  infecting  the  ureter  and  kidney,  so  that  the  greatest  possible  caution  in 
regard  to  asepsis  must  be  secured.  In  certain  cases  where  the  accumulation 
of  fluid  is  very  rapid,  and  where  the  symptorps  are  urgent,  aspiration  has 
been  practised,  but  this  is  not  devoid  of  danger,  and  gives  relief  in  only  about 
50  per  cent,  of  the  cases.  Morris  directs  that  the  needle  is  best  inserted  at 
the  most  bulging  point,  but  that  if  no  such  point  is  manifest  it  should  be 
driven  in  half-way  between  the  last  rib  and  the  crest  of  the  ilium  and  between 
two  and  two  and  a  half  mches  behind  the  anterior  superior  spine  of  the  ilium, 
if  it  is  the  right  kidney  which  is  in  trouble.  An  aspirating  needle  should  be 
used  instead  of  a  trocar  and  cannula.  WTien  repeated  aspirations  are  required 
for  relief ,  nephrotomy  is  necessary. 


CYSTIC   DISEASE   OF   THE  KIDNEY. 

Cysts  of  the  kidney  occur  as  congenital  malformations  and  are  acquired 
in  late  life.  There  is  perhaps  no  more  striking  object  to  be  found  in  a  col- 
lection of  pathological  specimens  than  a  congenital  cystic  kidney.  This 
condition  not  rarely  affects  both  kidneys,  which  is  an  important  point  to  bear 
in  mind  if  any  operation  on  one  kidney  is  thought  of.  These  cystic  kidneys 
are  not  composed  of  one  large  cyst,  but  of  a  multitude  of  cysts  massed 
together  regardless  of  shape  and  size,  and  separated  by  fibrous  bands  or  by 
strands  of  atrophied  renal  tissue.  The  contents  of  the  cyst  is  usually  a 
clear  yellow  fluid  with  an  acid  reaction  and  containing  urinary  salts,  but 
occasionally  the  fluid  is  opaque  and  may  contain  small  amounts  of  blood.- 
The  causes  and  processes  by  which  these  cysts  are  developed  are  not  definitely 
known,  but  it  is  thought  they  are  formed  by  extraordinary  dilatation  of  the 
tubules  or  of  Bowman's  capsules.  Shattock  believes  they  are  due  to  mal- 
development  of  the  mesonephron.  Such  kidneys  often  weigh  several  pounds. 
Although  congenital  in  origin,  it  is  to  be  remembered  that  life  may  be 
continued  far  into  adult  years  before  they  give  any  trouble. 

Congenital  cystic  kidney  (Fig.  98)  may  project  well  below  the  ribs  and 
give  rise  to  a  diagnosis  of  sarcoma,  hydronephrosis,  or  of  enlarged  spleen. 

Cysts  of  the  kidney,  single  or  multiple,  may  be  present  in  kidneys  which 
otherwise  show  no  abnormalities,  and  these  cysts  may  be  smaller  than  a 
pea  or  larger  than  an  orange.  Their  contents  may  be  clear  or  brown  in 
color,  and  may  be  gelatinous  in  character. 

Attention  has  already  been  called  to  the  small  cysts  which  are  seen  on  the 
surface  of  the  kidneys  in  chronic  interstitial  nephritis.    At  times  it  is  difficult 


CYSTIC  DISEASE   OF   THE  KIDNEY 


731 


to  determine  whether  the  kidney  is  the  site  of  acquired  or  congenital 
cysts  when  these  cysts  become  large  and  multiple. 

Echinococcus  cysts  of  the  kidney  also  occur.  (See  article  on  Para- 
sitism.) 

The  symptoms  of  congenital  cystic  kidney  are  in  no  way  peculiar  unless 
the  kidney  be  large  enough  to  project  in  the  manner  described.  Aside  from 
this  sign  the  patient  presents  no  signs  of  renal  disease  until  the  cyst,  by 
increase  in  growth  and  resulting  decrease  in  renal  tissue,  develops  renal 
failure,  and  the  signs  of  chronic  nephritis  ensue.    In  some  cases  a  sudden 


Fig.  98 


Congenital  cystic  kidney.     (Kast  and  Rumpler.) 


attack  of  uraemia  may  be  the  first  symptom  of  renal  difficulty.  "V^Tien  the 
condition  persists  and  adult  life  is  reached,  there  may  be  a  high  arterial 
tension  and  hypertrophy  of  the  heart,  as  in  ordinary  chronic  nephritis.  Often 
they  interfere  but  little  with  the  life  of  the  patient.  In  the  museum  of  the 
Jefferson  Medical  College  is  a  cystic  kidney  weighing  seven  pounds,  diag- 
nosed during  life  by  the  late  Dr.  J.  M.  Da  Costa,  and  carried  by  a  busy 


732 


DISEASES  OF  THE  KIDNEYS 


practitioner  of  medicine  for  over  two  years  afterward.     The  other  kidney 
was  but  shghtly  affected. 

Beyond  the  use  of  pain-reHeving  drugs,  there  is  nothing  that  can  be  done 
for  these  cases.  Operative  procedure  is  contraindicated  in  the  sense  of 
nephrectomy,  because  the  other  kidney  is  so  often  diseased  that  it  is  unable 
to  carry  the  burden  of  eUmination  if  left  by  itself. 


TUMORS  OP  THE  KIDNEY. 


Fig.  99 


The  kidney  is  not  rarely  the  seat  of  morbid  growths.    They  may  be  benign 
or  malignant.    The  benign  growths  are  the  fibromata,  which  chiefly  affect 

the  pyramids  of  the  kidney,  and  less 
commonly  the  lipomata  and  angiomata. 
Occasionally  papilloma  of  the  mucous 
membrane  of  the  pelvis  of  the  kidney 
develops.  The  most  common  malig- 
nant growth  in  the  kidney  is  sarcoma, 
which  is  by  no  means  very  rare  in 
young  children,  and  often  grows  to  a 
very  great  size.  Sarcoma  of  the  kidney 
secondary  to  sarcoma  elsewhere  is  also 
met  with  in  adults.  Endothelioma  may 
develop.  They  are  all  vascular  and 
often  bleed,  producing  hsematuria. 
Adenoma  of  the  kidney  usually  springs 
from  the  cortical  tissues,  but  it  may 
grow  to  so  large  a  size  that  it  takes  the 
place  of  most  of  the  renal  tissue.  They 
occur  frequently  in  children  and  are 
walled  off  from  the  rest  of  the  kidney  by 
a  fibrous  sheath.  Adenoma  is  found 
in  two  forms,  the  papillary  and  alveolar. 
Not  rarely  considerable  areas  of  necrosis 
develop  in  these  tumors.  Cancer  of  the 
kidney  as  a  primary  growth  is  rare.  As 
a  secondary  growth  it  is  more  common. 
Of  all  the  tumors  affecting  the 
kidney  those  arising  from  ectopic 
adrenal  tissue  are  probably  the  most 
frequent.  Such  tumors,  called  "hyper- 
nephromata,"  vary  in  size  from  almost 
microscopic  masses  to  growths  larger 
than  an  adult  head.  In  their  earlier  de- 
velopment such  neoplasms  are  benign, 
but  later  tend  to  involve  adjacent  struc- 
Sarcoma  of  the  right  kidney.    The  dark  line      turcs,  and  bv  metastasis  the  lungs.    If 

on  the  abdomen  IS  a  blue-pencil  outline  of  the         ,,  •'     ,,  •    i   .       •  i  ,^        ^• 

tumor.    (Le  Conte.)  they  occur  ou  the  right  side,    the  liver 


NEPHROLITHIASIS  733 

is  often  affected.  These  tumors  are  soft,  vascular,  yellowish,  or  blood- 
tinged  masses  developing  in  the  kidney,  and  often  cause  hsematuria. 

The  symptoms  of  renal  tumor,  if  the  growth  is  benign,  are  not  marked, 
unless  it  grows  large  enough  to  produce  pressure. 

When  the  tumor  is  malignant,  free  hcematuria,  with  clots  moulded  to  the 
shape  of  the  ureter,  may  be  present.  Pain  develops  only  when  the  growth 
presses  on  neighboring  parts  or  on  adjacent  nerve  trunks,  or  when  the 
weight  of  the  growth  is  such  as  to  cause  a  sense  of  weight  in  the  loin. 
Severe  attacks  of  colicky  pain  may,  however,  be  present  when  a  clot  is  being 
forced  through  the  ureter.  In  some  cases  marked  loss  of  flesh  takes  place, 
but  children  with  renal  sarcoma  often  remain  remarkedly  well  nourished. 
The  tumor,  if  large,  may  project  well  forward  in  the  belly  and  give  rise  to 
the  belief  that  it  is  an  enlarged  spleen  or  liver  (Fig.  99).  This  error 
is  frequently  made.  The  colon  may  give  tympany  on  percussion  over 
the  growth,  showing  that  it  springs  from  behind  that  part  of  the  bowel. 
Sarcoma  of  the  kidney  must  be  separated  from  sarcoma  of  the  retroperi- 
toneal space.  Care  should  be  taken  that  it  is  not  confused  with  cystic 
kidney,  or  hydronephrosis,  for  the  malignant  growth  may  be  nodular  and 
very  elastic,  or  even  give  a  sense  of  fluctuation  on  palpation. 

There  is,  of  course,  no  medical  treatment  of  this  state.  In  some  cases 
nephrectomy  of  the  sarcomatous  kidney  has  been  performed  in  young 
children  with  good  results,  but  there  is  usually  a  metastasis  elsewhere, 
which  ultimately  takes  life. 


NEPHROLITHIASIS. 

Definition. — ^This  condition  is  often  called  "  stone  in  the  kidney,"  or 
"  renal  calculus."  It  is  due  to  the  formation  in  the  tissues  of  the  kidney, 
or  in  its  calyces  or  pelvis,  of  concretions  composed  of  solids  derived  from 
the  urine. 

Etiology  and  Pathology. — ^The  concretions,  when  in  the  pelvis  of  the  kidney, 
may  be  single  or  multiple,  and  very  great  variations  in  their  size  may  be  met 
with.  In  some  instances  they  are  so  small  as  to  be  scarcely  larger  than  grains 
of  sand ;  in  other  cases  they  may  be  as  large  as  a  pea  or  bean,  and  in  still  other 
instances  a  large  calculus  may  form  which  completely  fills  the  renal  pelvis 
and  projects  itself  into  the  ureter  and  into  the  calyces  and  infundibula,  form- 
ing what  is  called  a  "coral  calculus."  The  latter  form  is,  of  course,  never 
passed  from  the  kidney,  but  the  smaller  stones  often  become  engaged  in  the 
ureter,  and  in  their  passage  through  it  to  the  bladder  cause  intense  pain. 
Not  rarely  the  fine  renal  sand  passes  so  readily  that  it  attracts  no  attention 
until  it  is  seen  in  the  urine. 

Not  only  are  concretions  found  in  the  calyces  and  pelvis,  but  also  in  the 
tissues  of  the  kidney.  Thus,  formations  of  uric  acid  may  take  place  in  the 
tips  of  the  pyramids  after  birth  and  cause  much  pain  in  the  first  month  of 
life.  Again,  accumulations  of  sodium  and  ammonium  urate  are  not  rarely 
found  in  adults  at  the  tips  of  the  pyramids,  particularly  in  gouty  invalids,  and 
in  very  old  persons  a  deposit  of  lime-salts  is  found  in  streaks  in  the  pyramids. 


734  DISEASES  OF    THE  KIDNEYS 

The  concretions  just  spoken  of  may  be  formed  of  a  number  of  urinary 
solids,  such  as  uric  acid,  calcium  oxalate  or  phosphate,  urate  or  carbonate. 
Cystin  and  xanthin  also  are  ingredients.  The  mere  existence  of  these  sub- 
stances in  the  urine  is  not  the  cause  of  the  formation  of  stone,  however, 
for  if  this  were  true  everyone  would  have  calculus.  There  are  at  least  two 
additional  factors  present,  one  of  which  is  the  presence  of  an  albuminoid 
substance,  which  serves  to  glue  together  tiny  particles  of  these  solids, 
and  a  condition  in  which  there  is  an  abnormal  tendency  to  crystallization 
of  these  bodies.  The  bacterial  origin  of  gallstones  and  the  presence  of 
micro-organisms  in  the  nuclei  of  renal  calculi  suggest  a  similar  origin  for 
both. 

The  most  common  ingredient  of  stone  is  uric  acid  or  the  urates.  Stones 
of  this  character  are  met  with  in  people  who,  because  of  small  quantities  of 
fluid  ingested,  have  a  scanty  urinary  flow,  or  who,  by  reason  of  great  activity 
of  the  sweat  glands,  have  little  urine.  As  a  consequence  of  concentration  and 
high  acidity  of  the  urine,  the  uric  acid  and  urates  are  readily  separated  in 
solid  form  and  held  together  by  the  albuminous  matrix.  Stones  of  this  char- 
acter are  quite  hard,  and  their  surface  is  smooth  and  reddish. 

Phosphatic  calculi  are  of  the  most  common  occurrence  after  those  formed 
from  uric  acid  and  the  urates.  They  are  composed  of  calcium  phosphate, 
ammoniomagnesic  phosphate,  or  both,  but  they  are  rarely  found  in  the  kid- 
ney, being  generally  developed  in  the  bladder.  They  are  usually  formed 
when  the  urine  is  persistently  ammoniacal. 

Next  to  phosphatic  calculi,  those  formed  of  calcium  oxalate  are  most 
commonly  met  with.  They  are  peculiar  in  respect  to  their  great  hardness 
and  their  roughened  surface  (mulberry  calculi).  Sometimes  when  they  are 
small  they  are  smooth  and  rounded,  "hemp-seed  calculi."  They  are  dark 
in  hue  and  not  infrequently,  on  being  split,  they  are  found  to  be  formed  about 
a  nucleus  of  uric  acid.  Oxalate  stones  are  only  met  with  in  those  who,  because 
of  digestive  or  metabolic  disorders,  pass  considerable  amounts  of  oxalates  in 
the  urine. 

The  effects  of  the  presence  of  stone  in  the  renal  pelvis  are  not  always 
marked.  Indeed,  calculi  may  be  present  for  years  without  causing  any  dis- 
comfort whatever.  Sometimes  they  suddenly  cause  trouble  if  the  patient 
suffers  from  a  fall  which  causes  the  stone  to  damage  the  lining  membrane  of 
the  pelvis,  and  as  a  result  hsematuria  may  ensue,  or  the  stone  may  be  started 
from  its  nest,  and,  proceeding  to  travel  down  the  ureter,  cause  an  attack 
of  colic.  In  still  other  cases  the  stone  may  cause  a  hydronephrosis  by  plug- 
ging the  orifice  of  the  ureter.  Again,  the  damage  done  by  the  sudden  move- 
ment of  a  stone  against  the  tissues  may  open  a  path  for  infection  and  conse- 
quent pyelitis  or  even  pyelonephritis. 

Frequency. — In  certain  parts  of  the  world  stone  is  very  prevalent,  notably 
in  some  counties  in  England.  This  is  probably  due  to  certain  mineral  ingre- 
dients of  the  water  which  is  taken  for  drinking  purposes.  Stone  is  also  very 
commonly  met  with  in  China  and  in  India.  The  late  Dr.  Kerr,  a  Chinese 
missionary,  removed  hundreds  of  vesical  calculi  during  his  residence  in 
China.  So  far  as  I  have  been  able  to  discover,  stone  is  not  much  more  preva- 
lent in  one  part  of  the  United  States  than  in  another. 


NEPHROLITHIASIS  735 

Prognosis. — -The  prognosis  of  nephrolithiasis  depends  entirely  upon  the 
question  of  the  state  of  the  kidney  tissues  about  the  stone  or  stones.  In  many 
cases  the  stone  produces  no  trouble  for  years.  If,  as  the  result  of  an  injury 
or  infection,  the  surrounding  tissues  become  diseased,  the  state  of  the  patient 
may  become  serious  from  pain  or  from  sepsis. 

Symptoms. — As  just  stated,  stones  may  be  in  the  kidney  for  years  without 
causing  any  signs.  When  they  escape  into  the  ureter  they  cause  renal  colic, 
which  is  due  to  three  causes:  first,  blocking  of  the  ureter  results  in  obstruction 
to  urinary  flow  which  causes  distention;  second,  the  pressure  of  the  urine  on 
the  stone  forces  it  forward  through  the  narrow  canal,  often  wounding  its 
lining,  and,  finally,  the  walls  of  the  ureter  are  spasmodically  contracted 
because  of  the  presence  of  the  stone.  The  pain  is  often  so  severe  as  to  be  a 
horrible  agony.  I  have  seen  a  strong  and  brave  man  grovel  on  the  floor 
groaning  with  anguish,  and  vomiting  because  of  its  severity.  The  fain 
extends  into  the  pelvis  and  the  inner  side  of  the  thigh  on  the  affected  side,  and 
even  into  the  testicle  and  penis.  It  also  radiates  into  the  back  of  the  chest. 
These  symptoms  may  persist  for  an  hour  or  for  several  hours.  In  the  latter 
instances  there  are  often  temporary  remissions  in  the  pain.  Not  rarely  the 
bladder  is  exceedingly  irritable,  and  the  patient  continually  passes  small  quan- 
tities of  urine  which  contains  traces  of  blood  from  the  affected  ureter,  but 
most  of  the  urine  comes  from  the  normal  side. 

In  cases  of  suspected  renal  calculus  the  urine  should  be  examined  micro- 
scopically for  blood  cells,  both  during  and  between  attacks.  They  are 
practically  never  absent  when  a  calculus  is  lodged  in  a  ureter. 

When  both  kidneys  are  affected,  total  suppression  of  urine  due  to  obstruc- 
tion of  the  ureter  or  to  reflex  irritation  may  ensue,  and  the  resulting  toxaemia 
produce  death.  It  is,  however,  a  noteworthy  fact  that  this  state  is  rarely  rapid 
in  onset  or  rapidly  fatal.  The  patient  often  lives  for  many  days,  unless  there 
has  been  renal  disease  present  for  some  time  with  some  degree  of  toxaemia. 
I  have  recently  seen  a  case  in  consultation  in  which  no  urine  had  been  passed 
for  a  week,  and  the  catheter  obtained  nothing  from  the  bladder,  yet  the 
patient  was  conscious  and  alert  when  spoken  to,  appearing  drowsy  only  when 
left  alone.  This  is  a  state  quite  separate  from  ordinary  uraemia,  and  has  been 
called  "latent  uraemia."     (See  Uraemia.) 

After  an  attack  of  renal  colic  has  passed,  pain  and  soreness  are  felt  for  some 
hours  or  days  in  the  affected  loin,  and  tenderness  on  pressure  may  be 
elicited. 

Diagnosis. — The  pain  of  renal  colic  must  be  separated  from  that  of  acute 
appendicitis,  that  of  gallstone  colic,  and  from  neuralgia.  It  must  also  be 
distinguished  from  the  pain  due  to  hydronephrosis  resulting  from  a  twist  in 
the  ureter.  Sometimes  a  diaphragmatic  pleurisy  may  mislead  us.  The 
peculiar  radiation  of  the  pain  into  the  groin,  penis,  and  inside  of  the  thigh  is 
diagnostic.  The  pain  of  gallstone  is  radiated  into  the  back,  and  is  often  asso- 
ciated with  jaundice.  Neuralgia  does  not  cause  bloody  urine.  Twist  of  the 
ureter  can  be  predicated  by  finding  a  floating  kidney.  Pleurisy  is  defined  by 
the  area  of  the  pain,  by  fixation  of  the  diaphragm,  and  by  a  friction  sound  in 
some  cases.  A  valuable,  but  by  no  means  absolutely  reliable,  method  of  diag- 
nosis is  the  use  of  the  Roentgen  rays,  which  may  or  may  not  reveal  a  stone, 


736  DISEASES  OF  THE  KIDNEYS 

and  which  sometimes  has  caused  the  surgeon  to  operate  when  no  stone  has 
been  found. 

Treatment. — The  treatment  of  nephroHthiasis  may  be  divided  into  two 
parts:  that  devoted  to  the  reHef  of  the  patient  at  the  time  of  the  attack  of  renal 
cohc,  and  that  devoted  to  the  prevention  of  the  formation  of  new  stones  or 
an  increase  in  the  size  of  those  already  present.  For  the  reHef  of  the  attack 
of  renal  colic,  a  hypodermic  injection  of  I  grain  of  morphine,  with  yw-q  grain 
of  atropine,  should  be  given  at  once;  or,  if  atropine  is  known  to  be  disagree- 
able in  its  effects  upon  the  patient,  nitroglycerin  may  be  used  hypodermically, 
for  the  double  purpose  of  aiding  in  relaxing  the  spasm  and  because  it  tends 
to  prevent  the  after-disagreeable  effects  of  the  opiate.  If  the  heart  is  in  a 
satisfactory  condition,  chloroform  may  be  given  by  inhalation,  and  if  the 
patient  will  lie  quietly  enough  to  permit  it,  hot  applications  may  be  made 
over  the  painful  kidney.  ' 

In  the  intervals  between  the  attacks  the  patient  should  be  instructed  to 
drink  large  quantities  of  some  pure  water  like  Poland  water,  or  one  of  the 
Lithia  waters,  which  depend  chiefly  for  their  effects  upon  their  purity  rather 
than  upon  their  lithia.  If  the  urine  is  alkaline,  lithia  waters  are  contra- 
indicated,  and  under  these  circumstances  it  is  well  not  only  to  use  copious 
draughts  of  water,  but  to  direct  the  patient  to  take  uritone,  urotropin,  or 
benzoate  of  ammonium,  for  the  purpose  of  making  the  urine  acid. 

When  the  urine  is  excessively  acid,  it  is  advisable  for  the  patient  not 
only  to  drink  large  quantities  of  water,  but  also  to  take  15  or  20  grains  of 
bicarbonate  of  potassium  three  or  four  times  a  day.  In  other  instances  the 
citrate  of  potassium  may  be  given.  Sometimes  good  results  follow  the  use 
of  Celestins  Vichy  water  when  the  urine  is  acid.  If  an  examination  of  the 
urine  reveals  the  presence  of  a  large  number  of  urates,  it  must  be  borne  in 
mind  that  these  have  their  origin  in  disordered  gastrointestinal  functions, 
and  the  diet  must  be  carefully  regulated,  and  nitromuriatic  acid  given  in  full 
doses.  Sometimes,  too,  these  cases  are  benefited  by  the  administration  of 
such  intestinal  antiseptics  as  salol,  or  aspirin,  in  the  dose  of  5  or  10  grains 
three  times  a  day. 

The  patient  should  be  forbidden  to  drink  any  sweet  wines  or  beer,  and  the 
only  form  of  alcoholic  stimulant  permitted  should  be  rye  or  Scotch  whiskey. 
If  the  patient  can  do  without  any  alcohol  at  all,  it  is  much  better  for  him  to 
be  content  with  non-alcoholic  drinks. 

If  the  patient  is  one  who  is  accustomed  to  leading  a  sedentary  life,  he 
should  be  instructed  that  an  amount  of  exercise  which  is  sufficient  to  pro- 
duce healthy  fatigue  is  absolutely  essential;  but  if  he  exercises  he  should 
also  drink  copiously  of  water. 

When  pain  in  the  kidney  is  continuous  or  so  frequent  in  its  recurrence  that 
the  enjoyment  of  life  is  impaired,  or  if  there  is  any  evidence  of  the  tissues  of 
the  pelvis  of  the  kidney  or  of  the  kidney  itself  being  irritated  or  infected,  the 
question  of  operative  interference  must  be  carefully  considered,  and  the 
patient  advised  to  seek  surgical  relief. 


DISORDERS  OF   URINARY  SECRETION  737 


PERINEPHRIC  ABSCESS. 

An  abscess  sometimes  forms  around  the  kidney  by  the  extension  of  infec- 
tion from  the  pelvis  of  this  organ,  because  of  transmitted  lymphatic  infection 
from  a  suppurative  appendicitis,  from  injury  to  the  tissues  by  a  blow  or  fall, 
by  extension  of  infection  from  spinal  disease,  from  perforation  of  the  stomach 
or  bowel  followed  by  subdiaphragmatic  abscess,  and  rarely  after  acute 
infectious  fevers,  as  typhoid  fever.  The  pus  may  cause  faiJi  and  bulging 
over  the  kidney;  it  may  burrow  upward,  and  escape  into  the  thorax,  or  down- 
ward and  resemble  a  psoas  abscess.  The  pus  is  usually  very  foul  and  distinct 
septic  symptoms  may  be  present.  On  the  other  hand,  I  have  seen  at  least 
two  cases  in  which  there  was  little  pain  and  no  fever.  There  was  nothing 
more  than  some  discomfort,  with  swelling,  over  the  Iddney.  Not  rarely  the 
spine  is  fixed,  and  the  leg  on  the  affected  side  is  drawn  up  when  the  patient 
lies  down. 

Treatment. — ^The  treatment  is,  of  course,  operative.  The  patient's  vitality 
should  be  supported  by  food  and  stimulants. 


DISORDERS  OF  URINARY  SECRETION. 

Anuria. — Anuria  is  a  condition  in  which  there  is  a  total  suppression 
of  urine.  It  arises  as  the  result  of  thrombosis  of  the  renal  vessels,  and 
an  intense  acute  nephritis  such  as  that  which  follows  the  ingestion  and 
elimination  of  very  irritant  poisons  as  cantharides  and  turpentine.  Some- 
times complete  anuria  also  follows  the  administration  of  ether  when  this 
anaesthetic  has  been  given  over  a  long  period  of  time  and  in  too  large 
quantities.  It  is  particularly  prone  to  occur  if  the  kidneys  are  already  in 
a  state  of  irritation.  In  other  instances  total  suppression  of  urine  results, 
reflexly,  from  the  irritation  produced  by  nephrolithiasis.  In  most  instances 
when  this  occurs  both  kidneys  are  affected.  Partial  or  complete  anuria  also 
sometimes  occurs  after  operations  upon  the  genito-urinary  tract.  A  care- 
ful distinction  should  be  made  between  anuria  when  no  urine  is  secreted 
and  retention  of  urine  in  which  no  urine  is  passed,  but  in  which  the  bladder 
is  found  to  be  well  filled. 

Treatment. — ^The  treatment  of  anuria  varies  somewhat  with  the  cause. 
When  the  arrest  of  secretion  is  due  to  the  presence  of  stone,  an  operation 
is  theoretically  demanded,  but  usually  the  diagnosis  as  to  the  cause  is  not 
completed  before  the  patient's  condition  has  become  so  grave  that  operative 
interference  is  of  questionable  propriety.  When  the  suppression  of  secre- 
tion is  not  due  to  stone,  but  to  reflex  irritation  or  spasm  of  the  renal  vessels, 
I  have  known  full  doses  of  nitroglycerin  given  every  three  or  four  hours, 
hypodermically,  to  relax  the  bloodvessels  and  cause  free  urinary  flow. 
This  is  particularly  apt  to  occur  if,  simultaneously,  the  patient  receives  a 
large  injection  of  cool  water  by  the  bowel.  If  saline  solution  is  used,  care 
should  be  taken  that  it  is  not  of  more  than  0.6  per  cent,  strength,  since 
strong  saline  solutions  abstract  liquids  from  the  tissues  instead  of  being 
47 


738  DISEASES  OF   THE  KIDNEYS 

absorbed.  In  these  instances  our  desire  is  that  fluid  shall  enter  the  tissues, 
find  its  way  to  the  bloodvessels  and  so  flush  the  kidneys.  Usually  about 
one  quart  of  liquid  should  be  given  by  gentle  hydrostatic  pressure.  Hot 
compresses,  or  poultices,  may  be  laid  across  the  loins,  and  if  there  is 
any  reason  to  believe  that  renal  congestion  is  present,  three  or  four  dry  or 
wet  cups  may  be  applied  over  each  kidney.  In  some  instances  moderate 
doses  of  the  bromides  and  the  vegetable  salts  of  potash,  like  the  citrate,  are 
advisable.  If  the  heart  is  strong  the  patient  may  be  subjected  to  a  hot  pack 
or  may  be  given  a  Turkish  bath  by  elevating  the  bed-clothes  and  allowing 
hot  air  to  surround  his  body.  Small  doses  of  pilocarpine  may  be  given  as 
a  diuretic,  particularly  if  the  heart  is  guarded  by  strychnine.  The  difiiculty 
in  using  large  doses  of  pilocarpine  is  that  it  is  prone  to  produce  pulmo- 
nary oedema. 

Haematuria. — Bloody  urine,  or  hematuria,  is  a  condition  in  which  there 
is  found  in  the  urine  not  only  the  coloring  matter  of  the  blood,  but  red  blood 
corpuscles  as  well.  It  sometimes  occurs  with  the  stage  of  onset  in  acute 
fevers  and  in  certain  cases  of  leukaemia.  It  is  also  met  with  in  certain  forms 
of  malarial  infection  of  the  sestivo-autumnal  type,  and  in  cases  of  infarction 
of  the  kidney  arising  during  an  attack  of  endocarditis  or  from  other  causes. 
When  there  is  stone  in  the  pelvis  of  the  kidney  or  any  part  of  the  conduct- 
ing tract,  and  the  patient  is  jarred  or  jolted,  the  stone  may  cause  suffi- 
cient local  damage  to  produce  bloody  urine.  Parasites  such  as  the  Filaria 
sanguinus  hominis  and  the  Bilharzia  may  produce  the  same  condition. 
Blood  also  appears  in  the  urine  as  the  result  of  papilloma,  cancer,  or  other 
neoplasm  of  the  bladder,  ureter,  renal  pelvis,  or  kidney,  ulceration  of 
the  urethra,  and  of  injuries  to  the  genito-urinary  tract  by  falls  or  blows. 
Sometimes,  too,  it  develops  in  the  course  of  scurvy  and  purpura  hemor- 
rhagica. In  acute,  and  even  in  chronic  parenchymatous,  nephritis  the  urine 
sometimes  contains  small  amounts  of  blood,  but  they  are  visible  only  under 
the  microscope. 

The  appearance  of  the  urine  when  it  contains  blood  is  quite  charac- 
teristic. It  is  not  only  dark  red  in  hue,  but  it  is  opaque  and  contains 
considerable  sediment,  which  is  chiefly  composed  of  fibrin  and  blood  cor- 
puscles. In  pure  renal  haematuria  the  voided  urine  is  more  of  a  smoky  hue, 
the  red  cells  are  of  the  shadow  or  phantom  type  and  clots  are  rarely  if  ever 
present.  If  the  urine  is  very  alkaline,  the  red  blood  corpuscles  may  be  dis- 
solved rapidly  or  become  colorless  and  diflicult  to  see.  Clots  formed  before 
the  urine  is  passed  nearly  always  arise  from  hemorrhage  in  the  bladder,  but 
occasionally  moulds  of  the  ureters  may  appear.  An  examination  by  means 
of  the  cystoscope  or  urethroscope  may  be  necessary  to  determine  the  source 
of  the  hemorrhage,  and  if  the  blood  comes  from,  the  kidney  it  may  be  neces- 
sary to  catheterize  the  ureters  to  determine  which  kidney  is  damaged. 

There  are  occasional  instances  of  hsematuria  in  which,  even  at  autopsy,  no 
sufficient  cause  can  be  found.  These  include  the  angioneurotic  haematuria 
of  Klemperer,  the  renal  hgemophilia  of  Senator,  and  Gull's  "renal  epistaxis." 

Treatment. — Treatment  of  haematuria  depends  largely  upon  its  cause. 
The  patient  should  be  put  absolutely  at  rest.  If  the  blood  comes  from  the 
kidney  there  is  no  treatment  which  can  be  relied  upon  as  being  efficacious. 


DISORDERS  OF  URINARY  SECRETION  739 

Chloride  of  calcium  in  the  dose  of  5  grains  three  or  four  times  a  day  may  be 
given  well  diluted  with  water  to  increase  the  coagulability  of  the  blood. 
Gallic  acid,  tannic  acid,  and  sulphuric  acid  have  been  largely  used  by  some 
practitioners,  but  it  is  doubtful  if  they  really  exercise  any  definite  influence. 
If  any  one  of  them  does  act  as  a  styptic  it  is  probably  sulphuric  acid.  Ten 
dropsof  the  aromatic  acid  maybe  given  everythree  or  four  hours, well  diluted, 
and  counterirritation  may  be  applied  in  the  shape  of  cups  or  hot  compresses 
over  the  kidneys.  Counterirritants  like  mustard,  turpentine,  and  cantharides 
should  be  avoided,  as  they  may  be  absorbed  and  increase  renal  irritation. 
The  patient  should  be  protected  from  cold.  If  the  hemorrhage  comes  from 
the  bladder,  an  injection  of  a  pint  of  normal  salt  solution  containing  J  to  1 
ounce  of  adrenalin  chloride  solution  1 :  1000  should  be  injected. 

When  the  hemorrhage  comes  from  the  urethra  a  similar  plan  of  treatment 
can  be  resorted  to,  simply  instilling  the  adrenalin  into  the  portion  of  the 
urethra  which  is  bleeding.  The  objection  to  the  use  of  substances  which 
cause  a  coagulation  of  the  blood  is  that  they  produce  clots,  which  may 
become  septic  or  give  rise  to  obstruction. 

Hsemoglobinuria. — In  all  probability  hsemoglobinuria  occurs  most  fre- 
quently as  a  complication  of  malarial  infection.  There  is  much  doubt  as  to 
the  actual  cause  of  this  condition.  In  some  instances  it  is  probably  due  to 
the  destructive  action  of  the  malarial  parasite  on  the  blood,  but  it  would 
seem  probable  that  in  other  instances  it  is  due  to  an  associated  infection 
or  a  condition  which  quinine  cannot  be  expected  to  remedy.  Indeed,  a 
large  number  of  cases  are  now  on  record  in  which  the  administration  of 
quinine  has  been  followed  by  hsemoglobinuria  or  hsematuria.  This  con- 
dition is  to  be  distinctly  separated  from  hsematuria,  for  in  this  case  no 
blood  corpuscles  are  present,  but  only  the  haemoglobin  or  coloring  matter 
of  the  blood.  Its  presence  does  not  indicate  any  lesion  in  the  genito-urinary 
tract.  Strictly  speaking  true  hsemoglobinuria  is  not  present,  but  methsemo- 
globinuria.  The  urine  is  clear,  but  may  be  quite  dark  in  hue,  and  deposits 
on  standing  a  heavy,  reddish-brown  sediment.  It  usually  gives  the  reaction 
for  albumin. 

Hsemoglobinuria  arises  from  the  ingestion  of  a  large  number  of  poisons, 
such  as  poisonous  mushrooms,  chlorate  of  potash,  pyrogallic  acid,  and  some 
of  the  coal-tar  products.  Not  long  since  I  had  under  my  care  a  physician 
who  suffered  from  repeated  attacks  of  hsemoglobinuria  whenever  he  tinkered 
with  his  automobile,  which  was  stored  in  a  small,  tightly  closed  shed  in  which 
the  fumes  of  gasoline  were  quite  concentrated.  He  never  suffered  with 
hsemoglobinuria  before  these  exposures,  and  since  avoiding  them  has  had 
no  return  of  his  trouble.  Hsemoglobinuria  sometimes  follows  severe  burns. 
It  may  also  develop  in  Raynaud's  disease.  The  discoloration  of  the  urine 
produced  by  carbolic  acid  is  not  due  to  hsemoglobinuria,  but  to  a  dark, 
oxidized  educt,  which  is  in  part  hydrochinon. 

Hsematinuria. — Under  the  name  of  paroxysmal  hsematinuria,  sometimes 
called  hcemoglobinurie  a  frigore,  a  condition  rarely  occurs  in  which  the 
urine  varies  in  color  from  a  port-wine  to  a  chocolate-brown,  or  almost  black 
hue,  the  alteration  in  its  appearance  lasting,  however,  for  but  a  few 
hours.     Its  specific  gravity  usually  ranges  from  1.025  to  1.027.     The  urea 


740  DISEASES  OF  THE  KIDNEYS 

is  increased.  The  quantity  of  blood  which  is  represented  has  been  estimated 
as  equivalent  to  from  seven  to  twelve  parts  in  one  hundred  of  urine.  Blood 
corpuscles  are  very  rarely  found  in  the  fluid.  The  urine  not  only  contains 
haemoglobin,  but  considerable  quantities  of  albumin  and  globulin.  Not 
infrequently  hyaline  and  granular  casts  are  present.  This  condition  is 
chiefly  provoked,  apparently,  by  exposure  to  cold — that  is,  by  chilling  of  the 
surface  of  the  body.  Aside  from  exposure  to  cold  and  chilling  of  the  surface 
of  the  body,  severe  muscular  exercise  seems  to  be  a  causative  factor,  and  not 
infrequently  there  is  also  a  tendency  to  vasomotor  disorders.  Indeed,  it  is 
probable  that  a  large  part  of  the  disorder  lies  in  an  abnormal  vasomotor 
condition.  Oilman  Thompson  has  recently  reported  two  cases  and  sum- 
marized the  literature.  It  appears  that  during  the  past  forty  years  only  206 
cases  have  been  reported,  and  that  most  of  these  have  appeared  in  England, 
Germany,  and  France,  and  that  very  few  indeed  have  been  reported  as 
occurring  in  the  United  States  and  Canada.  The  condition  affects  males 
very  much  more  frequently  than  females,  there  being  only  about  4  per  cent, 
of  females  in  the  206  cases  so  far  reported.  The  period  of  life  at  which  it 
commonly  occurs  is  between  thirty  and  forty  years,  but  cases  have  been 
reported  as  late  as  the  sixty-fourth  year.  At  the  time  of  the  attack  there  is 
usually  a  sharp  rise  of  temperature,  amounting  to  102°  or  103°,  but  this 
falls  to  normal  almost  as  rapidly  as  it  rises,  the  febrile  period  lasting  only  a 
few  hours.  Chills  are  often  present,  and  may  be  the  first  symptom  of  the 
attack.  Jaundice,  which  is  hsematogenous  in  origin,  develops.  Some  persons 
have  thought  that  the  jaundice  is  hepatogenous,  but  this  is  unlikely  in  view 
of  the  fact  that  the  urine  is  not  bile-stained  and  the  stools  are  not  lacking 
in  bile. 

Paroxysmal  hsemoglobinuria  is  to  be  separated  from  the  hsemoglobin- 
uria  met  with  in  some  cases  of  malaria  by  the  fact  that  the  latter  is  a  disease 
of  tropical  or  semi-tropical  regions,  whereas  paroxysmal  hcematinuria  usually 
occurs  in  cold  climates.  In  one  case  the  malarial  organism  is  present  and 
in  the  other  it  is  absent. 

Paroxysmal  haematinuria  is  also  associated  with  a  neurotic  condition, 
with  urticaria  and  with  localized  areas  of  cyanosis. 

Treatment. — The  treatment  consists  in  avoidance  of  exposure  to  cold 
and  to  causes  which  produce  nervous  excitement.  Tyson  has  suggested  the 
use  of  suprarenal  gland,  Thompson  suggests  the  use  of  thyroid  extract. 
Saundby  commends  calcium  chloride  and  Chvostek  believes  that  inhala- 
tions of  nitrite  of  amyl  may  be  useful  to  abort  an  attack.  If  the  circulation 
is  feeble,  rapidly  acting  diffusible  stimulants  like  Hoffmann's  anodyne, 
aromatic  spirit  of  ammonia,  and  small  doses  of  spirit  of  chloroform  are 
advantageous. 

The  treatment  of  hsemoglobinuria  cannot  be  direct.  Copious  draughts 
of  water  to  flush  the  kidneys,  careful  attention  to  the  state  of  the  bowels, 
protection  from  exposure  of  the  surface  of  the  body  to  cold,  and  the  use  of 
foods  which  are  not  highly  seasoned  and  irritating  to  the  liver  and  the  kidneys 
are  the  only  measures  which  the  physician  can  institute.  When  the  cause 
of  the  condition  is  malaria  the  debatable  question  of  administering  quinine 
must  be  discussed  and  decided.     (See  Treatment  of  Malarial  Fever.) 


DISORDERS  OF   URINARY   SECRETION  74^ 

Albuminuria. — Albuminuria  is  a  term  applied  to  a  condition  of  the  urine 
in  which  serum  albumin,  serum  globulin,  and,  by  some  writers,  other 
urinary  proteids,  including  nucleo-albumin,  albumose,  peptone,  or  fibrin 
is  found  in  it.  While  it  is  true  that  delicate  chemical  tests  will  frequently 
reveal  traces  of  albumin  in  the  urine,  it  is  also  a  fact  that  any  quantities 
which  can  be  appreciated  by  the  use  of  heat  and  nitric  acid  or  by  the 
potassium  ferrocyanide  or  mercuric  iodide  tests  are  to  be  regarded  as  ab- 
normal. 

As  albumin  is  a  colloid  substance  and  therefore  does  not  readily  diffuse 
through  animal  membranes  it  does  not  pass  through  the  bloodvessels  of  the 
kidneys  and  renal  tubules  unless  these  structures  have  undergone  some 
degenerative  change,  or  are  subjected  to  a  pressure  which  they  cannot  with- 
stand. Sometimes,  too,  albuminuria  may  be  due  to  changes  in  the  blood 
itself,  whereby  its  albuminous  ingredients  are  altered  or  the  renal  texture  is 
secondarily  affected.  The  presence  of  albumin  in  the  urine  when  disease 
of  the  conducting  apparatus  can  be  excluded  (accidental  albuminuria  may 
occur  through  contamination  of  the  urine  by  vaginal  discharges)  is  there- 
fore indicative  in  the  vast  majority  of  instances  of  some  renal  lesion,  and 
as  chronic  parenchymatous  nephritis  and  chronic  interstitial  nephritis  are 
the  most  common  renal  diseases,  it  is  usually  indicative  of  one  of  these 
maladies  or  of  a  subacute  nephritis  complicating  one  of  the  acute  infectious 
diseases.  Twenty  years  ago  albuminuria  was  considered  as  pathogno- 
monic of  Bright's  disease.  We  now  know  that  albumin  often  appears  in 
the  urine  when  Bright's  disease  is  not  present. 

As  a  general  rule  it  may  be  stated  that  the  quantity  of  albumin  is  in  direct 
ratio  to  the  severity  of  the  renal  lesion,  but  there  are  certain  notable  excep- 
tions to  this,  as  in  the  case  of  chronic  contracted  kidney,  in  which  disease 
the  kidney  is  seriously  affected,  yet  the  albumin  is  always  in  small  quantity 
and  may  be  absent  at  times. 

Albuminuria  is  not  rarely  met  with  in  cases  of  congestion  of  the  kidney 
due  to  cardiac  failure.  Under  these  circumstances  the  quantity  of  albumin 
present  may  be  very  large,  almost  as  great  as  that  which  is  found  in  chronic 
parenchymatous  nephritis.  It  is  due  under  these  circumstances  to  a 
structural  and  probably  nutritive  alteration  brought  about  by  passive 
renal  congestion,  and  the  use  of  cardiac  stimulants  usually  results  in 
its  disappearance,  at  least  to  some  degree.  So,  too,  albuminuria  may 
develop  in  certain  persons  after  severe  and  prolonged  exercise,  as  in 
soldiers  after  a  long  march,  or  in  athletes  after  a  long  run.  One  cause  of 
this,  at  least,  is  feebleness  of  the  heart  from  exhaustion. 

In  still  other  cases  what  is  known  as  "Cyclic  Albuminuria"  comes  on, 
which  is  sometimes  due  to  exposure  to  cold,  and  at  other  times  seems 
causeless.  Cyclic  albuminuria  is  sometimes  called  the  "  albuminuria  of 
adolescence,"  and  is,  as  its  name  implies,  intermittent  and  is  usually  not 
present  when  the  patient  rises  in  the  morning,  but  appears  as  the  day 
progresses.  The  upright  posture  is  in  some  cases  sufficient  to  induce  the 
condition — "orthostatic"  albuminuria.  Usually  the  urine  is  above  the 
normal  specific  gravity  and  contains  no  casts.  As  its  name  indicates,  it 
occurs  at  puberty,  in  easily  fatigued,  overgrown,  pallid  children.     It  usually 


742  DISEASES  OF   THE   KIDNEYS 

disappears  when  puberty  is  passed  and  the  system  is  established  on  an 
adult  basis. 

In  certain  persons  the  ingestion  of  excessive  quantities  of  albumin  in 
food  also  produces  albuminuria. 

A  very  high  arterial  tension  due  to  cardiovascular  disease  may  also  cause 
this  symptom.  While  it  is  true  that  the  cardiovascular  disease  usually  results 
in  some  impairment  of  the  kidney,  it  is  also  a  fact  that  reducing  arterial 
pressure  in  these  cases  by  the  use  of  nitroglycerin  often  stops  the  albuminuria. 

Albuminuria  may  be  due,  as  already  stated,  to  changes  in  the  condition 
of  the  blood  itself,  met  with  in  certain  cases  of  anaemia,  and  in  diseases  like 
purpura,  scurvy,  and  other  conditions  which  cause  marked  changes  in  the 
circulating  fluid. 

Tests. — Albumin  is  best  detected  in  the  urine  by  the  general  practitioner 
by  the  use  of  the  so-called  heat  and  nitric  acid  tests,  which  may  be  used  sepa- 
rately or  in  conjunction.  A  test-tube  is  two-thirds  filled  with  urine,  which  if 
cloudy  should  be  filtered,  and  if  alkaline  acidified,  and  the  upper  part  of  it  is 
held  over  a  lighted  alcohol  lamp  so  that  the  fluid  in  this  portion  of  the  tube 
soon  boils.  Under  these  circumstances  if  albumin  is  present  the  upper 
portion  of  the  urine  becomes  clouded  from  coagulated  albumin,  but  the 
portion  below  remains  clear  until  the  coagulated  albumin  is  precipitated. 
If  earthy  phosphates  are  present  some  cloudiness  of  the  fluid  develops, 
but  the  addition  of  a  few  drops  of  nitric  acid  disperses  the  cloud  if  it  is 
due  to  the  phosphates,  but  does  not  do  so  if  it  is  due  to  albumin.  Many 
physicians  use  a  somewhat  less  accurate  test,  which  consists  in  placing  one- 
half  to  one  drachm  of  nitric  acid  in  a  test-tube,  and  allowing  an  equal  quan- 
tity of  urine  to  trickle  down  the  side  of  the  tube  so  that  it  overlies  the  acid. 
If  albumin  is  present  a  layer  of  albumin  appears  at  the  point  of  juncture  of 
the  two  fluids.  Sometimes,  if  marked  intestinal  fermentation  is  present,  a 
reddish-brown,  but  transparent  zone,  appears  at  this  level  also. 

For  the  purpose  of  making  a  delicate  test  the  potassium  ferrocyanide 
method  may  be  employed.  The  writer  has  found  it  most  convenient  to  use 
for  this  purpose  the  so-called  urinary  test  tablets  which  are  now  placed  upon 
the  market.  Into  30  minims  of  Urine  is  placed  a  citric  acid  tablet  for  the 
purpose  of  acidification.  To  this  is  then  added  a  tablet  of  potassium 
ferrocyanide,  and  the  tube  is  shaken  or  allowed  to  stand  still  until  both 
tablets  are  completely  dissolved,  when  if  albumin  is  present  tiny  flocculi 
may  be  seen  floating  in  the  fluid,  which  settle  to  the  bottom  of  the  test-tube 
when  it  is  placed  at  rest.  This  is  a  delicate  test  for  albumin,  and  has  the 
advantage  that  it  does  not  precipitate  mucin,  peptones,  phosphates,  urates, 
or  vegetable  alkaloids.  If  the  physician  does  not  wish  to  use  these  tablets, 
he  may  add  to  a  test-tube  half-full  of  urine  5  or  6  c.c.  of  a  freshly-pre- 
pared solution  of  potassium  ferrocyanide  of  the  strength  of  one  in  twenty, 
adding  10  to  15  drops  of  acetic  acid.  In  other  instances  the  physician  may, 
if  he  chooses,  employ  potassiomercuric  iodide  test  tablets  in  the  same 
manner,  with  equally  good  results.  When  the  potassium  mercuric  iodide 
acid  test  is  used,  the  cloudiness  due  to  albumin  does  not  break  up  into 
flocculi,  as  it  does  when  potassium  ferrocyanide  is  employed. 

The  following:  facts  in  reo-ard  to  these  tests  should  be  remembered.     If 


DISORDERS  OF   URINARY   SECRETION  743 

the  specimen  of  urine  is  very  alkaline,  more  than  one  citric  acid  tablet,  or 
an  extra  quantity  of  acid  solution  should  be  added.  If  cloudiness  is  pro- 
duced by  the  acid,  it  is  due  to  mucin,  uric  acid,  or  some  oleoresin,  as,  for 
example,  when  copaiba  or  cubebs  have  been  taken  internally.  If  the  urine 
is  warmed  the  urates  dissolve,  but  the  mucin  remains.  The  precipitate 
produced  by  the  oleoresins  clears  up  by  boiling,  but  returns  as  soon  as  the 
urine  cools  slightly.  When  the  tablet,  or  solution,  of  potassium  mercuric 
iodide  or  potassium  ferrocyanide  is  added  to  the  acidulated  urine,  and 
cloudiness  is  produced,  the  urine  must  be  heated.  If  the  reaction  is  due  to 
albumin  the  precipitate  remains  undissolved,  but  if  it  clears  up  it  may  con- 
sist of  peptones  or  derivatives  of  vegetable  alkaloids  if  the  mercury  test  has 
been  employed.  When  the  potassium  ferrocyanide  test  is  used  peptones 
are  not  precipitated,  and  may  therefore  be  excluded. 

For  the  quantitative  estimation  of  albumin  Esbach's  method  is  most 
commonly  employed.  It  consists  in  using  a  graduated  test-tube  which  is 
called  an  albuminometer.  This  test-tube  is  marked  with  the  letter  "U," 
and  higher  up  with  the  letter  "R."  Below  the  letter  "U"  are  graduate  lines 
from  1  to  7.  Urine  is  placed  in  the  tube  to  the  level  of  the  letter  "U," 
and  the  following  solution  is  then  added  till  the  fluid  in  the  tube  reaches 
the  letter  "R."  The  solution  used  consists  of  10  grams  of  picric  acid;  20 
grams  of  citric  acid;  1000  cm.  of  distilled  water.  The  tube  is  now  corked 
and  inverted  several  times  until  the  test  solution  and  the  urine  are  com- 
pletely mixed.  It  is  then  allowed  to  stand  on  a  rack  in  a  perpendicular 
position  for  twenty-four,  hours.  At  the  expiration  of  the  twenty-four  hours 
the  albumin  is  found  to  be  at  the  level  of  one  of  the  numbers  cut  on  the  side 
of  the  tube,  and  this  represents  the  number  of  grams  of  albumin  per  litrje,t 
If  it  is  desired  to  know  the  percentage  of  albumin,  a  decimal  point  is  placed 
in  front  of  the  figure.  In  cases  where  the  quantity  of  albumin  is  so  great 
that  it  cannot  be  measured  by  the  ordinary  Esbach  tube,  the  urine  should 
be  diluted  with  water,  and  the  result  in  grams  multiplied  by  the  number 
of  times  the  urine  has  been  diluted. 

There  is  no  excuse  for  neglecting  examination  of  the  urine  for  albumin. , 
In  the  absence  of  other  apparatus  and  reagents  the  urine  may  be  acidified 
with  vinegar,  boiled  in  a  spoon  or  cup,  and  if  necessary  poured  into  a  glass 
for  inspection. 

From  what  has  been  said  it  must  be  evident  that  the  significance  of  albu- 
minuria varies.  Usually,  except  in  the  case  of  chronic  interstitial  nephritis, 
its  importance  from  a  prognostic  standpoint  is  in  direct  relation  to  its  quan- 
tity; its  cause  is  also  an  important  factor  concerning  prognosis.  The  pres- 
ence of  tube  casts  with  the  albumin  is  also  of  great  importance,  particularly 
if  these  tube  casts  are  granular  and  contain  fatty  globules.  Tube  casts 
should  always  be  sought  for  in  the  urine,  if  need  be  with  the  aid  of  the  centri- 
fuge, but,  on  the  other  hand,  it  should  be  remembered  that  if  the  centrifuge 
is  thoroughly  employed,  there  are  few  specimens  of  urine  which  will  not 
reveal  an  occasional  cast. 

No  one  perhaps  has  studied  more  carefully  than  has  Leube  this  question 
of  albuminuria.  His  view  is  that  while  in  many  cases  physiological  albu- 
minuria does  occur,  particularly  after  severe  exercise,  we  should  never- 


744  DISEASES  OF  THE  KIDNEYS 

theless  regard  all  such  instances  with  suspicion.  Washburn,  in  studying 
the  records  of  life  insurance  cases  who  were  supposed  to  have  physiological 
albuminuria,  found  that  the  death  rate  among  them  was  17.5  per  cent, 
instead  of  9  per  cent.,  as  it  should  have  been. 

A  careful  study  must  be  made  of  the  heart,  kidney,  lungs,  and  other 
organs  before  the  patient  is  given  a  favorable  prognosis. 

Wright  and  Ross  have  shown  that  it  is  sometimes  possible  to  differentiate 
the  albuminuria  of  renal  disease  and  physiological  albuminuria  by  increasing 
the  coagulability  of  the  blood  through  the  use  of  calcium  lactate.  (For 
dose  see  article  on  Purpura.)  If  the  use  of  this  drug  arrests  the  albuminuria 
it  does  not  depend  upon  actual  renal  disease. 

While  casts  may  be  present  in  the  urine  of  patients  who  are  thought 
to  be  healthy,  but  who  have  albuminuria,  these  casts  should  disappear  if 
the  patient  rests  in  bed,  and  they  should  not  be  epithelial  casts.  If  they  are 
present,  then  it  is  not  physiological  albuminuria.  It  is  perhaps  best  to  say 
that  albuminuria  ought  not  to  be  present,  and  that  its  existence  at  least 
excites  suspicion  of  some  renal  change.  But  it  does  not  necessarily  mean 
Bright's  disease,  and  I  have  seen  more  than  one  case  in  which  distinct 
albuminuria  was  present  without  the  association  of  casts  for  more  than 
fifteen  years. 

Pyuria. — Pus  in  the  urine  may  arise  from  pyelitis,  pyelonephritis,  cystitis, 
urethritis,  vaginitis,  or  the  rupture  of  an  abscess  into  the  urinary  passages 
from  contiguous  parts.  When  pus  is  in  urine,  it  gives  it  a  peculiar  opacity, 
and  on  sedimentation  the  bottom  of  the  vessel  contains  a  somewhat  ropy 
mass,  presenting  a  wavy  surface.  It  is  to  be  distinguished  from  the  phosphatic 
deposits  mixed  with  mucus  by  the  fact  that  it  is  not  so  white,  and  does  not  so 
closely  resemble  white  or  pinkish  powdered  chalk.  Further  than  this,  the 
phosphates  are  usually  cleared  up  by  boiling  or  by  the  addition  of  acid,  but 
urine  containing  pus  is  not  so  altered. 

The  treatment  of  pyuria  depends  upon  the  cause  of  the  presence  of 
pus.  If  there  is  an  abscess  in  the  kidney  surgical  measures  are  required, 
but  if  the  pus  is  due  to  a  pyelitis  or  cystitis  the  use  of  substances  which 
exercise  a  mild  antiseptic  influence  is  to  be  resorted  to,  at  least  for  a  time. 
For  this  purpose  the  patient  may  receive  5  grains  of  uritone  or  urotropin 
three  times  a  day  in  sparkling  water,  or  10  grains  of  benzoate  of  ammonium 
three  times  a  day  in  capsule.  For  the  methods  and  drugs  to  be  employed 
for  irrigating  the  bladder  the  reader  is  referred  to  works  on  genito-urinary 
diseases. 

Chyluria. — Chyluria  is  a  condition  in  which  the  urine  presents  a  milky 
appearance  owing  to  an  admixture  of  fat.  It  may  occur  in  some  cases  of 
pregnancy  and  during  lactation.  In  other  instances  it  follows  injury  to  the 
lymphatics  of  the  abdominal  cavity.  The  most  common  form  of  chyluria 
is  that  which  comes  on  as  a  complication  or  symptom  of  infection  by  the 
parasite  Filaria  sanguinis  hominis.  This  condition,  as  pointed  out  else- 
where, is  met  with  most  commonly  in  India,  China,  and  in  the  Straits 
Settlements,  and  its  cause  is  the  obstruction  of  the  lymphatics  produced  by 
the  presence  of  the  parasites  within  them.  Not  rarely  urine,  when  chylous, 
coagulates  in  the  vessel  holding  it  or  becomes  gelatinous  in  appearance. 


DISORDERS  OF   URINARY  SECRETION  745 

Phosphaturia. — This  term  is  applied  to  a  condition  of  the  urine  in  which 
it  contains  an  excess  of  phosphates  and  is  supposed  by  some  to  be  associated 
with  unusual  activity  of  the  nervous  system,  particularly  in  connection  with 
that  degree  of  excessive  nervous  strain  which  is  often  productive  of  neuras- 
thenia. Whether  this  view  is  correct  is  debatable.  There  can,  however, 
be  no  doubt  of  the  fact  that  in  certain  of  the  diseases  characterized  by  great 
loss  of  flesh,  such  as  tuberculosis,  an  excess  of  phosphates  is  present  in  the 
urine.  Such  a  condition  also  arises  in  acute  atrophy  of  the  liver  and  in  cer- 
tain forms  of  grave  anaemia.  On  the  other  hand,  acute  diseases  running  a 
febrile  course,  and  supposed  to  be  characterized  by  a  great  amount  of 
tissue  breakdown,  are  not  accompanied  by  this  manifestation.  In  some 
instances  in  which  there  is  an  excess  of  phosphates  present  in  the  urine  the 
patient  is  also  diabetic,  and  in  still  others  the  patient,  while  suffering 
from  polyuria  and  phosphaturia,  and  who  has  such  diabetic  symptoms  as 
thirst  and  loss  of  flesh,  nevertheless  does  not  develop  a  glycosuria,  sugar 
being  constantly  absent.  It  has  been  thought  by  some  that  these  cases  of 
so-called  "phosphatic  diabetes"  represent  an  early  stage  of  true  diabetes, 
for  in  some  of  them  glycosuria  ultimately  develops. 

The  best  remedy  for  the  purpose  of  cleaning  the  urine  of  an  excess  of 
phosphates  is  benzoate  of  ammonium  in  doses  of  10  to  20  grains  three 
times  a  day. 

Oxaluria. — Oxaluria  consists  in  a  condition  in  which  urine  of  high 
specific  gravity  contains  on  standing,  when  decomposition  is  absent, 
an  excess  of  calcium  oxalate  crystals.  The  condition  is  an  important 
one  in  that  it  frequently  points  the  way  to  the  correct  diagnosis  and 
treatment  of  patients  who  are  suffering  from  dyspepsia,  nervous  irritability, 
melancholy,  and  mental  depression  with  a  general  condition  of  wretched- 
ness. It  is  said  to  be  present  in  those  cases  in  which  there  is  lack  of  free 
hydrochloric  acid  in  the  secretion  of  the  stomach.  It  also  develops  in  patients 
who  eat  pears,  cabbage,  tomatoes,  and,  occasionally,  in  those  who  take 
coffee  to  excess.  In  many  patients  it  is  an  evidence  of  faulty  metabolism 
due  to  lack  of  fresh  air  and  exercise.  The  condition  is  of  interest  from  a 
therapeutic  standpoint  because  of  the  fact  that  these  patients  often  gain 
great  benefit  if  they  receive  moderate  doses  of  nitrohydrochloric  acid  and 
take  a  fair  amount  of  physical  exercise  and  lead  an  out-door  life. 

Indicanuria. — Traces  of  indican,  or,  to  speak  more  correctly,  indoxyl 
sulphate  of  potassium,  are  present  in  normal  urine,  being  derived  from  the 
indol  which  is  formed  in  the  intestine  by  the  decomposition  of  proteids 
through  the  action  of  bacteria.  If  this  indol  is  absorbed  from  the  intestine 
into  the  blood,  it  is  oxidized  and  forms  the  indoxyl  sulphate  of  potassium  just 
named. 

When  indicanuria  is  marked,  it  is  an  evidence  of  an  excessive  amount  of 
intestinal  putrefactive  change,  and  the  discovery  of  indicanuria  in  a  patient 
who  is  suffering  from  the  symptoms  of  autointoxication  is,  therefore,  of  value 
from  a  diagnostic  standpoint.  An  estimation  of  this  substance  in  the  urine 
is  also  useful  to  differentiate  intestinal  obstruction  from  ordinary  severe 
constipation,  for  in  the  former  indicanuria  is  usually  marked,  and  in  the 
latter  the  trace  of  indican  which  is  present  is  usually  not  above  the  normal. 


746  DISEASES  OF  THE  KIDNEYS 

In  rare  instances,  owing  to  decomposition  of  the  indoxyl  sulphate  of  potassium 
before  it  escapes  from  the  body,  the  urine  is  blue  when  it  is  passed,  but  in 
the  majority  of  cases  in  which  a  blue  urine  has  appeared  it  has  been  found 
that  the  patient  has  taken  methylene  blue  or  some  similar  aniline  dye, 
either  as  a  medicine  or  in  foodstuffs.  The  presence  of  indican  in  the  urine  is 
determined  by  heating  to  the  boiling  point  5  c.c.  of  nitric  acid  in  a  test-tube 
and  adding  5  c.c.  of  urine.  If  indican  is  present  in  excess,  a  bluish  ring 
develops  at  the  point  of  contact  between  the  two  fluids,  and  if  2  c.c.  of  chloro- 
form are  added  and  the  liquids  mixed  by  shaking,  and  the  test-tube  then  set 
aside  to  stand,  it  will  be  found  that  the  layer  of  chloroform  which  soon  sepa- 
rates has  a  violet  color. 

Lithuria. — Under  this  heading  is  mentioned  a  condition  in  which  an  excess 
of  uric  acid  occurs  in  the  urine,  chiefly  in  association  with  sodium  and  ammo- 
nium, and  sometimes  with  potassium,  lithium,  and  calcium.  An  examination 
of  the  urinary  sediment  under  the  microscope  may  reveal  small,  reddish  grains 
or  crystals,  looking  under  the  microscope  like  particles  of  red  pepper.  There 
is  no  condition  which  is  so  little  understood  at  the  present  time  as  is  this  one. 
Almost  every  layman,  and  a  multitude  of  doctors,  continually  speak  of  being 
"full  of  uric  acid,"  meaning  by  this  that  they  have  muscularstiffness,orthat  the 
urine  shows  an  excess  of  urates,  or  even  uric  acid  crystals.  In  the  majority  of 
instances  this  excessive  deposit  of  urates,  or  uric  acid,  depends  not  upon  any 
abnormality  in  bodily  metabolism,  but  upon  conditions  of  the  urine  which 
cause  the  precipitation  or  deposition  of  these  solids.  There  is  either  a  condi- 
tion of  acidity  or  a  minimum  quantity  of  mineral  salts,  and  as  a  result  pre- 
cipitation takes  place.  For  this  so-called  "uric  acid  diathesis,"  physicians 
prescribe  large  quantities  of  lithium  and  copious  draughts  of  water.  There 
can  be  no  doubt  that  the  water  is  advantageous,  but  the  lithium  only  does 
good  until  a  certain  degree  of  alkalinity  is  reached,  when  it  is  of  little  value, 
and  if  the  doses  are  large  it  acts  as  a  depressant  to  the  general  system.  It  is 
quite  true  that  persons  who  eat  heartily,drink  alcohol,  and  take  no  exercise  are 
not  infrequently  overloaded  with  effete  materials  representing  imperfect  meta- 
bolism, which  cause  disagreeable  symptoms.  It  is  also  perfectly  true  that 
exercise,  a  proper  diet,  and  the  use  of  plenty  of  drinking  water  will  overcome 
these  symptoms,  but  this  does  not  prove  that  the  patient  is  a  sufferer  from  the 
"  uric  acid  diathesis." 

Melanuria. — Melanuria  is  a  condition  in  which  the  urine  at  the  time  it  is 
passed,  or  shortly  after  its  exposure  to  the  air,  becomes  intensely  dark  in  hue, 
owing  to  the  presence  in  it  of  melanin.  It  is  found  in  certain  conditions  in 
which  this  substance  is  produced  in  the  body  by  pathological  processes,  such 
as  melanotic  growths.  If  a  solution  of  ferric  chloride  is  added  to  the  urine,  it 
becomes  inky  black.  If  caustic  potash  is  added,  it  becomes  at  first  violet  and 
then  claret  colored,  and  if  acetic  acid  is  added  to  this  mixture  it  may  become 
blue.  The  test  most  commonly  employed  is  the  solution  of  ferric  chloride 
mentioned. 

Myelopathic  Albumosuria. — ^The  presence  in  the  urine  of  the  so-called 
Bence-Jones  albumose  or  proteid  has  by  a  number  of  observations  been 
shown  to  be  most  suggestive  of  the  rather  rare  tumor  of  bone  known  as 
multiple  myeloma  or  medullary  osteosarcoma,  "Kahler's  Disease."    The  test 


DISORDERS  OF   URINARY  SECRETION  747 

is  quite  simple.  The  urine,  if  not  distinctly  acid,  should  be  made  so  with 
acetic  acid  and  then  heated.  At  50°  C,  if  it  contains  this  albumose,  it 
becomes  milky;  at  60°  C.  it  deposits  a  thick  precipitate  which  clings  to  the 
sides  of  the  tube  or  collects  on  the  surface.  Further  heating  to  100°  C. 
causes  the  almost  complete  disappearance  of  the  precipitate,  which,  how- 
ever, re-forms  as  the  urine  cools. 


DISEASES  OF  THE  DUCTLESS  GLANDS  AND 
LYMPHATIC  SYSTEM. 


DISEASES  OF  THE  THYROID  GLAND. 

GOITRE. 

Definition. — Under  the  term  goitre,  hronchocele,  thyreocele,  or  struma  is 
included  almost  all  enlargements  of  the  thyroid  gland,  but  the  application  of 
so  general  a  term  is  not  to  be  regarded  with  favor.  It  is  better,  therefore,  to 
consider  the  various  diseases  of  the  thyroid  as  inflammatory  (traumatic 
strumitis),  infectious  (tuberculous  or  syphilitic  strumitis),  and  parasitic 
(echinococcic)  strumitis.  Of  the  remaining  so-called  hypertrophies  of  the 
gland  it  may  be  said  that  some  of  them  at  least  are  apparently  not  of  the 
nature  of  neoplasms,  and  to  these  the  term  "simple"  or  "benign  goitre"  is 
applied;  whereas,  in  the  case  of  those  enlargements  which  are  due  to  the 
development  of  tumors  within  the  gland,  we  apply  the  term  "neoplastic 
goitre,"  as,  for  example,  endotheliomatous,  sarcomatous,  and  cancerous 
growths  (malignant  goitre).     (See  Tumors  of  the  Thyroid.) 

With  regard  to  some  of  the  simple  or  benign  goitres,  it  is  still  unsettled  as  to 
whether  they  are  neoplastic,  that  is,  adenomatous,  in  every  instance.  In  some 
cases  they  are  undoubtedly  adenomatous.  In  still  other  cases  the  greatly 
enlarged  gland  may,  under  the  microscope,  have  a  histological  formation  like 
that  of  the  normal  organ.  To  this  type  of  goitre  the  name  "hyperplastic 
goitre"  is  applied,  including  those  varieties  characterized  by  reproduction 
of  the  parenchyma  of  the  gland  and  called  by  some  writers  "  parenchymatous 
goitre."  When  the  enlarged  gland  contains  cysts  developing  from  its  acini, 
the  mass  is  called  a  "cystic  goitre."  Cystic  goitres  result  from  the  distention 
of  the  gland  spaces,  with  absorption  of  the  intervening  walls,  thereby  giving 
rise  to  cavities  of  various  sizes.  The  contents  of  these  cysts  may  be  gelatin- 
ous or  colloid.  In  some  instances  the  enlargement  depends  upon  dilatation 
of  bloodvessels,  and  apparently  upon  the  overgrowth  and  dilatation  of  new 
bloodvessels,  forming  the  so-called  vascular  goitre,  and  not  rarely  there  is  a 
blending  of  two  or  more  of  the  types  already  mentioned.  Such  conditions 
are  known  as  "mixed  goitres." 

In  ordinary  goitre  there  takes  place  an  increase  in  the  size  of  the  alveoli 
in  the  thyroid  gland  and  a  simultaneous  formation  of  new  glandular  tissue. 
Side  by  side  with  this  increase  there  is  often  colloid  degeneration,  and  when 
this  degenerative  process  is  marked  the  state  is  called  colloid  struma  or 

(749) 


750  DISEASES  OF   THE   THYROID   GLAND 

colloid  goitre.  Not  uncommonly  still  other  degenerative  changes  take  place, 
in  which  the  walls  of  the  alveoli  break  down,  and  in  this  way  several 
cavities  are  thrown  together,  forming  cysts,  which  may  hold  colloid  matter 
and  blood  derived  from  the  vessels  in  the  alveolar  walls.  This  is  called  cystic . 
goitre.  In  still  other  cases  the  bloodvessels  of  the  gland  become  dilated,  so 
that  a  telangiectatic  state  develops.  Finally,  it  sometimes  happens  that  all  of 
these  changes  take  place  in  the  same  gland,  and  upon  them  may  be  super- 
imposed acute  inflammation  and  even  malignant  growth.  The  increase  in 
size  may  be  limited  to  a  single  part  of  the  gland  or  be  widely  diffused. 

Etiology. — The  cause  of  ordinary  enlargement  of  the  thyroid  gland  of  the 
fibroid  and  cystic  type  is  unknown,  but  there  can  be  no  doubt  that  it  depends, 
at  least  in  part,  upon  the  character  of  the  drinking  water  used.  My  colleague, 
Professor  Keen,  has  just  investigated  a  very  remarkable  prevalence  of  the 
disease  in  the  interior  of  the  State  of  Pennsylvania,  in  which  the  relationship 
of  water  supply  and  goitre  is  extraordinary,  a  very  large  number  of  the  people 
on  one  side  of  a  mountain  ridge  being  affected,  and  those  across  the  divide 
escaping.  The  disease  is  also  said  to  be  very  common  in  some  parts  of 
Michigan  and  in  Switzerland.  The  suggestion  of  Grasset  that  goitre  is  of 
protozoal  origin  has  not  been  favorably  received.  In  support  of  his  view  he 
calls  attention  to  the  fact  that,  like  malaria,  goitre  is  endemic  in  certain 
areas,  and  he  is  inclined  to  believe  that  the  thyroid  enlargement  is  anal- 
ogous to  the  splenic  tumor  of  chronic  malarial  infection.  The  disease  is 
more  frequent  in  women  than  in  men,  and  in  adults  than  in  children,  in 
which  class  it  is  very  rare. 

Symptoms. — The  symptoms  of  goitre  are  usually  of  no  consequence  until 
the  growth  is  large  enough  to  be  seen  or  until,  by  its  pressure  on  the  adjacent 
tissues,  it  causes  difficulty  in  breathing  and  interferes  with  swallowing  or  with 
the  function  of  the  vagus  nerves.  The  goitre  may  involve  all  of  the  gland, 
its  isthmus,  or  either  one  of  the  lateral  lobes.  Rarely  aberrant  goitres  arise 
in  ectopic  or  misplaced  thyroid  tissues,  and  they  may  be  intrathoracic  or 
occur  at  the  base  of  the  tongue  (lingual  goitre).  In  still  other  instances  they 
have  been  known  to  develop  along  the  course  of  the  thyroglossal  ducts  or  in 
adjacent  areas.  The  degree  to  which  the  cervical  tissues  are  displaced  in 
those  cases  in  which  the  growth  is  chiefly  in  one  lobe  is  remarkable.  Not 
long  since  I  sent  to  Dr.  Keen  for  operation  a  patient  whose  hyoid  bone  was 
pushed  to  one  side  so  that  it  rested  nearly  under  his  right  ear. 

Treatment. — There  is  no  medicinal  treatment  of  much  value  in  goitre. 
Painting  the  part  with  iodine  and  the  use  of  various  counterirritant  ointments 
have  been  resorted  to,  but  they  have  no  real  effect  over  the  growth.  If  it 
becomes  very  large,  it  must  be  excised  if  the  pressure  symptoms  are  severe. 


SWELLING  OF  THE  THYROID. 

This  occurs  from  two  chief  causes,  namely,  from  inflammation  and  from 
hyperaemia  or  congestion.  Some  writers  have  described  an  angioneurotic 
form.  When  the  swelling  is  due  to  inflammation  it  may  arise  from  infection 
of  the  gland,  as  in  typhoid  fever  or  other  acute  infectious  diseases,  and  may 


EXOPHTHALMIC   GOITRE  751 

follow  vaccination  or  sepsis;  or,  again,  it  may  be  due  to  tuberculosis  of  the 
gland,  or  to  syphilis  with  the  formation  of  gummata.  Occasionally  marked 
swelling  arises  from  trauma,"  and  this  may  be  acute  or  chronic. 

It  is  asserted  by  Fothergill  that  there  are  recorded  five  cases  of  enlargement 
of  the  fetal  thyroid  due  to  the  administration  of  potassium  chlorate  to  the 
mother. 

Some  years  ago  I  reported  the  case  of  a  woman  who,  in  stooping  in  a  dark 
room,  struck  her  neck  against  the  edge  of  a  chair  and  at  once  felt  violent  pain 
in  the  thyroid  gland.  The  gland  rapidly  became  swollen,  and  the  patient 
presented  all  the  symptoms  seen  in  persons  to  whom  large  doses  of  thyroid 
gland  have  been  given,  such  as  headache,  a  rapid  pulse,  and  a  tendency  to 
syncope.  In  still  another  case,  seen  by  me,  an  army  surgeon  on  the  fight- 
ing line  received  a  severe  blow  in  the  thyroid,  and  developed  a  chronic 
enlargement  of  the  thyroid  gland,  with  some  tachycardia. 

The  thyroid  gland  is  also  found  enlarged  by  hypersemia  in  young  girls, 
particularly  at  the  menstrual  period,  and  in  young  women  in  their  first  preg- 
nancy. It  also  occurs  in  young  persons  who  suffer  from  cardiac  disease. 
Such  an  enlargement  usually  passes  away  when  the  cause  is  removed. 

Sometimes  thyroiditis  occurs  in  the  insane,  but  its  etiology  and  symp- 
tomatology need  further  study. 

TUMORS  OF  THE  THYROID  GLAND. 

The  tumors  of  this  gland  are  adenoma,  in  which  state  the  condition  is 
practically  that  of  goitre  as  already  described,  carcinoma,  sarcoma,  and 
endothelioma.  The  sarcomata  are  usually  primary.  Morf  has  been  able 
to  collect  but  39  instances  of  carcinoma  of  the  thyroid;  he  himself  adds 
1  case.  Of  the  173  cases  of  cancer  of  the  thyroid  collected  by  Orcel,  14 
invaded  the  trachea. 

Carcinomata  are  also  usually  primary  and  undergo  metastasis  to  nearby 
tissues  or  even  to  distant  structures.  The  growth  may  develop  in  the 
parenchyma  or  in  the  connective  tissue  of  the  gland. 

An  interesting  form  of  tumor  of  the  thyroid  is  the  so-called  carcino- 
sarcoma, or  mixed  tumor  of  this  gland. 

Occasionally  old,  quiescent  goitres  may  become  malignant,  undergoing 
either  sarcomatous  or  carcinomatous  degeneration. 

An  anomalous  condition  in  this  group  of  affections  is  thyroid  metastasis, 
consisting  in  the  growth  of  typical  thyroid  tissue  at  points  distant  from  the 
glands.  These  growths  are  quite  commonly  in  bones  and  are  seldom 
malignant.     The  thyroid  itself  may  show  no  change. 

EXOPHTHALMIC  GOITRE. 

Definition. — ^Exophthalmic  goitre  is  often  called  "Basedow's  disease," 
"Parry's  disease,"  or  "Graves'  disease."  Parry  described  it  (1825)  ten 
years  before  it  was  described  by  Graves  (1835)  and  fifteen  years  before  it 
was  described    by  Basedow  (1840).     Exophthalmic  goitre  is  an   entirely 


752  DISEASES  OF   THE   THYROID  GLAND 

different  disease  from  ordinary  goitre  or  simple  enlargement  of  the  thyroid 
gland.  It  is  a  malady  in  which,  as  its  name  implies,  there  is  protrusion  of 
the  eyeballs,  and,  in  addition,  palpitation  of  the  heart,  with  a  very  rapid 
pulse.  There  are  fine  tremors  in  the  hands,  arms,  and  head,  and  disordered 
vascular  tone.  A  tendency  to  abnormal  sweating  of  the  palms  of  the  hands, 
and  great  mental  depression  is  often  present. 

Satterthwaite  recognizes  acute,  subacute,  and  chronic  forms  of  Graves'  dis- 
ease, and  says  we  may  speak  of  acute  or  temporary  and  essential  or  chronic 
forms.  A  secondary  form  is  that  in  which  an  old  goitre  takes  on  the  symp- 
toms of  Graves'  disease. 

Frequency. — In  10,603  cases  admitted  to  the  Jefferson  Hospital,  there  were 
11  cases  of  exophthalmic  goitre,  or  1  in  964.  In  the  University  Hospital,  out 
of  35,076  cases,  there  were  48  cases  of  exophthalmic  goitre,  or  1  in  730.  Of 
7270  cases  treated  at  the  Dispensary  for  Nervous  Diseases  at  the  Orthopaedic 
Hospital  and  Infirmary  for  Nervous  Diseases,  Eshner  found  that  30  were 
exophthalmic  goitre,  or  1  in  242.    It  is  therefore  by  no  means  a  rare  disease. 

Etiology. — ^The  cause  of  exophthalmic  goitre  is  not  known,  but,  as  is  the 
case  with  most  diseases  of  obscure  causation,  a  multitude  of  factors  have  been 
named  as  possible  causes  for  its  development,  varying  all  the  way  from  rheu- 
matism and  tonsillitis  to  fright  and  traumatism.  The  disease  is  very  much 
more  frequent  in  women  than  in  men.  Thus,  out  of  1839  cases  collected  from 
various  sources,  1553  were  females  and  286  males,  a  proportion  of  about  6  to  1, 
and  its  average  age  incidence  is  between  sixteen  and  forty  years.  Cases 
are  on  record  in  which  it  has  affected  children  as  young  as  two  and  a  half 
years.  In  some  statistics,  collected  by  me  some  years  ago,  it  was  shown  that 
there  is  a  very  distinct  hereditary  influence  present  in  many  cases.  There 
can  be  little  doubt  that  the  symptoms  which  are  present  in  exophthalmic 
goitre  are  dependent  upon  excessive  internal  secretion  of  the  th}Toid  gland, 
or,  if  not  upon  excessive  secretion,  to  the  entrance  into  the  general  system 
of  more  of  the  active  principle  of  the  th}Toid  gland  than  is  normal.  It  has 
been  claimed  that  the  cause  lies  in  disorder  of  the  sympathetic  ganglia,  but 
there  is  no  adequate  proof  of  the  correctness  of  this  view. 

Pathology  and  Morbid  Anatomy. — So  far  as  the  morbid  changes  are  con- 
cerned, there  is  an  excess  of  fat  in  the  orbit  as  compared  to  the  quantity  of 
fat  in  other  portions  of  the  body. 

The  heart  may  be  normal  or  dilated.  Not  rarely  there  is  some  undue 
relaxation  of  the  sphincteric  fibres  around  the  mitral  orifice  of  the  heart. 
The  thyroid  is  enlarged,  the  veins  covering  it  are  dilated  and  numerous, 
and  the  arteries  supplying  its  tissues  are  enlarged  and  tortuous.  On  the 
other  hand,  certain  observations  have  shown  that  in  many  instances  there  is 
no  remarkable  change  in  the  vascularity  of  the  organ. 

A  microscopic  examination  of  the  thyroid  gland  reveals,  in  many  instances, 
however,  a  very  marked  increase  in  the  development  of  its  parenchyma,  and 
the  epithelium  lining  its  vesicles  is  changed  in  appearance.  The  colloid 
substance  in  the  vesicles  partly  or  entirely  disappears  and  is  replaced  by 
mucoid  material  which  takes  a  stain  badly.  The  epithelial  cells  lining 
the  vesicles  frequently  desquamate.  Greenfield  has  shown  that  additional 
tubules  lined  by  a  layer  of  epithelium  are  also  developed.    After  the  disease 


EXOPHTHALMIC   GOITRE  753 

has  lasted  for  a  considerable  period  of  time,  there  is  not  infrequently  an 
overgrowth  of  connective  tissue  in  the  gland.  MacCallum  finds  that,  as  a 
whole,  the  changes  resemble  most  closely  those  found  in  experimentally 
produced  compensatory  hypertrophy  of  the  thyroid. 

The  thymus  gland  is  enlarged  in  a  very  considerable  proportion  of  cases, 
but  a  microscopic  examination  of  it  does  not  show  pathological  changes  in 
most  instances. 

The  parathyroids  are  often  found  to  be  atrophied  and  the  thymus  gland 
is  persistent  and  often  hypertrophic. 

Certain  alterations  have  been  described  in  the  sympathetic  system  and  in 
the  central  nervous  system,  but  it  has  not  been  proved  that  these  have  any 
close  relationship  with  the  disease. 

Symptoms. — ^The  'protrusion  of  the  eyeballs,  even  when  it  is  present  to  a 
moderate  degree,  is  so  striking  that  attention  is  directed  to  this  symptom 
almost  as  soon  as  the  patient  is  seen.  It  varies  greatly  in  degree.  In  some 
cases  the  eyeballs  may  be  so  prominent  that  it  is  impossible  for  the  lids  to 
completely  close,  whereas  in  others  the  exophthalmos  may  be  very  slight 
indeed.  ^Vhile  it  is  true  that  the  exophthalmos  may  not  be  equally  developed 
on  both  sides,  it  is  nearly  always  bilateral,  although  a  few  instances  of  uni- 
lateral exophthalmos  have  been  reported. 

Under  the  name  of  von  Graeje's  sign,  a  condition  is  found,  in  which,  if 
the  patient  is  directed  to  look  at  the  floor,  the  upper  eyelid  does  not  follow 
the  eyeball  in  its  downward  rotation  as  rapidly  as  it  should.  This  sjTuptom 
is  not  always  present.  Stelwag's  sign  consists  in  a  widening  of  the  palpebral 
fissure,  with  retraction  of  the  lids,  to  such  an  extent  that  the  sclerotic  coat  of 
the  eye  is  seen  above  and  below  the  iris.  This  very  distinctly  increases  the 
exophthalmic  effect.  With  this  symptom  there  is  also  diminished  reflex 
excitability,  so  that  winking  is  delayed  when  a  sudden  movement  is  made 
toward  the  patient.  Under  the  name  of  Mohius'  sign  is  described  a  con- 
dition in  which  there  is  a  lack  of  power  of  convergence,  so  that  if  a  pencil 
is  brought  near  the  patient's  face  the  eyes  cannot  converge,  as  they  do  in  a 
normal  individual. 

Notwithstanding  the  exophthalmos,  vision,  as  a  rule,  is  not  interfered  with, 
but  ulceration  of  the  cornea  sometimes  occurs  as  the  result  of  the  inability  of 
the  eyelids  to  protect  the  eye.     (See  Fig.  100.) 

The  increase  in  the  size  of  the  thyroid  gland  is  usually  not  very  great,  and 
it  never  becomes  as  large  as  in  many  cases  of  ordinary  goitre. 

On  inspection  the  gland  may  seem  to  pulsate,  and  on  palpation  it  often 
transmits  a  thrill  to  the  finger-tip.  If  the  stethoscope  be  placed  over  the 
gland,  a  distinct  humming  murmur  can  be  heard.  This  same  murmur  is 
also  detected,  even  more  clearly,  if  the  stethoscope  be  placed  over  the 
carotid  arteries. 

The  gland  is  never  very  hard,  but  may  be  soft  and  fluctuating,  and  is  apt 
to  vary  in  size  considerably  from  week  to  week  or  from  day  to  day.  Tachy- 
cardia is  practically  always  present  in  these  cases.  The  pulse  varies  from 
90  to  100  or  even  200  beats  a  minute,  the  ordinary  rapid  pulse  being  very 
much  increased  on  exertion  or  excitement. 

If  the  finger-tips  of  the  patient  are  rested  upon  the  finger-tips  of  the  physi- 
48 


754 


DISEASES  OF   THE   THYROID  GLAND 


cian,  there  can  be  felt  not  infrequently  a  fine  tremor,  sometimes  called  "  rail- 
road bridge  tremor,"  owing  to  its  resemblance  to  the  sensation  produced  in 
one's  feet  when  standing  upon  a  railroad  bridge  during  the  time  a  train  is 
passing  over  it.  In  other  instances  the  tremor  is  very  marked  and  coarse  in 
character. 

The  patient  nearly  always  complains  of  feebleness  and  mental  depression, 
and  in  some  cases  melancholia  may  be  so  profound  as  to  result  in  suicide,  as 
in  a  patient  recently  under  my  observation.  An  irritating  nervous  cough  and 
occasional  attacks  of  dyspncea  may  occur,  and  cases  are  on  record  in  which 


Fig. 100 


Exophthalmic  goitre.     The  illustration  shows  the  enlarged  thyroid  gland.     The  exophthalmos  was  so 
great  that  the  lids  had  to  be  sewed  together  to  protect  the  eyes. 

the  patient  has  suddenly  died  from  urgent  dyspnoea,  which  has  had  its  origin 
in  intense  swelling  of  the  thyroid  gland,  so  that  it  has  pressed  upon  the  trachea 
in  much  the  same  manner  as  does  the  enlarged  thymus  in  status  lymphaticus. 
Another  symptom  which,  when  it  develops,  must  always  be  regarded  with 
alarm,  is  excessive  and  obstinate  vomiting.  This  condition  may  speedily  pass 
by,  but  in  some  cases  it  has  persisted  until  death  has  ensued.  Sudden  attacks 
of  diarrhoea  are  not  rare.  The  digestion  is  fairly  good,  but  the  appetite  is 
uncertain,  and  the  patient  craves  abnormal  things  as  she  does  in  hysteria. 
Oftentimes  a  constant  "rifting  up"  of  wind  gives  great  annoyance.  The 
nervousness  is  so  intense  that  in  many  cases  the  patient's  life  is  almost  unbear- 
able because  of  the  irritation  produced  by  noises  and  other  sources  of  irrita- 
tion which  ordinarily  would  not  be  noticed.  Nervous  chills  or  tremblings  are 
often  a  source  of  great  annoyance  to  the  patient,  and  the  palms  of  the  hands 


EXOPHTHALMIC  GOITRE  755 

are  prone  to  be  wet  with  excessive  perspiration.  Patches  of  pigmentation  on 
the  skin  often  develop.  There  is  usually  distinct  loss  of  weight  and 
strength. 

Prognosis. — A  certain  number  of  cases  of  exophthalmic  goitre  undoubtedly 
recover,  but  they  are  always  liable  to  relapse.  Rapid  loss  of  flesh  and 
strength,  marked  tachycardia,  persistent  vomiting,  and  diarrhoea  are  all  of 
them  symptoms  which  would  cause  us  to  give  a  guarded  or  unfavorable 
prognosis.  Whereas,  if  the  symptoms  are  mild,  we  have  a  right  to  feel  corre- 
spondingly encouraged.  Sometimes  exophthalmic  goitre  may  last  so  short 
a  time  as  a  few  days  or. weeks.  In  other  instances  it  may  continue  for  many 
years. 

Treatment. — The  treatment  of  exophthalmic  goitre  is  not  very  satisfactory. 
When  the  thyroid  gland  was  first  used  as  a  therapeutic  agent  it  was  given  to 
a  considerable  number  of  persons  suffering  from  exophthalmic  goitre,  with 
the  idea  that  it  might  do  good,  but  from  the  first  it  must  have  been  manifest 
that  it  could  not  be  of  value  because  the  patient  is  suffering  from  too  much 
thyroid  secretion,  and  the  addition  of  more  of  the  thyroid  substance  must  in 
consequence  be  disadvantageous. 

Lupine  has  recommended  antithyroid  serum  in  the  treatment  of  Graves' 
disease.  This  serum  is  obtained  from  animals  immunized  against  hyper- 
thyroidism. Under  the  name  of  thyroid  serum  Moebius  has  given  us  serum 
derived  from  sheep  from  which  the  thyroid  gland  had  been  removed  six 
weeks  before.  The  dose  is  1  to  5  c.c.  three  times  a  day,  given  by  the  mouth. 
A  similar  preparation  is  prepared  in  this  country  by  Parke,  Davis  &  Co., 
and  is  called  "Thyroidectin."     The  dose  is  5  to  10  grains  t.  i.  d.,  in  capsules. 

In  most  instances  the  patient  should  receive  a  carefully  carried  out  rest 
cure,  extending  over  a  period  of  from  four  to  six  weeks,  with  regulation  of 
the  diet  and  massage  and  electricity.  Sometimes  a  course  of  hydrotherapy 
is  advantageous,  and  change  of  air  and  scene  is  particularly  valuable  if  the 
patient  has  been  subjected  to  nervous  stress.  All  forms  of  exercise  or  gayety 
which  tend  to  exhaust  the  nervous  system  should  be  forbidden. 

The  drugs  which  seem  to  be  of  most  benefit  are  those  which  belong  to 
the  class  of  sedatives.  When  the  heart's  action  is  very  excessive,  I  have 
known  full  doses  of  tincture  of  veratrum  viride  to  be  most  advantageous, 
in  that  they  quiet  the  heart  not  only  by  depressing  its  muscle,  but  also  by 
stimulating  the  pneumogastric  nerve.  In  other  instances  the  bromides  may  be 
employed.   In  still  other  cases  I  have  seen  gelsemium  employed  to  advantage. 

The  disadvantage  of  opium  or  morphine,  for  the  production  of  nervous 
quiet,  is  the  danger  of  establishing  the  "habit."  This  is  a  very  real  danger 
in  these  patients,  because  of  their  lack  of  nervous  equilibrium.  Sometimes 
belladonna  may  be  given  with  advantage  to  quiet  the  circulatory  and 
nervous  excitement. 

Within  the  last  twenty  years  a  very  large  number  of  operations  have 
been  performed  upon  patients  with  exophthalmic  goitre,  with  the  object  of 
curing  the  disease.  In  some  instances  the  thyroid  arteries  have  been  tied. 
In  others  the  capsule  of  the  gland  has  been  stripped  from  it  and  made  fast 
in  the  wound,  so  that  the  tissues  will  shrivel.  In  still  another  class  of  cases 
the  cervical  sympathetic  has  been  cut,  and  Jaboulay  has  strongly  advocated 


756  DISEASES  OF   THE   THYROID  GLAND 

this  measure.  The  value  of  operative  procedure  is,  however,  well  summed 
up  by  my  colleague,  J.  Chalmers  Da  Costa,  who  says: 

"  Treat  most  cases  medically  and  by  rest;  if  medical  treatment  fails, 
consider  the  advisability  of  surgical  treatment. 

"  Do  not  operate  if  there  is  great  hysteria;  if  the  gland  is  very  large, 
thyroidectomy  will  fail;  if  the  gland  is  very  small,  it  will  do  no  good  to 
remove  it. 

"  If  the  symptoms  are  urgent,  if  the  goitre  is  distinct,  but  not  excessively 
large,  if  it  has  relapsed  under  medical  treatment,  or  if  the  patient  refuses  to 
submit  to  the  necessary  restrictions  of  medical  treatment,  perform  thyroid- 
ectomy. 

"  Take  Kocher's  advice,  and  do  not  promise  cure,  but  realize  that  the 
patient  may  die  or  there  may  be  a  partial  cure. 

"When  thyroidectomy  is  performed  do  not  remove  the  entire  gland.  Remove 
one  lobe  only,  or  one  lobe  and  a  half  or  two-thirds  of  the  remaining  lobe. 
Even  so-called  complete  thyroidectomies  are  not  often  really  complete,  as  a 
remnant  of  the  processus  pyramidalis  is  usually  left  behind.  In  addition  to 
removing  a  part  of  the  gland,  take  Kocher's  advice  and  tie  three  of  the  four 
thyroid  arteries. 

"  Do  not  give  a  general  anaesthetic,  but  produce  local  ansesthesia  (Kocher). 
A  general  anaesthetic  is  very  dangerous  in  goitre  operations." 

In  advanced  cases  with  threatened  suffocation,  it  may  be  necessary  to  do 
tracheotomy.  If  the  goitre  is  small,  if  the  symptoms  are  marked,  and  do 
not  yield  to  rest  and  medical  treatment,  and  the  patient  refuses  thyroid- 
ectomy, we  can  perform  bilateral  resection  of  the  cervical  sympathetic 
ganglia. 

MYX  (EDEMA. 

Definition. — Myxoedema  is  a  disease  in  which  extraordinary  nutritional 
changes  take  place  in  the  body  as  the  result  of  absence,  atrophy,  removal, 
or  inactivity  of  the  thyroid  gland.  It  is  characterized  by  a  peculiar  swelling 
of  the  subcutaneous  tissues,  by  falling  of  the  hair,  by  mental  failure,  and  by 
feebleness  of  the  circulation.  Myxoedema  is  closely  related  to  cretinism  in 
children.     It  is  sometimes  called  "Athyrea"  and  "Gull's  disease." 

Etiology. — The  cause  of  myxoedema  is  failure  of  the  body  to  receive  the 
normal  quantity  of  secretion  from  the  thyroid  gland.  In  this  sense  it  may 
be  considered  the  antithesis  of  exophthalmic  goitre.  The  cause  of  the 
atrophy  or  inactivity  of  the  gland  is  unknown. 

Myxoedema  occurs  more  frequently  in  married  than  in  single  women,  and 
it  appears  most  commonly  after  thirty  years  of  age.  It  affects  women  and 
men  in  the  proportion  of  6  to  1. 

Pathology  and  Morbid  Anatomy. — When  the  thyroid  gland  undergoes 
atrophy,  when  it  is  removed  by  surgical  operation,  and  when,  as  the  result  of 
a  specific  infection,  as  actinomycosis  or  morbid  growth,  its  function  is 
destroyed,  myxoedema  ensues.  In  most  cases  the  atrophy  of  the  thyroid 
gland  can  be  readily  recognized,  but  in  others  the  gland  may  seem  larger 
than  normal.    This  increase  in  size  may  be  due  to  infiltrations,  tumors,  cysts, 


MYXCEDEMA  757 

subacute  or  chronic  inflammatory  processes  leading  to  an  overgrowth  of 
the  connective  tissue  of  the  gland,  and  is  not  a  sign  of  any  actual  increase  in 
glandular  structure. 

The  state  of  the  subcutaneous  tissues  is  very  remarkable.  They  are  puflpy 
and  swollen,  and  if  incised  are  found  infiltrated  with  a  mucoid  or  jelly-like 
material.  This  material  is  present  in  such  excessive  quantities  that  the 
cutaneous  glands  are  pressed  upon  and  their  nutrition  interfered  with,  so  that 
the  skin  becomes  dry  and  harsh,  and  the  hair  falls  out.  Nor  does  this  process 
of  infiltration  cease  with  the  involvement  of  the  subcutaneous  tissues,  for 
in  the  liver  and  in  the  kidneys  the  cells  are  pushed  apart  and  compressed. 
The  kidneys  are  larger  than  normal,  and  considerably  toughened  in  texture. 

Frequency. — Myxoedema  is  a  rare  disease,  particularly  in  the  United  States. 
Physicians  connected  with  large  hospitals  may  see  a  case  only  once  in  many 
years. 

Symptoms. — ^The  symptoms  of  myxoedema  are  infiltration  of  the  tissues  of 
the  entire  body,  so  that  they  appear  at  first  glance  to  be  dropsical,  but  they 
do  not  "pit"  on  pressure  and  are  quite  firm  and  resistant.  The  skin  is  dry, 
pallid,  and  poorly  nourished,  the  hair  falls  till  only  a  few  strands  are  left,  and 
the  eyebrows  disappear.  The  expression  is  altered  by  the  obliteration  of  the 
facial  lines,  and  by  the  stupidity  from  which  the  patient  suffers,  for  a  form  of 
mental  inertia  develops.  As  the  disease  advances  muscular  feebleness  often 
arises,  so  that  the  patient  falls,  and  there  may  be  difficulty  in  holding  the 
head  erect.  The  temperature  is  slightly  subnormal,  the  heart  is  feeble,  and 
albuminuria  is  sometimes  present. 

Prognosis. — The  prognosis  depends  entirely  upon  the  treatment.  If  no 
specific  treatment  is  resorted  to  death  invariably  ensues  as  a  result  of  general 
asthenia  or  from  some  intercurrent  malady.  If  specific  treatment  is  adequate 
recovery  usually  takes  place,  provided  the  patient  is  not  seen  until  after  the 
disease  is  very  far  advanced. 

Treatment. — Aside  from  the  use  of  antitoxin  in  diphtheria,  there  is  no 
therapeutic  measure  which  produces  such  extraordinary  results  and  acts  in 
so  specific  a  manner  as  the  administration  of  thyroid  gland  in  myxoedema 
and  in  cretinism.  The  dried  thyroid  gland  of  the  sheep  should  be  given  the 
patient  in  gradually  ascending  doses,  beginning  with  2  grains  in  capsule 
twice  or  thrice  a  day,  and  gradually  increasing  the  amount  until  10  to  15 
grains  are  taken  daily,  provided  the  patient  does  well  on  these  doses  and 
seems  to  need  large  quantities.  When  the  extract  of  the  thyroid  gland  is 
used,  the  dose  is  ^  grain  three  times  a  day  to  start  with.  Meltzer  states  that 
the  extract  and  dried  gland  prepared  by  Parke,  Davis  &  Co.  have  given  him 
the  best  results.  When  overdoses  are  taken  symptoms  of  cardiac  weakness 
develop.  These  are  dangerous  and  should  be  controlled  by  the  use  of  strych- 
nine and  by  insisting  that  the  patient  remain  in  bed  for  several  days.  Indeed, 
rest  in  bed  is  the  safer  plan  whenever  ascending  doses  are  being  employed. 
After  thyroid  gland  has  been  given  long  enough  to  cause  great  improvement, 
so  that  the  patient  is  practically  well,  it  is  essential  that  about  one-half  the 
dose  be  continued  indefinitely  or  at  certain  periods,  in  order  to  prevent  a 
relapse,  for  the  sheep's  thyroid  must  take  the  place  of  the  wasted  gland  in 
the  neck. 


758 


DISEASES  OF  THE  THYROID  GLAND 


As  these  patients  are  very  susceptible  to  cold,  they  should  be  carefully 
clothed  and  sent  to  a  warm  climate  in  the  winter  months,  if  possible. 


CRETINISM. 

Definition. — Cretinism  is  sometimes  called  congenital  myxoedema,  or  the 
myxoedema  of  childhood,  and  depends  upon  the  same  causes  as  does  myx- 
oedema, in  that  the  curious  systemic  changes  which  develop  in  the  patient  are 
the  result  of  an  absence  of  the  secretion  of  the  thyroid  gland. 

Cretinism  occurs  in  two  forms,  as  endemic  cretinism  and  sporadic  cretinism. 

The  conditions  leading  to  thyroid  absence  or  inadequacy  are  not  known. 
It  is  true  that  in  some  instances  the  results  of  the  marriage  of  near  relatives 


Fig.  101 


Fig.  102 


A  case  of  cretinism,  showing  the  improvement  produced  by  the  administration  of  thyroid  gland. 

(Davisson's  case.) 

or  the  presence  of  a  tuberculous  history  has  seemed  to  indicate  that  there 
might  be  some  connection  between  these  factors  and  the  development  of  the 
disease,  but  in  most  cases  these  causes  are  absent. 

Symptoms. — The  symptoms  of  cretinism  rarely  develop  before  the  end  of 
the  second  year,  but  the  symptoms  may  be  noticeable  from  the  time  the  child 
is  twelve  months  of  age,  when  the  parents  usually  consider  that  the  child  is 
somewhat  "backward."  At  this  time  it  is  found  to  be  stunted  and  mentally 
dull.    The  head  and  the  hands  and  feet  may  seem  unduly  large  in  proportion 


CRETINISM  759 

to  the  size  of  the  trunk  and  Hmbs.  The  face  is  stupid  and  heavy,  and  the  eyes 
dull.  The  palpebral  openings  are  narrow  and  elongated,  and  the  nose  is  broad 
and  flat,  with  heavy  nostrils.  The  lips  are  coarse,  are  apt  to  protrude,  are 
usually  held  apart,  and  not  infrequently  there  is  a  good  deal  of  dribbling  of 
saliva.  The  tongue  is  swollen,  and  there  seems  to  be  some  weakness  of  the 
cervical  muscles,  so  that  the  head  is  not  well  carried  on  the  shoulders.  An 
anteroposterior  curvature  of  the  spinal  column  is  often  present,  so  that  the 
abdomen  is  very  much  protruded.  The  legs  are  short  and  bent,  as  in  rickets, 
and  the  skin  is  sallow  and  greasy.  The  hair  is  scanty  and  brittle,  and  the  skin 
is  badly  nourished.  The  temperature  is  subnormal,  but  there  are  no  important 
changes  in  either  the  urine  or  the  blood.  The  most  marked  alterations  from 
normal  in  the  blood  are  a  diminution  in  the  quantity  of  haemoglobin.  In 
many  instances  the  child  has  little  more  intelligence  than  that  which  is 
needed  to  take  its  food.    In  other  cases  it  is  vicious  and  dirty. 

An  autopsy  in  a  case  of  cretinism  usually  reveals  an  absence  of  the 
thyroid  gland,  its  place  being  taken  by  a  few  fatty  granules,  or  by  a  fibro- 
cystic growth.  On  opening  the  skull  there  is  found  to  be  an  excess  of  intra- 
ventricular and  interarachnoid  fluid. 

Diagnosis. — There  is  no  difficulty  in  diagnosticating  cretinism  if  a  typical 
case  is  presented.  Given  a  patient  suffering  from  rickets  and  idiocy,  some 
resemblance  to  true  cretinism  may  be  present,  but  the  state  of  the  skin  and 
hair  and  the  absence  of  the  thyroid  gland  in  true  cretinism  render  a  separa- 
tion possible. 

Prognosis. — The  prognosis  in  cretinism  is  very  good,  even  better  than  in  the 
myxoedema  of  adults,  provided  the  treatment  is  instituted  while  the  patient 
is  yet  a  child  in  years.  If  the  patient  has  survived  till  adult  years  are  reached, 
the  results  are  not  so  satisfactory  and  extraordinary. 

Treatment. — The  treatment  consists  in  the  administration  of  thyroid  gland 
or  thyroid  extract,  beginning  with  |  of  a  grain  of  the  extract  three  times  a 
day  and  gradually  increasing  it,  or  using  1  or  2  grains  of  the  dry  gland  once, 
twice,  or  thrice  a  day,  according  to  the  size  and  age  of  the  child.  Under  the 
administration  of  these  substances  the  most  remarkable  change  takes  place 
in  the  patient.  The  first  noticeable  alteration  is  a  great  decrease  in  body 
weight,  with  a  similar  decrease  in  the  bulkiness  of  the  child.  The  skin 
becomes  more  moist  and  appears  better  nourished,  and  the  expression 
improves.  There  is  also  an  improvement  in  the  color  of  the  skin  and  in  the 
quantity  of  haemoglobin  in  each  blood  corpuscle.  Still  later,  after  this  pri- 
mary decrease  in  weight,  a  real  improvement  in  nutrition  takes  place,  and 
the  child  begins  to  gain,  so  that  it  no  longer  looks  stunted,  but  appears  more 
like  a  healthy  individual.  The  mental  improvement  is  perhaps  the  slowest 
part  of  the  cure,  and  in  some  instances  the  mind  never  fully  reaches  the 
development  of  that  of  a  healthy  child,  although  the  nutrition  of  the  body  may 
be  excellent.  The  effect  of  the  administration  of  thyroid  upon  the  growth  of 
the  teeth  is  equally  remarkable  with  that  upon  the  general  nutrition.  Before 
thyroid  is  given  the  milk  teeth  are  usually  badly  formed  and  rapidly  decay; 
but  if  thyroid  is  administered  freely  before  the  permanent  tooth  appear,  they 
are  often  developed  as  they  would  be  in  the  jaws  of  a  healthy  child. 


760  DISEASES  OF   THE  SUPRARENAL  GLANDS 

DISEASES  OF  THE  SUPRARENAL  GLANDS. 

ADDISON'S  DISEASE. 

Definition. — The  name  Addison's  disease  is  applied  to  a  condition  in  which 
the  patient  suffers  from  a  characteristic  pigmentation  of  the  skin,  pallor,  and 
loss  of  strength,  and  in  which  the  chief  microscopic  changes  are  alterations  in 
the  suprarenal  bodies. 

History. — Addison's  disease  gets  its  name  from  Thomas  Addison,  the 
physician  who  first  clearly  described  the  malady  in  1849  at  Guy's  Hospital, 
London.  The  condition  did  not  receive  attention  from  the  profession  in 
general  until  1854,  when  Addison  wrote  a  special  monograph  on  the 
subject. 

Etiology  and  Pathology. — ^The  cause  of  Addison's  disease  is  not  known  in 
the  sense  that  we  recognize  a  cause  which  is  responsible  for  all  cases.  In 
about  50  per  cent,  of  the  cases  so  far  reported  which  have  come  to  autopsy, 
tuberculosis  of  the  suprarenal  glands  has  been  found.  That  this  lesion  is  not 
sufficient  in  all  cases  to  cause  the  general  systemic  manifestations  of  the  dis- 
ease is  proved  by  the  fact  that  identical  changes  have  been  found  in  the  supra- 
renal bodies  when  none  of  these  s}Tiiptoms  have  been  present.  In  certain 
cases  hemorrhages  into  the  suprarenal  bodies  as  the  result  of  injuries  have 
caused  the  symptoms  to  develop. 

As  a  matter  of  fact,  the  view,  as  to  the  relationship  of  these  causes  to  the 
disease,  expressed  by  Addison  fifty  years  ago  is  probably  correct,  namely, 
that  any  lesion  of  these  bodies  which  interferes  with  their  function  may  cause 
the  malady. 

In  some  instances  the' disease  seems  to  be  primarily  the  result  of  patholog- 
ical changes  in  the  semilunar  ganglia  of  the  abdominal  sympathetic  nervous 
system.  Rolleston  has  expressed  the  plausible  view  that  in  these  cases  the 
disease  arises  in  all  probability  by  reason  of  the  fact  that  the  glands  are 
cut  off  in  circulation  and  nerve  supply  by  growths  or  inflammatory  exu- 
dates. 

Morbid  Anatomy. — -The  common  lesion  in  cases  of  Addison's  disease  is, 
as  already  stated,  tuberculosis,  and  next  to  this  in  frequency  is  atrophy.  The 
tuberculous  change  is  of  the  fibrocaseous  type,  except  in  rare  instances,  and 
usually  begins  in  the  medulla  of  the  gland.  The  stage  of  infiltration  is 
followed  by  caseation  and  commonly  more  or  less  fibrosis;  in  other  words, 
there  is  an  attempt  at  healing.  The  fibrocaseous  area  may  be  restricted  to 
the  adrenal  or  extend  beyond  it.  Calcification  is  not  uncommon,  and 
pyogenic  infection  may  cause  abscess.  The  tuberculous  process  may  be 
primary  and  confined  to  the  adrenal  body,  as  in  the  two  cases  reported  by 
Symes  and  Fisher. 

In  the  form  of  the  disease  in  which  atrophic  changes  occur  in  the  glands, 
the  wasting  may  be  so  complete  that  only  a  small  fibrous  mass  remains  to 
indicate  their  former  existence.  In  still  others  an  overgrowth  of  fibrous  tissue 
resembling  the  sclerosis  found  in  the  other  organs  of  the  body  may  take  place. 


ADDISON'S  DISEASE  761 

with  secondary  atrophy  of  the  parenchyma.  Peterson  has  collected  26  such 
cases.  In  still  other  cases  the  glands  have  been  found  to  be  the  seat  of  hemor- 
rhage (adrenal  apoplexy),  thrombosis  of  the  vessels,  or  malignant  disease. 
The  changes  found  in  the  semilunar  ganglia  and  in  the  plexuses  composing 
the  abdominal  sympathetic  system  are,  as  already  stated,  in  all  probability, 
indirect  causes  of  the  disease,  although  Hale  White  has  shown  that  changes 
take  place  in  these  tissues  in  ordinary  individuals  as  the  result  of  advancing 
age.  It  is  difficult  to  determine,  therefore,  whether  the  reports  of  changes  in 
these  tissues  made  by  some  observers  have  been  really  etiological  factors  in 
the  disease.  Further,  a  very  large  proportion  of  cases  in  which  Addison's 
disease  has  been  present  have  failed  to  show  alterations  in  the  semilunar 
ganglia  or  in  the  abdominal  sympathetic.  In  some  cases  a  hyperplasia  of 
the  lymphoid  structures  in  the  alimentary  canal  has  been  noted. 

Finally,  it  is  not  to  be  forgotten  that  Addison's  disease  may  be  present 
without  noticeable  lesions  in  the  suprarenal  bodies,  and  it  is  also  a  fact  that 
these  bodies  may  be  almost  completely  destroyed  by  a  growth  or  by  tuber- 
culosis without  any  symptoms  of  this  malady  developing. 

The  pigmentation  of  the  skin  is  due  to  the  deposition  of  pigment  in  the 
cells  of  the  Malpighian  stratum,  and  according  to  Earkshevitch,  who  studied 
the  skin  removed  from  a  living  subject,  in  the  subjacent  tissues.  The  pig- 
mented cells  are  supposed  to  obtain  their  pigment  from  the  haemoglobin  of 
the  blood,  but  they  contain  no  iron.  The  discoloration  of  the  mucous  mem- 
branes is  due  also  to  the  deposit  of  pigment.  The  pigmentation  of  the 
mucous  membranes  is  in  patches,  and  Mann  asserts  that  it  is  deposited  only 
where  the  parts  are  rubbed  or  subjected  to  causes  that  produce  hypersemia. 

That  there  have  been,  and  are  in  existence  at  present,  several  theories  as 
to  the  lesions  which  result  in  Addison's  disease  must  have  been  evident  from 
what  has  already  been  said.  The  only  ones  that  have  received  general 
recognition  have  been  the  "nervous  theory,"  that  the  disease  was  due  to 
changes  in  the  abdominal  nervous  apparatus;  or  the  original  theory  of 
Addison,  that  it  is  due  to  failure  of  the  suprarenal  glands  to  carry  out  their 
normal  function.  The  nervous  theory  has  now  been  generally  cast  aside, 
and  we  have  left  Addison's  own  proposition  modified  by  our  extended 
knowledge  of  internal  glandular  secretion.  Space  does  not  permit  a  discus- 
sion of  the  views  for  and  against  this  opinion.  These  can  be  found  exhaust- 
ively, and  most  capably,  discussed  by  Rolleston  in  Allbutt's  System  of 
Medicine,  vol.  iv.  Suffice  it  to  say,  that  the  opinion  generally  held  to-day  is 
that  these  symptoms  come  on  because  the  suprarenal  secretion  fails  to  find 
its  way  into  the  general  economy.  Changes  in  the  sympathetic  nervous 
system  may  also  be  a  factor. 

Symptoms. — The  symptoms  of  Addison's  disease  are  chiefly  those  which 
are  represented  by  the  term  general  asthenia.  The  patient  gives  the  history 
of  being  easily  tired  and,  indeed,  of  a  constant  sense  of  fatigue.  Even  after 
a  night's  rest  he  feels  as  weary  in  the  morning  as  when  he  went  to  bed.  The 
sensation  of  feebleness  is  associated  with  profound  muscular  weakness  as 
the  disease  progresses,  but  there  is  little  or  no  true  emaciation.  The  term 
"  invincible  languor  "  used  by  Rolleston  well  describes  the  patient's  state.  An 
examination  of  the  heart  shows  its  muscle  is  greatly  enfeebled,  so  that  the 


762  DISEASES  OF    THE  SUPRARENAL  GLANDS 

cardiac  sounds  are  lacking  in  normal  tone.  The  'pulse  is  so]t,  and  easily 
extinguishable  by  the  pressure  of  the  finger.  The  extremities  are  cold  and 
the  general  body  temperature  may  be  subnormal.  Anae.mia  is  well  marked, 
but  usually  not  excessive,  the  blood  cells  being  decreased  to  3,000,000  or  a 
little  lower. 

No  mention  as  yet  has  been  made  among  this  list  of  symptoms  of  the  one 
characteristic  manifestation  of  the  malady  which  is  practically  pathog- 
nomonic, namely,  the  pigmentation  of  the  skin.  While  its  peculiarities 
would  naturally  lead  one  to  speak  of  it  first,  mention  of  it  has  been  delayed 
because  its  appearance  is  often  delayed  until  the  other  symptoms  are  quite 
well  developed.  In  other  words,  it  usually  follows  and  does  not  precede 
the  constitutional  manifestations  of  the  disease.  There  are,  however,  rare 
exceptions  to  this,  and  cases  have  been  recorded  in  which  the  pigmentation 
has  been  present  for  long  periods  before  any  other  signs  of  Addison's  dis- 
ease developed.  The  pigmentation  may  be  over  the  entire  body,  but  as  a 
rule  it  is  in  patches,  and  chiefly  affects  the  skin  of  the  face,  of  the  neck,  and 
the  extensor  surfaces  of  the  hands  and  forearms.  If  the  mucous  membrane 
of  the  mouth  is  examined  the  lips  at  the  point  of  contact  are  noticeably 
darkened  and  the  edges  of  the  tongue,  particularly  on  its  under  surface,  may 
show  discoloration  as  if  ink  had  been  taken  into  the  mouth. 

Diagnosis. — Except  in  well-defined  cases  it  may  require  weeks  or  months 
of  watching  to  determine  that  a  patient  has  this  malady.  Pregnancy  not 
rarely  is  associated  with  the  presence  of  pigmented  spots  on  the  skin,  but 
the  condition  of  the  uterus  and  its  contents  prevent  a  mistake  being  made 
as  to  the  cause.  In  some  cases  of  hypertrophic  cirrhosis  of  the  liver  there 
may  be  in  addition  to  jaundice  very  marked  pigmentation.  I  have  under 
my  care  at  the  time  this  is  written  a  man  who  has  hypertrophic  cirrhosis, 
jaundice,  and  such  deep  pigmentation  of  the  skin  that  he  looks  as  if  coated 
with  coal-dust.    In  such  a  case  the  state  of  the  liver  reveals  the  cause. 

In  the  rare  malady  called  diabetes  bronze,  in  which  there  is  hypertrophic 
cirrhosis,  jaundice,  diabetes,  and  pigmentation  of  the  skin,  the  state  of  the 
liver  and  urine  will  aid  in  the  differentiation.  In  certain  cases  of  advanced 
pulmonary  tuberculosis  the  skin  is  pigmented  a  dirty  brown,  and  in  patches 
may  be  considerably  discolored,  but  here  the  pulmonary  state  prevents  con- 
fusion as  to  its  cause. 

The  prolonged  use  of  arsenic  may  have  a  similar  effect,  not  only  on  the 
extremities,  but  on  the  skin  of  the  chest  and  abdomen,  which  may  become 
much  darker  than  normal  without  any  neuritis  being  present.  In  syphilitics 
the  site  of  old  eruptions  may  be  stained,  and  in  vagabonds  who  are  infested 
with  lice,  and  have  been  much  exposed  to  the  weather,  areas  of  discoloration 
of  the  skin  may  be  present.  It  is  said  that  the  discoloration  of  the  skin  called 
chronic  argyria,  due  to  the  prolonged  use  of  silver  internally,  has  been  con- 
fused with  the  state  of  the  skin  in  Addison's  disease.  This  would  be  scarcely 
possible  if  the  observer  had  ever  seen  a  case  of  chronic  silver  poisoning, 
for  the  discoloration  of  argyria  is  a  peculiar  lividity  rather  than  a  pigmenta- 
tion, and  it  is  uniform  on  exposed  parts  of  the  body. 

As  Addison's  disease  is  due  in  a  large  proportion  of  cases  to  tuberculosis 
of  the  adrenal  bodies,  the  tuberculin  test  may  be  employed  to  give  additional 


ADDISON'S   DISEASE  763 

information  In  the  case;  but  even  if  this  test  is  positive  the  possibihty  of 
tuberculous  foci  elsewhere  giving  the  reaction,  and  the  fact  that  syphilitics 
sometimes  react,  should  make  us  hesitate  before  resting  too  heavily  upon 
this  means  of  diagnosis. 

Prognosis. — It  may  be  stated  that  given  a  patient  w^ith  Addison's  disease 
developed  so  far  that  a  diagnosis  is  certain,  then  death  from  the  malady  is 
certain  also.  Lewin  in  a  collection  of  500  cases  found  that  5  were  cured 
and  28  improved.  In  the  2  cases  I  have  seen,  1  of  which  is  now  under' 
observation,  the  disease  had,  at  times,  certainly  been  arrested  in  its  progress 
under  the  use  of  full  doses  of  suprarenal  gland.  Because  of  the  gradual 
development  of  the  malady,  its  average  duration  is  difficult  to  determine, 
but  its  course  is  not  very  rapid.  Wilks  believes  it  to  be  about  eighteen 
months,  but  in  some  cases  it  lasts  for  years.  Very  rapidly  fatal  cases  are 
also  on  record. 

Treatment. — ^The  question  of  the  proper  plan  of  treatment  of  Addison's 
disease  cannot  be  answered  positively  until  the  pathologist  is  able  to  give  us 
a  clear  conception  of  the  morbid  processes  which  produce  the  chain  of 
symptoms  already  described.  The  very  fact  that  different  pathological 
changes,  or  diseases,  affect  the  suprarenal  bodies,  and  so  produce  the  symp- 
toms of  this  malady,  indicates  that  the  therapy  must  vary  with  the  cause. 
Theoretically  the  use  of  suprarenal  gland  of  the  sheep  is  indicated  in  every 
case,  but  practical  experience  has  shown  that  only  in  a  small  proportion  of 
those  cases  in  which  it  has  been  used  has  it  done  good.  It  is  not,  therefore, 
to  be  compared  to  the  value  of  thyroid  gland  in  myxoedema  or  cretinism. 
It  has  been  proved  that  suprarenal  gland  has  little  effect  on  blood  pressure 
if  it  is  taken  by  the  stomach,  arid  that  its  active  principle  when  in  concen- 
trated form  often  causes  abscess  when  it  is  given  hypodermically.  Probably 
the  best  plan  is  to  give  the  patient  adrenalin  chloride  in  normal  salt  solution 
by  hypodermoclysis  every  day  or  every  other  day,  using  1  to  2  drachms  of 
the  adrenalin  chloride  (1 :  1000  solution),  as  put  upon  the  market,  to  a  half- 
pint  or  pint  of  saline  fluid.  When  the  desiccated  gland  is  used  by  the 
mouth,  from  2  to  10  grains  may  be  given  three  times  a  day  in  capsule.  It 
is  unfortunately  true  that  even  when  the  adrenalin  gland  is  freely  used,  the 
disease  is,  at  the  best,  only  delayed  in  its  progress  in  most  cases. 

Adams  has  collected  97  cases  treated  with  suprarenal  gland.  Of  these 
7  were  made  worse,  43  experienced  no  real  benefit,  31  showed  marked 
improvement,  and  16  were  said  to  be  cured.  In  the  successful  cases  the 
gland  was  given  solely  by  the  mouth.  If  the  patient  is  at  all  feeble  he  should 
be  kept  in  bed,  not  only  because  in  this  manner  we  conserve  his  flagging 
energies,  but  also  because  a  number  of  cases  of  syncope  and  sudden  death 
from  this  disease  have  occurred  in  patients  who  have  made  a  sudden  effort. 
An  easily  digested  diet,  the  avoidance  of  purgatives  which  may  induce 
dangerous  purging,  and  the  use  of  iron  and  arsenic  as  tonics  form  the  rest 
of  the  treatment. 


764  DISEASES  OF  THE  SPLEEN 


DISEASES  OF  THE  SPLEEN. 

Diseases  of  the  spleen  occurring  independently  of  other  diseases  may  be 
said  not  to  exist.  In  myelogenous  leuksemia,  in  splenic  ansemia,  in 
malarial  fever,  and  in  cases  of  hepatic  cirrhosis  or  heart  disease,  the  spleen  is 
often  greatly  enlarged,  but  in  no  case  is  this  condition  primary.  So,  too, 
in  the  prolonged  infectious  fevers,  such  as  typhoid  fever,  the  spleen  is 
usually  swollen. 

In  some  cases  the  surface  of  the  spleen  may  be  traversed  by  a  crevice  or 
indentation  which  almost  divides  its  body  into  different  parts,  and  in 
others  there  may  be  found  an  accessory  spleen  or  accessory  spleens  in 
nearby  parts  of  the  abdominal  cavity.  In  very  old  people  the  spleen  is  often 
greatly  atrophied. 

An  infarct  of  the  spleen  is  due  to  an  embolus  which  usually  has  its  origin 
in  the  heart,  or  which  arises  from  some  area  of  septic  infection,  or  in  other 
cases  a  thrombus  forms  in  the  splenic  vein  and  produces  a  similar  effect. 
The  latter  condition  is  the  cause  of  the  infarct  met  with  in  typhoid  fever 
and  in  leukaemia. 

Abscess  of  the  spleen  as  the  result  of  septic  infection  is  by  no  means  rare, 
and  such  abscesses  always  depend  upon  infected  emboli. 

Hydatid  cyst  of  the  spleen  is  rare  not  only  because  hydatid  cyst  is  rare  in 
this  country,  but  also  because  it  seldom  develops  in  this  gland  even  in  those 
parts  of  the  world  in  which  hydatid  disease  is  common. 

Malignant  growths  in  the  spleen  are  among  the  rarest  pathological  lesions. 
Primary  growths  are  practically  unknown  and  secondary  growths  are  also 
very  rare.  From  statistics  at  St.  George's  Hospital,  London,  collected  by 
Walker,  it  is  found  that  in  161  cases  of  carcinoma  involving  all  parts  of  the 
body  secondary  growths  appeared  in  the  spleen  seven  times,  and  in  50 
cases  of  sarcoma  the  spleen  was  affected  once.  Taylor  in  677  cases  of 
carcinoma,  epithelioma,  and  sarcoma  found  secondary  growths  in  the 
spleen  in  twenty-three  instances.  Sometimes  in  cases  of  cancer  of  the 
gall-bladder  or  of  the  pylorus  the  growth-  extends  to  the  spleen  by  direct 
invasion. 

Movable  spleen,  like  movable  kidney,  is  a  condition  in  which  this  organ 
wanders  away  from  its  normal  position  so  that  it  may  be  found  far  removed 
from  its  ordinary  area,  and  even  so  low  as  the  pelvis.  Its  displacement  is 
usually  associated  with  a  sense  of  dragging  in  the  left  hypochondrium  or 
loin,  and  if  the  pedicle  becomes  twisted  great  pain  may  be  suffered,  with  fever, 
collapse,  and  finally  necrosis  of  the  splenic  tissues.  Osier  records  a  case  in 
which  this  occurred  and  in  which  abdominal  section  resulted  in  recovery, 
although  a  considerable  part  of  the  spleen  was  lost  by  sloughing. 

It  is  necessary  to  separate  wandering  spleen  from  floating  kidney.  This 
can  be  done  by  the  discovery  of  the  splenic  notch,  by  the  greater  sense  of 
resistance  in  the  otherwise  normal  kidney,  and  by  the  presence  of  reson- 
ance on  percussion  in  the  splenic  area  where  splenic  dulness  is  usually 
demonstrable. 

Rupture  of  the  spleen  is  a  rare  accident,  but  occurs  occasionally  in  those 


SPLENIC  ANEMIA  765 

who,  while  suffering  from  great  congestion  or  enlargement  of  this  organ, 
meet  with  an  accident  in  which  the  splenic  area  is  subjected  to  a  severe 
blow.  Cases  are  also  on  record  in  which  the  spleen  has  ruptured  as  the 
result  of  great  distention.  Rupture  of  the  spleen  will  be  found  discussed 
under  Malaria.  The  symptoms  are  those  of  internal  hemorrhage  and 
demand  an  immediate  abdominal  section. 

The  treatment  of  wandering  spleen  consists  in  the  wearing  of  a  bandage 
and  pad  to  retain  the  organ  in  its  place,  and,  if  need  be,  we  may  resort  to 
an  operation  to  fix  it  by  causing  adhesions  to  form  around  it.  Extirpation 
of  the  spleen  has  been  advised  in  cases  in  which  the  symptoms  are  very  dis- 
tressing, but  this  should  be  done  only  when  the  condition  is  very  urgent; 
for  while  the  spleen  has  been  proved  to  be  not  necessary  to  life,  its  removal 
jeopardizes  existence  and  the  patient  passes  through  a  long  period  of  con- 
valescence before  recovery  occurs. 


SPLENIC  ANEMIA. 

Definition. — ^Axnong  the  types  of  splenomegaly  the  condition  known  as 
splenic  anaemia  is  one  about  which  great  difference  of  opinion  has  existed. 
Its  existence  has  been  denied  by  some  physicians  and  asserted  by  others. 
At  present  it  is  generally  considered  that  a  distinct  morbid  state  to  which 
this  name  may  be  applied  really  exists.  It  is  essentially  a  condition  of 
anaemia  with  enlargement  of  the  spleen,  and  lacks  all  of  the  additional 
conditions  which  are  associated  with  these  states  in  other  maladies,  as,  for 
example,  leukaemia,  lymphadenoma,  or  lymphatic  leukaemia. 

Etiology. — ^This  is  unknown,  but  some  suppose  it  to  be  due  to  intestinal 
infection. 

Pathology  and  Morbid  Anatomy. — An  examination  of  the  spleen  in  this  dis- 
ease shows  that  it  is  not  only  greatly  enlarged,  but  that  it  shows  signs  of  the 
existence  of  a  perisplenitis  with  localized  areas  of  capsular  thickening.  In 
some  portions  of  the  organ  old  infarcts  may  be  found  which  in  turn  have 
caused  puckering  of  its  surface  or  depressed  scars.  When  the  spleen  is  cut 
it  is  found  to  be  more  resistant  to  the  knife  than  normal,  and  it  is  somewhat 
fibroid.  If  a  section  is  placed  under  the  microscope  it  is  found  that  the  con- 
nective tissue  is  increased  and  the  lymphoid  elements  wasted.  The  Mal- 
pighian  bodies  are  fibroid.  There  is  also  in  some  cases  a  marked  prolifera- 
tion of  the  endothelial  cells  which  line  the  blood  sinuses.  These  cells  are 
very  large  and  may  be  so  numerous  as  to  fill  these  spaces  till  they  resemble 
an  endotheliomatous  growth. 

Dock  and  Warthin  have  called  particular  attention  to  hyperplasia  of  the 
haemolymph  nodes  and  thrombosis  of  the  splenic  vein.  The  association  of 
splenic  fibrosis  with  enlargement  and  cirrhosis  of  the  liver  constitute  the 
type  studied  by  Banti  (Banti's  disease),  and  this  is  thought  to  be  a  later 
stage  of  the  process  characterized  in  its  early  manifestations  by  splenic 
enlargement. 

Symptoms.— The  symptoms  of  splenic  anaemia  are  pallor,  dyspnoea  on 
exertion,  and  feebleness  associated  with  enlargement  of  the  spleen.    An  exami- 


766  DISEASES  OF  THE  SPLEEN 

nation  of  the  blood  does  not  throw  any  great  Ught  on  the  character  of  the 
case.  Indeed,  the  blood  changes  are  often  in  no  way  different  from  those 
of  lymphadenoma  or  gumma  of  the  spleen.  The  red  cells  number  about 
3,500,000,  and  the  haemoglobin  equals  about  50  per  cent.  When  the  disease 
is  advanced  poikilocytes  and  nucleated  red  cells  are  present.  The  white 
cells  are  not  increased  as  in  leukaemia,  but  usually  are  below  the  normal 
number,  amounting  to  about  4500  per  c.mm. 

Diagnosis. — The  diagnosis  of  splenic  ansemia  is  very  difficult  and  should 
not  be  reached  until  a  careful  study  of  the  patient's  past  and  present  condi- 
tion has  been  carefully  made  and  his  blood  repeatedly  examined.  A  con- 
siderable number  of  cases  of  so-called  splenic  ansemia  have  proved  to  be 
other  diseases  when  studied  longer  or  examined  postmortem.  All  possible 
causes  for  enlargement  of  the  spleen  should  be  excluded  before  a  decision 
is  reached. 

Splenic  ansemia  must  be  separated  from  the  "  ansemia  infantum  "  of  von 
Jaksch,  in  which  the  spleen  is  enlarged,  but  in  which  the  changes  in  the 
blood  and  in  the  liver  and  spleen  in  no  way  correspond  to  those  seen  in 
splenic  ansemia.  This  condition  must  also  not  be  confused  with  enlargement 
of  the  spleen  due  to  syphilis  with  the  formation  of  gummata;  nor  with  sar- 
coma of  the  spleen ;  nor  with  the  ansemia  of  chronic  malarial  poisoning,  with 
secondary  splenic  enlargement,  nor  with  amyloid  disease.  It  must  also  be 
separated  from  the  ansemia  associated  with  enlargement  of  the  spleen  sec- 
ondary to  cirrhosis  of  the  liver,  and  from  a  condition  described  by  Gaucher 
of  chronic  inflammation  of  the  spleen  {epitheliome  'primitive).  Sometimes, 
too,  in  children  suffering  from  rickets  and  marasmus  with  gastrointestinal 
intoxication,  there  is  a  considerable  degree  of  ansemia  and  some  enlarge- 
ment of  the  spleen.  Such  cases  have  been  thought  to  represent  an  infantile 
form  of  splenic  ansemia,  but  the  subsequent  history  of  the  patient  seems  to 
contradict  this  view. 
RoUeston  gives  the  following  as  the  clinical  characteristics  of  splenic  ansemia: 

1.  Splenic  enlargement  which  cannot  be  correlated  with  any  known  cause. 

2.  Absence  of  enlargement  of  the  lymphatic  glands. 

3.  Ansemia  of  a  type  midway  between  secondary  ansemia  and  chlorosis. 

4.  Leukopenia,  or  at  most  no  increase  in  the  number  of  white  blood 
corpuscles. 

5.  An  extremely  prolonged  course  lasting  years. 

6.  A  tendency  to  periodic  hemorrhages,  especially  from  the  gastrointes- 
tinal tract. 

Prognosis. — The  prognosis  under  medical  treatment  is  always  unfavorable. 

Treatment. — ^The  treatment  consists  in  the  administration  of  full  doses 
of  arsenic,  but,  so  far  as  we  know,  no  method  of  treatment  has  yet  been 
devised  which  materially  alters  the  general  progress  of  the  disease. 

According  to  Harris  and  Herzog,  of  19  cases  subjected  to  splenectomy, 
14  recovered.  To  these  series  Scott  has  added  6  cases  with  4  recoveries. 
Queen  and  Duval  collected  6  cases  and  added  1  original  case  in  which 
removal  of  the  spleen  was  followed  by  a  cure.  They  state  in  addition  that 
a  beginning  hepatic  cirrhosis  may  be  arrested  by  splenectomy,  although  it 
is  difficult  to  understand  how  this  operation  can  exercise  this  effect. 


HODGKIN'S  DISEASE  767 


BANTI'S  DISEASE. 

Under  the  name  of  Banti's  disease  a  condition  characterized  by  enlarge- 
ment of  the  spleen,  an£emia,  cirrhosis  of  the  hver,  jaundice,  and  ascites  is 
met  with.  It  is  thought  by  some  that  Banti's  disease  is  a  terminal  stage  of 
splenic  anaemia;  but,  on  the  other  hand,  it  is  certain  that  this  is  not  always 
the  case.    The  disease  is  very  rare. 


HODGEIN'S  DISEASE. 

Definition. — Hodgkin's  disease  is  a  condition  in  which  there  is  marked 
swelling  and  overgrowth  of  the  lymphatic  glands,  both  internal  and  external, 
with  a  moderate  degree  of  anaemia  which  is  in  no  way  peculiar  to  this  malady. 
The  spleen  is  usually  enlarged.  The  overgrowth  of  the  lymph  nodes  and 
lymphatic  tissues  generally  is  closely  allied  to  malignant  lymphadenoma. 
Another  name  for  the  disease  is  "  pseudoleuksemia." 

History. — Although  a  difference  between  this  state  and  scrofulous  enlarge- 
ment of  the  lymph  nodes  had  been  made  prior  to  1830,  it  w^as  not  until 
Hodgkin  in  1832  described  cases  seen  at  Guy's  Hospital  that  it  was  gen- 
erally recognized.  In  1856  Wilkes  in  London  and  Bonfils  in  France  still 
further  illuminated  the  subject. 

It  was  not  until  Virchow  completed  his  work  on  the  histology  of  the  blood 
that  Hodgkin's  disease  became  clearly  differentiated  from  leukaemia  of  the 
lymphatic  type.  The  fact  that  changes  of  a  peculiar  character  exist  in  the 
lymph  nodes  was  not  known  until  1897,  when  several  investigators,  notably 
Fischer,  described  them. 

Etiology. — ^The  cause  of  Hodgkin's  disease  is  unknown.  Within  the  last 
few  years  the  view  that  it  was  a  peculiar  condition  due  to  infection  by  the 
Bacillus  tuberculosis  gained  a  number  of  adherents,  and  there  are  without 
doubt  certain  facts  connected  with  the  malady  which  tend  to  substantiate 
this  view.  On  the  other  hand,  it  may  be  considered  as  pretty  well  settled 
that  this  view  is  erroneous,  for  Dorothy  Reed,  Longcope  and  Simmons  have 
published  careful  investigations  which  seem  to  prove  that  Hodgkin's  disease 
possesses  definite  pathological  characteristics  peculiar  to  itself.  The  disease 
is  more  frequent  in  males  than  in  females,  and  in  adults  than  in  childhood. 

Pathology  and  Morbid  Anatomy. — The  changes  which  are  most  marked 
are  enlargement  of  the  lymphatic  glands  at  first  in  limited  areas  and  later 
all  over  the  body.  The  cervical  and  inguinal  glands  are  usually  the  most 
prominent,  and  the  outlines  of  the  neck  may  be  completely  obliterated. 
At  autopsy  the  retrobronchial  and  retroperitoneal  glands  may  be  found 
enormously  increased  in  size,  forming  a  mass  as  large  as  the  arm,  and  pressing 
on  adjoining  tissues  such  as  the  thoracic  duct  and  the  bloodvessels.  The 
affected  nodes  are  discrete  and  regularly  enlarged.  Their  consistency  varies. 
Sometimes  they  are  firm  and  dense,  at  others  so  soft  as  to  fluctuate.  The 
cut  surface  of  these  glands  is  translucent,  gray,  or  more  rarely  yellowish, 
and  the  tissues  of  the  glands  bulge  forward.  An  overgrowth  of  lymphoid 
tissue  may  take  place  at  the  apices  of  the  lungs  and  lead  to  a  diagnosis  of 


76g  DISEASES  OF  THE  SPLEEN 

tuberculosis.  Death  may  be  due  to  pressure  on  the  thoracic  bloodvessels, 
and  perhaps  to  pulmonary  infiltration  and  exudation.  Osier  asserts  that 
infiltration  of  the  lung  does  not  occur  in  this  disease,  and  that  when  such 
an  infiltration  does  take  place  the  disease  is  true  lymphosarcoma.  There 
is  also  enlargement  of  the  spleen  with  overgrowth  of  the  lymphoid  bodies, 
which  are  gra}^sh-white  in  appearance,  and  consist  of  lymph  follicles  held 
too-ether  by  a  reticulum  of  connective  tissue.  The  marrow  of  the  long  bones 
may  be  lymphoid  or  purulent  in  appearance,  as  it  is  in  some  cases  of 
myelogenous  leukaemia.  The  liver  and  kidneys  may  also  be  enlarged 
and  contain  lymphoid  masses. 

The  characteristic  lesions  of  Hodgkin's  disease  are  an  early  increase  in  the 
lymphadenoid  tissues  with  a  proliferation  of  endothelial  cells,  the  formation 
of  uninuclear  and  multinuclear  giant  cells,  thickening  of  the  reticulum,  and 
lastly  an  overgrowth  of  the  connective  tissue  of  the  lymph  nodes  to  the 
development  of  which  the  increased  density  of  these  masses  is  due.  Eosino- 
phile  cells  in  most  cases  are  present  in  very  large  number  in  the  b/mph  nodes 
and  in  the  bone-marrow.  Not  only  is  the  disease  characterized  by  these 
changes  in  the  pre-existing  lymph  nodes,  but  there  is  a  constant  formation 
of  new  nodes  which  soon  become  similarly  affected. 

The  blood  changes  are  most  variable.  In  some  cases  they  are  moderate, 
in  others  severe,  in  that  the  red  cells  may  be  decreased  in  number,  but  even 
when  the  patient  is  at  death's  door  there  may  be  fully  3,000,000  cells  present. 
The  red  cells  are  not  altered  in  a  manner  which  is  in  any  way  characteristic. 
The  chancres  consist  solely  in  a  diminution  in  number  to  a  moderate  degree, 
and  in  a  reduction  of  the  amount  of  haemoglobin.  The  leukocytes  are  not 
increased  as  in  true  leukaemia,  but  are  often  actually  diminished.  Pinkus 
thought  a  relative  increase  of  the  lymphocytes  constant,  but  this  change  was 
present  in  but  1  of  Ivongcope's  7  cases,  although  a  very  large  proportion  of  the 
white  cells  may  be  of  this  variety.  Occasionally  the  increase  of  white  cells 
may  rise  to  the  number  seen  in  certain  inflammatory  states,  as  from  30,000 
to  40,000.  In  the  later  stages  the  blood  picture  may  assume  all  the  charac- 
teristics of  an  intense  secondary  anaemia. 

Symptoms. — ^The  symptoms  of  pseudoleukaemia  are  those  of  ordinary 
severe  secondary  anaemia,  with  shortness  of  breath  and  palpitation  of  the 
heart  on  exertion.  The  enlarged  masses  of  glands  in  the  neck  and  groins 
may  be  very  characteristic  in  appearance,  associated  as  they  are  with  pallor 
and  pujjiness  of  the  face,  ^^^len  the  internal  glands  are  primarily  and  chiefly 
involved  the  diagnosis  from  tuberculosis  may  be  difficult  because  the  pressure 
may  cause  consolidation  with  patches  of  dulness  on  percussion,  and  because 
a  distinct  febrile  movement  is  often  present. 

These  masses  by  producing  pressure  may  give  rise  to  paroxysms  of  cough 
or  of  pain  or  constant  dyspncea.  ^^^aen  the  inguinal  glands  are  affected 
oedema  of  the  lower  extremities  may  develop,  and  shooting  pains  may  be  felt 
in  the  legs.  After  the  glandular  masses  become  very  large,  superficial 
sloughing  may  occur,  and  therefore  the  resemblance  to  a  suppurating  tuber- 
culous mass  may  be  increased  (Fig.  103).  I  have  seen  an  actinomycosis 
of  the  neck  produce  similar  s}Tnptoms.  Bronzing  of  the  skin  may  occur. 
Moderate  fever  is  often  present.     It  may  be  low  and  regular  or  high  and 


HODGKIN'S  DISEASE 


769 


irregular  in  type.  Occasionally  it  has  an  intermittent  character  with  sharp 
exacerbations,  so  that  it  resembles  intermittent  or  remittent  malarial  fever. 
Jaundice  due  to  pressure  on  the  bile-ducts  may  appear. 

Additional  symptoms  met  with  in  some  cases  are  murmurs  in  the  great 
vessels,  produced  partly  by  the  ansemia  but  chiefly  by  the  pressure  caused 
by  the  growths.  Deafness  due  to  closure  of  the  Eustachian  tubes  by  growths 
in  the  pharynx  and  unequal  pupils  due  to  pressure  on  the  cervical  sym- 
pathetic, may  be  present. 


Fig.  103 


Hodgkin's  disease. 

Diagnosis. — From  true  leukaemia  pseudoleuksemia  is  to  be  separated 
by  the  absence  of  the  large  excess  of  leukocytes,  and  the  lack  of  the  leuko- 
cytes peculiar  to  that  disease.  From  enlargement  of  the  lymph  glands  due 
to  tuberculosis  it  is  to  be  separated  by  the  test  with  tuberculin  (see  Tuber- 
culosis), and  by  the  fact  that  tuberculosis  rarely  produces  enlargement  of 
the  cervical  glands  on  both  sides  and  in  both  groins,  and  by  the  absence  of 
a  tuberculous  focus  elsewhere.  When  doubt  exists  a  part  or  all  of  an 
enlarged  mass  of  glands  may  be  excised  and  examined  microscopically  to 
determine  the  character  of  the  disease, 
49 


770  DISEASES  OF   THE  SPLEEN 

In  many  cases  the  clinical  diagnosis  is  most  difScult.  I  have  seen  the 
most  eminent  clinicians  mistake  this  malady  for  tuberculosis.  Very  rarely 
a  form  of  multiple  lipoma  distributed  in  the  l}miph-node  areas  closely 
resembles  Hodgkin's  disease;  the  picture  may  further  be  confused  by  the 
presence  of  glandular  and  calcific  masses  in  the  fatty  tumors;  such  a  case 
has  been  observed  in  the  Jefferson  Medical  College  Hospital;  Chantemesse 
and  Podwyssotsky  figure  such  a  case  under  the  name  adenolipomatosis. 

Prognosis. — The  prognosis  in  Hodgkin's  disease  is  absolutely  bad.  Not 
one  recovers.  These  patients  have  periods  of  improvement  when  courage 
runs  high,  but  after  all  the  inevitable  progress  is  downward.  Death  comes 
from  interference  with  circulation  or  respiration  or  by  general  asthenia. 

Treatment. — The  best  treatment  is  the  use  of  arsenic  in  full  doses.  Re- 
cently excellent  results  have  been  obtained  by  Senn,  Finch,  and  others  in 
some  of  these  cases  by  the  use  of  the  a--rays,  the  parts  involved  being  exposed 
to  the  rays,  repeatedly,  over  a  long  period  of  time. 


STATUS  LYMPHATICUS. 

Definition. — The  term  status  lymphaticus  or  "l}Tnphatic  constitution," 
sometimes  called  "  const itutio  lymphatica,"  is  applied  to  a  state  which  occurs 
chiefly  in  children  or  infants,  and  wliich  is  characterized  by  hyperplasia,  of 
the  lymph  nodes,  the  thymus  gland,  and  the  spleen,  and  by  a  hypoplasia  of 
the  heart  and  arteries.  The  lymphoid  bone-marrow  is  also  affected.  The 
fact  of  particular  'nterest  is  that  patients  with  this  condition  sometimes  suffer 
sudden  death,  which,  coming  on  in  children  who,  on  superficial  examination, 
appear  unusually  robust  and  plump,  is  all  the  more  startling. 

History. — As  long  ago  as  1614  Plater  made  note  of  the  fact  that  the  thymus 
gland  was  found  enlarged  in  certain  cases  of  sudden  death,  and  in  1830  Kopp 
described  a  form  of  difficult  breathing  which  he  called  "thymic  asthma," 
and  which  he  considered  was  due  to  pressure  upon  the  trachea  by  an  enlarged 
thymus  glanrl.  This  view,  which  was  apparently  disproved  by  Friedleben  in 
1858,  received  no  further  support  until  in  1888  it  was  revived  by  Grawitz, 
only  to  be  controverted  again  by  Paltauf  in  1889. 

Etiology. — The  etiology  of  this  state  is  not  known,  but  it  is  apparently  a 
congenital  fault,  and  is  associated  vnth  a  low  degree  of  vital  resistance  to 
infection.  Hedniga  has  reported  an  instance  in  which  out  of  a  family  of 
nine  children,  five  died  of  this  malady. 

Blumer  has  recently  put  forward  certain  facts  which  seem  to  show  that 
this  condition  is  the  result  of  the  development  in  the  body  of  a  toxic  sub- 
stance, a  c}i:otoxin.  To  this  state  the  term  lymphotoxismus  has  been  appfied. 
According  to  this  view,  the  overgrowth  of  the  lymphatic  tissues  in  the  differ- 
ent parts  of  the  body  is  a  sequence  of  the  action  of  this  poison  and  not  the 
cause  of  its  development. 

Pathology  and  Morbid  Anatomy. — An  autopsy  in  a  case  of  this  character 
reveals  an  overgrowth  and  swelling  of  the  lymph  glands  in  the  thorax,  abdo- 
men, and  cervical  and  inguinal  chains,  and  enlargement  of  the  tonsils.  The 
lymph  nodes  of  the  intestinal  tract  are  very  markedly  swollen  and  sharply 


STATUS  LYMPHATICUS  771 

defined.  The  spleen  appears  larger  than  normal,  and  the  lymphoid  tissue 
of  the  Malpighian  bodies  is  in  a  state  of  overgrowth.  The  changes  in  the 
thymus  gland  are,  however,  the  most  important,  because  it  is  supposed  that 
the  sudden  congestion,  hyperplasia,  and  swelling  of  the  gland  which  occurs 
causes  death  by  pressure  upon  the  great  vessels  of  the  neck  and  upon  the 
trachea.  The  thyroid  gland  may  also  be  enlarged.  If  the  shafts  of  the  long 
bones  are  opened,  yellow  marrow  is  found  to  be  substituted  for  red  marrow. 
The  heart  and  aorta  are  poorly  developed. 

Congestion  and  oedema  of  the  lungs  have  been  found  in  some  cases  at 
autopsy,  and  in  others  atelectatic  patches  have  been  discovered.  In  all 
of  these  cases  the  pressure  upon  the  air  passages  was  responsible  for  these 
changes. 

Symptoms. — There  are  no  symptoms  in  any  way  characteristic  of  this  state, 
except  that  the  child  may,  on  close  examination,  be  found  to  suffer  from 
rickets,  some  enlargement  of  the  lymphatics,  and  a  rather  feeble  heart.  The 
recollection  of  the  possible  presence  of  this  state  should  make  the  physician 
particularly  careful  when  administering  an  anaesthetic  to  a  child  of  the 
lymphatic  type,  especially  if  the  condition  to  be  relieved  is  overgrowth  of  the 
lymph  tissues,  such  as  the  postnasal  adenoids  and  spongy  tonsils,  as  sudden 
death  may  ensue.  Hand  has  reported  a  case  in  which  tetany  was  present.  In 
a  case  recently  reported  by  Musser  and  Ullom  an  unusually  robust  and  well- 
developed,  but  overfat,  boy  of  five  years  suffered  from  a  little  hoarseness  on 
one  day,  and  on  the  next  seemed  about  as  well  as  usual.  That  same  night 
he  went  to  sleep  at  the  usual  time,  but  at  2  a.m.  was  seen  to  be  somewhat 
pinched  and  livid.  A  few  hours  later  he  became  more  cyanosed  and  pre- 
sented a  rapid  pulse  and  labored  breathing.  His  respirations  were  character- 
ized by  loud  rales  in  the  bronchial  tubes  and  larynx.  His  temperature  grad- 
ually rose  till  it  reached  105°,  at  which  time  convulsions  developed,  and  he 
died  shortly  afterward.    The  urine  was  loaded  with  albumin. 

Several  cases  of  so-called  teething  convulsions  in  infants  have  been  found 
at  autopsy  to  be  due  to  this  disease.  Sometimes  the  child  is  found  dead 
in  bed. 

Treatment. — We  know  so  little  of  the  cause  of  this  state,  and  so  few  cases 
have  been  subjected  to  treatment,  that  no  definite  plan  of  treatment  can  be 
outlined,  save  that  fresh  air  and  sunshine  and  iron  iodide,  and  arsenic  are 
useful. 

If  the  thymic  enlargement  be  demonstrable,  operation  might  be  resorted 
to.  Rehn  opened  the  mediastinum,  drew  the  gland  forward  and  stitched  it 
in  position;  recovery  followed.  Carter  operated  on  a  case  for  tracheal 
obstruction,  recognized  the  thymic  enlargement,  and  introduced  a  tube  which 
gave  temporary  relief,  but  the  child  died. 


772  DISEASES  OF   THE   THYMUS  GLAND 


DISEASES  OF  THE  THYMUS  GLAND. 

The  thymus  gland  is  found  well  developed  in  infants  up  to  the  second  year 
of  life,  after  which  time  it  gradually  decreases  in  size  till  it  reaches  a  degree 
of  degeneration  and  atrophy  in  which  it  may  be  said  to  no  longer  exist.  This 
occurs  about  the  time  of  puberty.  In  fully  developed  adults  it  is  represented 
by  a  small  aggregation  of  lymphoid  and  fatty  cells.  Very  rarely  the  thymus 
persists  without  any  change  in  its  tissues,  even  in  adult  life.  When  it  remains 
large,  or  increases  in  size  as  the  result  of  disease,  as  in  the  status  lymphaticus, 
it  may  cause  symptoms  by  pressing  on  the  trachea  and  the  great  vessels  of 
the  neck  and  chest. 

Diseases  of  the  thymus  gland  are  very  rare.  In  some  cases  a  state  of 
so-called  hypertrophy  is  present,  but  this  is  rarely  a  true  hypertrophy,  the 
gland  being  swollen  and  filled  with  lymphoid  cells.  Occasionally  minute 
hemorrhages  may  take  place  into  its  tissues  or  beneath  its  capsule.  Abscess 
has  been  recorded  as  having  occurred,  and  growths,  benign  and  malignant, 
have  been  found  in  its  tissues.    It  has  been  found  affected  by  tuberculosis. 

Many  years  ago  enlarged  thymus  was  supposed  to  be  the  cause  of  spas- 
modic croup.  That  an  enlarged  gland  may  cause  some  interference  with 
respiration  is  conceivable,  but  we  now  know  that  spasmodic  croup  is  usually 
due  to  rickets  or  postnasal  adenoids.  Those  interested  in  this  subject  should 
read  Jacobi's  essay  published  in  1888  in  the  Transactions  of  the  Association 
of  American  Physicians,  vol.  iii.  p.  297. 


DISEASES  OF  THE  BLOOD. 


ANiEMIA. 

Definition.— The  word  ansemia  signifies  a  state  of  the  blood  in  which  there 
is  lacking  the  normal  quantity  of  red  cells  or  of  haemoglobin  in  these  cells. 
When  the  cause  of  this  state  is  due  to  some  disorder  of  the  blood-making  or 
blood-destroying  tissues,  it  is  called  essential  or  primary  antemia.  When  due 
to  some  other  cause,  such  as  hemorrhage  or  one  of  the  acute  infectious  dis- 
eases, it  is  called  secondary  anaemia.  Fortunately,  most  cases  of  anaemia 
belong  to  this  latter  class,  and  they  will,  therefore,  be  considered  first. 

Secondary  Anaemia. 

Secondary  anaemia  arises  from  a  host  of  causes  and  is  characterized  in  most 
cases  by  a  diminution  in  the  number  of  the  red  cells,  and  an  even  greater 
reduction  in  the  haemoglobin  content  of  each  cell.  In  some  cases  it  comes  on 
as  a  result  of  breathing  vitiated  air,  as  in  factory  girls  and  stenographers. 
In  other  cases  it  is  due  to  overwork  and  insuflficient  or  improper  food,  and  in 
still  other  cases  to  protracted  digestive  disturbance  or  to  chronic  constipation, 
which,  by  causing  autointoxication,  is  the  active  factor  in  producing  the 
condition.    The  late  Sir  Andrew  Clark  was  an  earnest  exponent  of  this  view. 

Hemorrhage  is,  of  course,  a  very  potent  cause.  When  it  is  profuse  the 
change  appears  so  promptly  that  the  cause  is  evident,  but  in  many  cases 
anaemia  arises  as  the  result  of  repeated  small  losses  of  blood,  as  from  hemor- 
rhoids when  the  patient  is  at  stool.  Under  conditions  of  hemorrhage, 
nucleated  cells  and  a  few  poikilocytes  may  be  found.  After  a  single  large 
hemorrhage  the  rapidity  of  recovery  is  extraordinary,  being  more  rapid  than 
when  the  loss  of  blood  has  been  prolonged.  Cases  are  occasionally  met  with 
in  which,  by  reason  of  lack  of  regenerative  power  in  the  blood-making  organs, 
a  sharp  hemorrhage  is  followed  by  death  in  a  short  time. 

Toxic  states  due  to  renal  disease  or  to  the  various  infectious  maladies, 
particularly  malaria  and  syphilis,  often  cause  anaemia,  and  prolonged  lacta- 
tion, frequent  child-bearing,  and  the  growth  of  tumors  of  large  size  also 
produce  it.  When  the  tumors  are  malignant,  the  anemia  is  also  partly  toxic. 
Not  infrequently  we  meet  with  cases  in  which  the  anaemia  is  due  to  chronic 
metallic  poisoning,  as  from  arsenic,  lead,  and  mercury.  In  other  instances 
the  anaemia  is  due  to  intestinal  parasites,  such  as  the  Ankylostomum  duo- 
denale  or  the  tapeworm. 

In  all  cases  of  marked  and  apparently  causeless  anaemia,  the  possibility  of 
the  condition  being  due  to  intestinal  parasites  should  be  borne  in  mind,  and 

(773) 


774  DISEASES  OF   THE  BLOOD 

the  stools  examined,  not  only  for  the  ordinary  tapeworm,  but  for  uncinaria 
as  well.  Further  than  this,  the  marked  increase  in  the  eosinophiles  in  the 
blood  in  nearly  all  cases  of  parasitic  infection  should  be  recalled.  Walker  has 
collated  the  following  interesting  table  in  this  connection: 


Large 

Eosinophiles. 

Polymorphonuclears. 

mononuclears. 

Normal 

1  to    4  per  cent. 

60  to  70  per  cent. 

5  to  8  per  cent. 

Taenia    . 

6  to  13       " 

Ankylostoma  duodenale 

12.43  " 

Filaria  medinensis  . 

6  to  36       " 

Filaria  loa 

53       " 

23        " 

Oxyuris  vermicularis 

0.4  to  13.7   " 

Bilharzia  hsematobia 

16  to  48       " 

44  to  58 

12.5     " 

He  makes  the  interesting  statement  that  a  practical  application  of  this  has 
been  already  made.  In  the  feces  obtained  from  one  of  the  closets  in  a  large 
college  the  eggs  of  the  Ankylostomum  duodenale  were  found.  The  pupils 
who  had  used  the  receptacle  on  the  specified  day  were  asked  to  submit  them- 
selves to  examination,  but  their  feces  yielded  negative  results.  An  examina- 
tion of  the  blood  of  each  pupil  was  made,  eosinophilia  was  observed  in  2 
cases,  and  ova  subsequently  detected  in  their  feces. 

Symptoms. — ^The  symptoms  of  secondary  anoemia  vary  greatly  in  different 
individuals,  some  patients  with  marked  pallor  presenting  no  other  noteworthy 
symptoms,  while  others  whose  cheeks  have  color,  nevertheless,  suffer  from 
'palpitation  and  dyspnoea  on  exertion.  It  is  important  to  bear  in  mind  that 
there  are  fat  ansemics  and  red-cheeked  ansemics,  and  that  many  persons  who 
look  pallid  really  have  a  normal  number  of  red  cells  and  a  normal  percentage 
of  haemoglobin.  Headache,  neuralgia,  loss  of  appetite,  constipation,  and 
attacks  of  syncope  are  sometimes  due  to  anaemia,  and  in  women  amenorrhosa 
is  often  due  to  this  cause. 

Diagnosis. — The  diagnosis  between  secondary  and  primary  anaemia  is  to  be 
made  by  the  history  of  the  patient,  and  chiefly  by  the  fact  that  the  abnormal- 
ities, as  to  the  shape  and  character  of  the  red  cells  found  in  the  primary 
anaemias  (which  see),  are  far  more  marked  than  in  the  secondary  forms. 

Treatment. — In  the  treatment  of  secondary  anaemia  three  things  are  abso- 
lutely essential:  the  removal  of  the  cause,  if  possible,  the  institution  of  a 
proper  diet,  and  a  hygienic  mode  of  life,  and  the  administration  of  iron  and 
arsenic,  and  often  of  the  bitter  tonics,  in  order  that  the  condition  of  the  blood 
may  be  directly  improved.  If  the  method  of  life  of  the  patient  is  unhealthy, 
it  must  be  corrected,  and,  above  all,  plenty  of  fresh  air  and  sunshine  must  be 
obtained.  The  sleeping-rooms  should  be  well  ventilated,  and  the  patient 
must  be  dieted  in  such  a  way  that  the  bowels  are  moved  regularly  and 
adequately  every  day,  at  least  once,  for  constipation,  as  already  stated,  is 
usually  present,  and  is  often  the  cause.  Under  these  circumstances  aloes  and 
cascara  sagrada  are  probably  the  best  laxatives  to  administer,  particularly 
if  iron  is  given.  When  persistent  diarrhoea  is  the  cause  of  the  anaemia,  I  have 
found  that  Rockbridge  Alum  Spring  water  is  a  useful  remedy,  and  in  some 
instances  it  is  advisable  to  give  one  of  the  astringent  preparations  of  iron  like 
the  dried  sulphate  in  the  dose  of  ^  to  ^  grain  three  times  a  day.     If  the 


ANEMIA 


775 


ansemia  is  due  to  a  loss  of  blood  by  hemorrhoids,  this  loss  must  be  arrested 
by  local  treatment.  The  appetite  should  be  stimulated  by  the  use  of  drugs 
like  nux  vomica,  quinine,  or  other  bitter  tonics  like  cardamom  or  gentian.  A 
good  prescription  for  many  of  these  cases  is  a  pill  composed  as  follows: 

Be — Ferri  redact!       .  .  .  .  .  .  .  .     gr.  v. 

Acid,  arsenosi     .  .  .  .  .  .  .  .     gr.  J. 

Ext.  nucis  vomicae       .......     gr.  v. — M. 

Ft.  in  pil.  No.  xx. 

Sig. — One  t.  i.  d.  after  meals. 

The  nux  vomica  may,  in  some  cases,  be  replaced  by  2  grains  of  quinine. 
If  the  digestion  is  impaired,  hydrochloric  acid  and  pepsin,  or  pancreatin  and 
bicarbonate  of  soda,  or  taka-diastase  in  2  to  3  grain  doses  with  meals  is 
advisable. 

Primary  or  Essential  Anaemias. 

Chlorosis.  Definition. — Chlorosis  is  a  condition  of  the  blood  usually  met 
with  in  young  girls,  and  characterized  by  a  marked  diminution  in  the  quantity 
of  haemoglobin,  and  by  a  less  marked  decrease  in  the 
red  cells.  Until  recently  it  was  considered  a  second- 
ary anaemia  but  hsematologists  now  class  it  in  the 
primary  aneemias  chiefly  because  it  is  believed  to  be 
due,  at  least  in  part,  to  defective  hsemogenesis. 

Etiology. — ^There  are  still  many  who  believe  that 
chlorosis  is  a  secondary  anaemia.  It  is  certainly 
associated  with  many  causes  of  secondary  anaemia, 
such  as  constipation,  inanition,  and  bad  air.  What- 
ever influence  these  causes  may  have,  there  can  be 
no  doubt  that  the  processes  which  take  place  about 
the  age  of  puberty  in  the  female  sex  are  closely  con- 
cerned in  its  production,  for  the  disease  is  scarcely 
ever  met  with  except  at  a  period  of  life  near  these 
changes.  Occasionally,  however,  it  develops  in  later 
life,  and  it  is  then  called  "chlorosis  tarda."  Bramwell 
and  others  have  shown  that  there  is  also  a  heredi- 
tary influence. 

The  two  chief  causes  are  a  natural  predisposition 
to  anaemia  and  an  inability  to  utilize  iron  from  the 
food.  Some  believe  that  the  intestinal  mucosa  is  at 
fault,  others  that  the  spleen  is  functionally  perverted,  but,  as  Ewing  well  says, 
there  can  be  no  doubt  that  chlorosis  results  from  a  functional  insufficiency 
of  the  bone-marrow,  which  is  prone  to  occur  at  puberty. 

Pathology. — ^The  following  are  the  chief  changes  in  the  blood :  The  chief 
alteration  is  the  decrease  of  the  haemoglobin  in  each  corpuscle,  so  that  a  low 
color  index  is  one  of  the  points  necessary  to  a  diagnosis  of  the  disease.  So 
low  a  percentage  of  haemoglobin  as  10  has  been  recorded  by  Bramwell,  but 
the  average  low  limit  is  from  30  to  40  per  cent.,  and  the  color  index  about 
0.5  per  cent.    The  second  change  is  a  diminution  in  the  number  of  the  red 


Fig.   104 

46 

43                             , 

42                            / 

41                            1 

40                                   1 

39                                    \ 

34                                        \ 

«)  30        r 

m   29 

M    28 

"    26 

a    23 

16 

15 

13                                                            ..--.- 

11 j 

9                                                      /W. 

8                                                 /          I 

4                                                                  " 

3      ;                                       \    \ 

AGE  2Pi:ss::2:sssssssss|sssss 

Age  incidence  of  chlorosis. 
(Bramwell.) 


776  DISEASES  OF   THE  BLOOD 

cells,  but  usually  this  is  not  so  marked.  Taking  the  normal  for  a  woman  as 
approximately  4,800,000  to  the  cubic  millimetre,  the  fall  is  usually  not  more 
than  from  500,000  to  1,000,000.  When  a  very  great  fall  in  the  number  of  red 
cells  is  present,  they  may  amount  to  only  2,000,000,  but  in  such  a  case  a  sus- 
picion of  pernicious  ansemia  comes  forward. 

If  the  chlorosis  is  severe,  the  red  cells  vary  as  to  size  and  shape,  and  a 
number  of  large  red  cells,  with  a  full  complement  of  haemoglobin,  may 
be  present.  As  a  rule,  the  size  of  the  red  cells  is  reduced.  Imperfectly 
formed  cells  (poikilocytes)  are  found,  but  they  are  present  in  very  small 
numbers.  Granular  degeneration  of  the  red  cells  has  been  particularly 
well  studied  by  the  chief  of  my  medical  clinic.  Dr.  J.  C.  Da  Costa,  Jr.,  and 
by  Stengel,  White,  and  the  yoimger  Pepper. 

The  leukocytes  in  cases  of  chlorosis  do  not  suffer  much  change,  as  a  rule, 
but  some  patients  show  an  increase  of  the  lymphocytes.  Dr.  Da  Costa 
has  shown  that  most  of  these  are  large  lymphocytes,  and  that  the 
lymphocytes  may  amount  to  40  per  cent,  of  all  the  white  cells.  The 
specific  gravity  of  the  blood  is  reduced  pari  passu  with  the  haemoglobin. 
Although  extravascular  coagulation  is  retarded,  in  some  cases  there  is  a 
tendency  to  thrombosis. 

Aside  from  the  blood  changes,  a  state  of  hypoplasia  of  the  tissues  of  the 
heart  and  larger  arteries  is  often  present,  but  this  condition  is  not  peculiar  to 
chlorosis,  but  to  the  lymphatic  constitution.  When  recovery  begins  to  take 
place  the  number  of  undersized  red  cells  decreases  and  the  cells  of  normal 
size  increase  their  haemoglobin  content. 

Symptoms. — The  symptoms  of  chlorosis  are  a  peculiar  pallor  of  the  skin, 
which  often  has  a  greenish  hue,  whence  the  name  "green  sickness."  The 
patient  is  nearly  if  not  always  plump  and  possessed  of  a  good  quantity  of 
subcutaneous  fat.  Occasionally  the  superficial  vessels  are  well  supplied  with 
blood,  so  that  the  patient  is  ruddy,  thereby  misleading  the  physician  who  fails 
to  study  the  blood.  This  type  is  called  chlorosis  florida.  The  subjective 
symptoms  a.re  dyspnoea  on  exertion,  palpitation  of  the  heart,  vertigo,  and 
perhaps  attacks  of  partial  syncope.  Constipation  is  nearly  always  marked. 
Headache  is  quite  constant,  and  there  is  usually  a  most  persistent  absence  of 
appetite.  There  is  also  mental  depression  and  apathy.  Physical  examination 
will  reveal  a  diastolic  hsemic  murmur  at  the  third  left  costal  cartilage,  and  over 
the  right  carotid  artery  a  bruit  is  often  heard. 

The  complications  of  chlorosis  which  are  serious  are  the  development  of 
thrombi  in  the  veins  of  the  legs  and  in  the  cerebral  sinuses.  From  such 
thrombi  fragments  may  arise,  which  may  result  in  pulmonary  embolism. 
Slight  fever  may  occur,  but  the  hands  and  feet  are  usually  cold.  Amenorrhcea 
is  a  very  constant  symptom. 

The  blood  changes,  as  discovered  by  the  hsemoglobinometer  and  hsemato- 
cytometer  have  already  been  described. 

Diagnosis. — ^The  well-nourished  state  of  the  chlorotic  patient  is  also 
present  in  pernicious  anaemia,  but  the  differentiation  is  found  in  the  blood 
count  (see  Pernicious  Anaemia),  for  in  that  disease  the  decrease  in  the  white 
cells  is  usually  marked.  The  irritability  of  the  heart  must  not  be  taken  for 
a  sign  of  cardiac  disease  because  a  murmur  is  present,  nor,  in  the  absence  of 


ANEMIA  777 

urinary  changes,  should  the  puffy  face  and  ankles  be  thought  to  be  due  to 
renal  disease,  unless  the  urine  reveals  albumin  and  casts. 

Prognosis. — The  ultimate  prognosis  in  cases  of  chlorosis  is  usually  very 
good,  but  a  long  period  often  passes  without  much  improvement.  When  the 
number  of  the  red  cells  is  not  greatly  reduced  and  they  are  normal  in  shape 
and  size,  recovery  under  proper  treatment  is  usually  rapid.  This  holds  true 
even  if  the  color-index  is  very  low^.  When  the  red  cells  are  as  low  as  3,000,000, 
are  badly  shaped,  and  many  of  them  undersized,  the  prognosis  as  to  rapid 
recovery  is  bad.  So,  too,  when  the  lymphocytes  are  very  numerous,  a  speedy 
cure  is  rarely  seen.    Relapses  are  very  frequent. 

Treatment. — The  treatment  of  chlorosis  does  not  differ  materially  from 
that  which  was  given  for  the  treatment  of  ordinary  secondary  anaemia,  except 
that  chlorotic  patients  are  usually  more  obstinately  constipated,  and, 
therefore,  particular  attention  must  be  given  to  the  state  of  the  bowels. 
Fresh  air  and  sunshine  are  also  very  essential  in  these  cases.  More  important 
than  all,  it  must  be  remembered  that  chlorotic  patients  usually  need  very 
much  larger  quantities  of  iron  than  do  ordinary  anaemic  cases.  Whether  this 
is  due  to  an  inability  to  absorb  iron  or  whether  there  is  an  excess  of  sulphides 
in  the  bowels,  which  change  a  goodly  portion  of  the  iron  into  a  sulphide  of  iron, 
is  not  known.  During  the  winter  months  chlorotic  patients  usually  do  best 
at  seaside  resorts  or  at  places  like  Lakewood,  N.  J.,  which  are  low  in  altitude. 
In  the  summer  months  they  should  be  sent  to  high  altitudes,  varying  from 
3000  to  5000  feet,  unless  these  high  altitudes  tend  to  increase  palpitation  of 
the  heart  and  dyspnoea. 

Pernicious  Anaemia.  Definition. — Pernicious  anaemia  is  a  disease  of 
the  blood  arising  from  faulty  haemogenesis  and  excessive  haemolysis  or 
blood  disintegration.  It  is  a  fatal  malady  characterized  by  three  chief 
changes,  viz.,  an  extraordinary  decrease  in  the  number  and  alterations 
in  the  morphology  of  the  red  cells  and  by  certain  changes  in  the  bone- 
marrow. 

History. — Andral  in  France,  in  1821,  reported  cases  of  what  was  probably 
this  disease,  and  Channing  in  Boston  recognized  them  in  1832.  Pepper  and 
Tyson  showed  the  bone-marrow  changes  in  1875.  Sorenson,  in  1874,  made 
the  first  observations  as  to  the  number  of  the  red  cells,  reporting  cases  with 
only  470,000  corpuscles. 

Etiology. — ^The  etiology  is  still  unknown,  but  it  is  probable  that  certain 
of  the  causes  of  ordinary  secondary  anaemia  may  antedate  pernicious  anaemia. 
Age  has  no  great  influence.  Most  cases  appear  between  twenty  and  forty 
years  of  age,  but  even  young  children  of  less  than  five  years  have  been  seen 
with  the  malady.  In  some  of  the  reported  cases  the  Ankylostomum  duodenale, 
the  Bothriocephaliis  lotus,  or  tapeworm,  and  the  Oxyuris  vermicularis  have 
been  found.  The  first-named  parasites  can  cause  grave  anaemia,  but  it  is 
doubtful  if  any  of  them  alone  can  cause  pernicious  anaemia.  So,  too,  severe 
hemorrhage,  syphilis,  and  pregnancy  have  been  found  associated  with  the 
development  of  the  disease.  They  are  not  the  actual  cause,  but  rather 
predisposing  causes.  The  various  fevers,  as  malaria  and  typhoid  fever,  only 
exert  an  indirect  effect,  and  the  condition  of  the  gastrointestinal  tract,  at 
one  time  thought  to  be  responsible,  has  been  proved  to  be  only  a  predis- 


778  DISEASES  OF   THE  BLOOD 

posing  or  secondary  condition.    Hunter  thinks  the  disease  is  due  to  bacterial 
infection  of  the  ahmentary  canal  from  a  foul  mouth. 

Morbid  Anatomy. — The  most  noteworthy  pathological  changes  are  the  alter- 
ations in  the  blood  and  in  the  bone-marrow.  Unlike  cases  of  chlorosis,  the 
blood  may  be  difficult  to  obtain.  In  marked  cases  it  does  not  form  a  rounded 
drop,  but  flows  from  the  puncture  made  by  the  needle  or  scalpel  sometime 
after  the  wound  is  inflicted.  Coagulation  is  usually  delayed,  and  even  at 
an  autopsy  made  many  hours  after  death  the  blood  may  still  be  fluid.  The 
red  cells  are  decreased  to  2,000,000,  then  to  1,000,000,  and  sometimes  to  less 
than  500,000  to  the  cubic  milhmetre.  A  great  proportion  of  the  remaining 
cells  are  larger  than  normal  (megalocytes),and  some  are  smaller  (microcytes). 
Many  of  the  red  cells  are  misshapen  (poikilocytes) ,  and  the  amount  of 
hgemoglobin  in  most  of  the  red  cells  is  considerably  increased,  although 
some  of  them  may  be  poor  in  hsemoglobin.  Red  cells  possessing  nuclei 
(erythroblasts)  are  also  present  in  considerable  number.  Some  of  these 
are  large  (megaloblasts)  and  others  of  normal  size  (normoblasts).  Small 
nucleated  red  cells  called  microblasts  are  also  present.  The  presence  of 
the  megaloblast  is  an  important  aid  in  reaching  a  positive  diagnosis.  These 
nucleated  cells,  both  large  and  small,  contain  a  great  amount  of  hsemo- 
globin,  and  some  of  them  differ  from  ordinary  red  cells  in  one  very  im- 
portant particular — namely,  they  possess  amoeboid  movement — and,  further, 
when  the  blood  is  examined,  they  are  seen  to  form  rouleaux  as  do  ordinary 
red  cells.  A  granular  degeneration  which  permits  basophilic  staining  also 
occurs  in  the  red  cells. 

In  mild  cases  the  leukocytes  may  not  be  altered  in  number,  although 
usually  they  are  slightly  reduced.  Rarely  they  are  greatly  reduced  in 
number  if  the  case  is  severe.  As  a  rule,  but  few  myelocytes  occur  and  the 
lymphocytes  may  be  increased. 

The  haemoglobin  is  reduced,  the  average  being  25  to  30  per  cent.,  but  not 
in  proportion  to  the  red  cells,  hence  a  high  color  index  is  the  rule. 

When  the  bone-marrow  is  examined  very  marked  changes  are  manifest. 
There  is  an  excess  of  large  nucleated  red  cells,  many  of  which  are  giganto- 
blasts.  The  Hver,  spleen,  lymph  glands,  and  particularly  the  liver,  are 
loaded  with  iron  derived  from  the  destroyed  red  blood  cells,  and  even  the 
urine  contains  pigment  from  this  source;  Hunter  denies  an  excess  of  iron 
in  the  spleen.  Fatty  degeneration  of  the  liver,  kidneys,  and  of  the  heart 
muscle  are  often  present,  and  because  of  similar  changes  in  the  walls  of 
the  arteries  and  of  the  altered  character  of  the  blood,  hemorrhages  into  the 
retina  and  into  other  parts  may  occur.  In  some  cases  marked  atrophy  of 
the  gastric  tubules  is  found.  A  diffuse  degenerative  change  occurs  in  the 
posterior  and  lateral  columns  of  the  spinal  cord. 

Symptoms. — A  patient  with  pernicious  anaemia  usually  first  seeks  medical 
advice  because  he  is  feeling  weak  and  lacks  initiative.  Often  he  suffers 
from  some  dyspncea  on  exertion  and  has  a  throbbing  headache  or  attacl'cs  of 
vertigo.  His  tissues  are  well  filled  with  fat  and  his  appearance  is  plump, 
but  he  is  pallid  and  cheesy  looking.  The  sclerotic  part  of  the  eyes  is  pecu- 
liarly pearly  and  the  lips,  gums,  and  tongue  are  prone  to  be  very  pale  and 
bloodless.    There  may  be  slight  puffiness  of  the  face  on  the  dependent  side 


ANEMIA  779 

if  the  patient  lies  on  his  side  in  bed.  A  purring  hcomic  murmur  is  often 
heard  over  the  pulmonary  artery  at  the  third  left  costal  cartilage,  and  the 
arteries  of  the  neck  pulsate  and  throb  with  a  peculiar  jerking,  expansile 
movement.  An  irregular  fever  is  very  constantly  present.  When  the  disease 
is  far  advanced  a  state  of  mental  torpor  with  muttering  delirium  may  occur. 

Diagnosis. — The  fact  that  the  patient  is  in  middle  life,  or  even  older, 
serves  to  separate  this  state  from  chlorosis,  which  has  its  greatest  fre- 
quency at  the  eighteenth  or  nineteenth  year.  Again,  pernicious  anaemia  is 
more  common  in  men,  chlorosis  in  women.  The  skin  in  pernicious  anaemia 
is  prone  to  show  a  cheesy-yellow  hue  in  distinction  from  the  greenish- 
yellow  of  chlorosis.  From  the  blood  of  the  chlorotic  that  of  pernicious 
anaemia  differs  so  radically  that  a  diagnosis  is  readily  made  in  typical  cases, 
for  in  the  former  we  have  cells  poor  in  haemoglobin  and  here  we  have 
cells  rich  in  haemoglobin.  In  the  former  the  red  cells  are  not  greatly 
decreased  in  number,  here  they  are  markedly  diminished.  In  chlorosis  the 
size  of  the  red  cells  is  below  the  normal,  in  pernicious  anaemia  the  average  is 
above  the  normal.  Again,  in  chlorosis  we  do  not  find,  to  the  same  degree, 
nucleated  red  cells  or  cells  with  mitotic  nuclei,  nor  red  cells  with  amoe- 
boid movement.  The  color-index  in  chlorosis  is  low  and  in  pernicious 
anaemia  high.  In  cases  of  gastric  cancer  there  is  present  ordinary  sec- 
ondary anaemia  and  the  presence  of  gastric  symptoms  to  aid  the  diagnosis. 
Finally,  Ewing  states  that  unless  at  least  33  per  cent,  of  the  red  cells  are 
oversized,  the  diagnosis  of  pernicious  anaemia  must  be  made  with  reserve. 

Prognosis  and  Treatment. — The  prognosis  of  true  pernicious  anaemia  is 
almost  invariably  fatal,  although  there  have  been  a  considerable  number 
of  cases  in  which  recovery  has  been  said  to  have  occurred.  Many  cases 
have  periods  of  extraordinary  improvement  in  all  the  symptoms  as  well 
as  in  the  blood,  and  then  a  disheartening  relapse  takes  place.  This  may 
be  repeated  several  times.  Most  cases  die  within  a  year  after  they  are 
first  seen.  A  great  decrease  in  the  number  of  red  cells  and  a  large  number 
of  megaloblasts  are  bad  signs. 

The  prognosis  in  pernicious  anaemia  depends  not  a  little  upon  the  quan- 
tities of  arsenic  which  the  patient  can  take  without  developing  disagree- 
able symptoms  from  its  use,  for  many  of  these  cases  are  markedly 
benefited  if  they  can  take  what  might  be  called  massive  doses  of  this  drug. 
By  a  process  of  training  with  ascending  doses  I  have  known  patients  to  take 
as  much  as  30  minims  of  Fowler's  solution  three  times  a  day  with  no  bad 
results  except  some  exfoliation  of  the  skin  of  the  hands  after  several  weeks' 
treatment.  Arsenic  administered  in  this  manner  up  to  the  point  of  tolerance 
sometimes  produces  periods  of  remarkable  improvement  in  this  disease,  the 
patient's  symptoms  becoming  modified  and  the  number  of  red  blood  cells 
becoming  markedly  increased. 

Of  course,  all  measures  which  tend  to  increase  the  general  health  of 
the  patient  are  advantageous,  such  as  plenty  of  sunshine,  fresh  air,  and  good 
food.  Small  quantities  of  iron  may  be  given  from  time  to  time  with  advan- 
tage. Diarrhoea  is  to  be  controlled  by  the  use  of  sulphuric  acid  or  one  of  the 
vegetable  astringents,  such  as  fluid  extract  of  haematoxylon,  kino,  or  catechu. 
Constipation,  if  present,  is  to  be  relieved  by  the  use  of  cascara  sagrada  and 


780  DISEASES  OF   THE  BLOOD 

aloes.  In  some  instances  hypodermic  injections  of  arsenic  have  been 
resorted  to  with  asserted  advantage,  but  this  is  a  method  of  treatment  which 
is  rarely  if  ever  justified.  If  the  patient  is  very  anxious  to  carry  out  a  plan 
of  treatment  which  may  possibly  be  advantageous,  inhalations  of  oxygen 
may  be  suggested. 

In  the  treatment  of  pernicious  anaemia  it  is  the  universal  experience  of 
clinicians  that  iron  is  by  no  means  as  beneficial  as  is  arsenic.  Indeed, 
the  general  proposition  may  be  stated  that  if  ansemia  is  associated  with 
diminution  in  the  number  of  red  blood  cells,  arsenic  is  more  advan- 
tageous than  iron;  whereas,  in  those  anaemias  which  are  characterized  by 
a  low  color-index  or  a  diminution  in  haemoglobin,  iron  is  more  useful  than 
arsenic. 


LEUE.SMIA. 

Definition. — Leukaemia  is  a  disease  in  which  the  blood  suffers  an  extra- 
ordinary increase  of  leukocytes  with  associated  alterations  in  the  bone- 
marrow,  the  spleen,  and  in  the  lymphatic  glands.  It  is  divided  into  two 
types,  that  form  in  which  the  spleen  and  bone-marrow  are  chiefly  affected, 
and  that  in  which  the  lymphatic  glands  are  chiefly  involved,  the  first  being 
called  splenomedullary  leukoemia  and  the  second  lymphatic  leukcemia.  Be- 
cause of  the  important  role  played  by  the  bone-marrow  in  splenomedullary 
type  it  is  sometimes  called  myelogenous  leukcBmia.  Leukaemia  is  also  some- 
times called  leukocythcemia. 

Although  a  division  of  the  disease  into  two  types  is  to  some  extent  justified 
because  it  renders  the  study  of  leukaemia  less  difficult,  and  because  changes 
in  certain  tissues  preponderate  in  one  instance  and  in  other  tissues  in  other 
instances,  it  is  not  to  be  forgotten  that  intermediate  cases  occur  in  which 
both  types  of  the  malady  are  represented,  or  at  least  in  which  no  definite 
dividing  line  can  be  drawn.  Thus  cases  are  recorded  in  which  the  blood 
cells  presented  the  picture  of  lymphatic  leukaemia,  but  the  lymphatic  glands 
were  not  involved  but  the  bone-marrow  was  altered.  Again,  it  has  been 
thought,  in  times  past,  that  acute  and  rapidly  progressive  leukaemia  was  usu- 
ally of  the  lymphatic  type,  and  that  the  subacute  or  chronic  form  of  the 
disease  was  commonly  of  the  splenomedullary  variety.  "\^Tiile  this  view  still 
holds  true,  we  have  been  forced  to  recognize  the  fact  that  acute  cases  may 
be  of  splenomedullary  type  and  that  some  of  the  chronic  cases  may  be 
lymphatic. 

History. — As  long  ago  as  1801  Bichat,  in  France,  noted  a  condition  of 
the  blood  which  was  probably  identical  with  leukaemia  as  we  know  it  to-day. 
Thirty  years  later  because  of  the  peculiar  appearance  of  the  blood  it  was 
called  "suppurative  haematitis,"  and  in  1839  Donne  described  the  blood 
in  these  cases  as  consisting  largely  of  "  white  or  mucous  globules."  Virchow, 
about  the  middle  of  the  last  century,  described  it  as  "Weisses  Blut,"  and 
showed  that  there  was  no  suppurative  process  present.  Bennett  made  the 
first  complete  study  of  the  disease  in  1851.  Since  then  a  host  of  investiga- 
tors have  thrown  light  upon  its  characteristics. 


LEUKEMIA  781 

Etiology. — The  cause  of  leukaemia  is  unknown.  It  may  occur  at  any 
time  of  life,  but  is  most  frequently  met  with  about  the  fourth  decade.  It  is 
about  twice  as  common  in  males  as  in  females.  A  very  large  number  of  condi- 
tions have  been  brought  forward  as  causes,  but  none  of  them  have  been  proved 
to  exercise  a  determining  influence.  Among  these  may  be  named  syphilis, 
maaria,  and  intestinal  intoxication.  The  view  has  been  advanced  that 
leukaemia  and  tuberculosis  are  nearly  related  in  the  sense  that  the  latter 
may  act  as  a  cause  of  the  former.  This  view  is  incorrect.  Gowers  tells  us 
that  the  appearances  of  the  lungs  in  one  or  two  cases  have  been  those  of 
tubercle,  that  extravasations  of  blood  into  the  lungs  are  common,  and  that 
these  organs  may  undergo  caseation  and  a  tuberculous  process  may  be  simu- 
lated. Cavities  may  result  from  lymphoid  infiltration.  This,  however,  is  not 
phthisis.  Susmann  has  been  able  to  collect  only  25  cases  from  literature 
in  which  tuberculosis  and  leukaemia  were  even  associated.  Further,  when 
the  diseases  are  combined  there  is  a  tendency  to  a  decrease  in  the  number 
of  leukocytes.  A  number  of  observers  are  strongly  inclined  to  the  belief  that 
the  condition  is  due  to  an  infection  by  a  parasite,  but  careful  observation 
and  experimental  studies  have  afforded  no  conclusive  result.  I.owit  and 
others  have  sought  to  establish  a  protozoal  origin,  but  their  observations  are 
inconclusive,  and  bacteriology,  so  far,  has  yielded  no  promising  results. 

Pathology  and  Morbid  Anatomy. — When  defining  the  disease  leukaemia 
it  was  stated  that  it  is  a  malady  which  appears  in  two  forms,  and  that  these 
forms  may  be  quite  dissimilar  in  their  chief  features,  or  overlap  one  another, 
according  to  the  degree  to  which  the  lymphatic  system  and  the  bone-marrow 
are  chiefly  affected.  It  is  probable  that  in  nearly  every  instance  the  bone- 
marrow  is  involved  in  the  disease  process,  and  almost  never  are  the  lesions 
situated  only  in  the  lymph  nodes  and  other  lymphatic  tissues.  Further, 
although  the  lymphocytes  of  a  person  in  good  health  are  usually  derived 
from  the  lymphatic  system,  in  the  patient  suffering  from  lymphatic  leu- 
kaemia they  are  derived,  to  a  large  extent,  from  the  bone-marrow  as  well. 

Having  made  these  preliminary  remarks,  we  can  best  proceed  to  the  study 
of  two  forms  of  leukcsmia  by  considering  them  separately. 

Splenomedullary  Leukaemia. — The  color  of  the  blood  may  be  normal  in 
some  cases,  but  if  the  disease  is  well  developed  it  is  much  paler  in  hue  because 
of  the  anaemia  and  the  excess  of  white  cells.  The  coagulability  of  the  blood  is 
greatly  decreased  or  lost.  The  red  corpuscles  are  not  very  greatly  diminished 
in  number  until  the  disease  is  far  advanced,  and  sometimes  not  then.  They 
rarely  fall  below  3,000,000  to  the  cubic  millimetre,  but  they  may  drop  to 
1,000,000.  Nucleated  red  cells,  especially  normoblasts,  are  present  in  varying 
numbers,  but  megaloblasts  are  rarely  present  in  any  great  degree.  There 
is  a  decrease  of  haemoglobin  so  that  the  color-index  is  about  0.5  to  0.7. 

The  white  cells  show  remarkable  changes  as  to  number,  shape,  size,  and 
variety.  Even  in  cases  which  may  be  called  moderate  they  usually  amount 
to  100,000  or  200,000  to  the  cubic  millimetre,  and  as  high  as  1,000,000  have 
been  reported,  as  against  a  normal  of  about  6000  to  10,000.  Of  the  varieties 
of  white  blood  cells  we  find  a  form  which  never  appears  in  normal  blood, 
and  which,  if  present  in  considerable  numbers,  is  pathognomonic  of  the 
disease,    namely,    large    mononuclear    leukocytes   containing    neutrophile 


782 


DISEASES  OF  THE  BLOOD 


granules.  These  cells  are  called  neutrophile  myelocytes  and  appear  in 
two  forms,  \nz.,  the  smaller  myelocytes,  about  the  size  of  the  polymorpho- 
nuclear leukocyte,  possessing  a  central  nucleus  which  stains  quite  deeply, 
and  a  larger  cell,  which  has  a  pale  staining  nucleus  placed  at  one  side  of 
the  corpuscle.  Eosinophilic  and  basophilic  myelocytes  also  may  be  found. 
The  relative  percentage  of  polymorphonuclear  cells  is  decreased,  although 
the  total  number  of  these  corpuscles  far  exceeds  the  normal.  The  presence 
of  the  myelocytes  is  at  the  expense  of  the  polymorphonuclear  cells.  ^ 

The  eosinophile  cells,  leukocytes  the  granules  of  which  stain  intensely 
with  eosin,  are  generally  increased  in  myelsemia,  although  they  are  never 
as  number ous  as  are  the  other  forms  already  named. 

The  number  of  hmiphocytes,  both  large  and  small,  varies  within  wide 
limits  in  most  cases  of  splenomedullary  leukemia,  and  at  different  times 
in  the  same  case.  Relatively  they  are  reduced  (as  low  as  2  per  cent.),  but 
even  in  this  percentage  the  blood  may  contain  more  mononuclears  to  the 
cubic  millimetre  than  in  health.  Very  large  mononuclear  leukocytes  with 
faintly  staining  nuclei  are  rarely  conspicuous  by  their  number.  "  iVIast-cells  " 
are  usually  present,  not  infrequently  reaching  5  or  10  per  cent.  When 
present  in  large  numbers  they  are  second  to  myelocytes  only  in  diagnostic 
significance.  These  mast-cells  are  polynuclear  cells  with  coarse  basophile 
granules. 

The  onset  of  any  one  of  the  acute  infections  may  completely  change  the 
appearance  of  the  blood  so  that  it  is  no  longer  characteristic  and  there  may 
be  a  great  increase  in  polymorphonuclear  cells. 

The  normal  red  bone-marrow  shows  marked  hyperplasia  and  the  fatty 
marrow  of  the  long  bones  undergoes  a  similar  transformation.  It  con- 
tains nucleated  red  cells  in  unusual  numbers,  and  is  crowded  with  leu- 
kocytes which  are  ancestral  to  those  found  in  the  blood,  including  all 
forms,  but  particularly  myelocytes.  In  some  cases,  however,  these  changes 
appear  in  patches  rather  than  all  through  the  bone  cavity.  At  certain  points 
the  compact  portion  of  the  bone  may  atrophy  before  the  hyperplastic 
marrow,  and  new  subperiosteal  nodes  may  develop. 

The  spleen  is  very  much  enlarged,  sometimes  to  fifteen  times  its  normal 
size.  It  is  frequently  attached  to  adjacent  tissues.  Its  capsule  is  usually 
thickened  and  roughened,  and  the  consistency  of  the  organ  increased.  On 
section  it  is  seen  to  be  mottled  red  and  gray,  or  it  may  be  a  homogeneous 
red.  The  trabeculse  may  be  thickened  and  hemorrhagic  infarctions  may  be 
present.  The  venous  system  is  engorged  and  purulent-looking  clots  may 
be  found  in  the  heart  and  vessels.  The  Hver  is  often  enlarged  and  leuksemic 
nodules  may  be  found  in  it  and  in  the  kidneys  and  thymus  gland. 

LjTDiplia'tic  Leukaemia. — The  conspicuous  blood  changes  in  this  disease 
are  confined  to  the  lymphocytes,  which  are  greatly  increased  in  number  so 
that  they  may  exceed  80  per  cent,  of  the  total  number  of  white  cells.  For 
this  reason  the  condition  is  sometimes  called  lymphsemia.  Usually  most  of 
the  cells  are  small  lymphocytes,  but  the  large  form  may  predominate, 
especially  in  the  acute  t}^e  of  the  disease.  The  total  increase  in  leukocytes 
rarely  approaches  that  seen  in  the  splenomedullary  form.  Nucleated  red 
cells   are  rarely  encountered. 


LEUKEMIA  783 

The  lymphatic  glands,  particularly  those  which  are  deeply  situated, 
are  enlarged,  but  the  spleen  and  the  medulla  of  the  long  bones  are  not 
greatly  altered.  Cases  are  on  record  in  which  chronic  lymphatic  leukaemia 
has  occurred  without  any  enlargement  of  the  l}Tiiph  nodes. 

Symptoms. — The  symptoms  of  splenomedullary  leukoemia  are  at  first  those 
of  anoBmia,  the  patient  presenting  himself  because  of  dyspnoea  on  exertion,  or 
because  of  lack  of  energy  and  poor  digestion.  Sometimes  the  swollen  spleen 
first  calls  his  attention  to  his  condition.  In  other  cases  nose-bleed  or  gastric 
hemorrhage  or  reiial  hemorrhage  comes  on  very  early  in  the  disease.  In  other 
cases  there  is  purpura  hoBmorrhagica.  If  the  hand  is  placed  over  the  splenic 
area  and  the  abdominal  wall  moved  over  the  enlarged  spleen  a  creaking 
sensation  may  sometimes  be  felt.  Not  rarely  the  liver  is  greatly  enlarged, 
and  ascites  may  be  present.  There  is  dizziness  and  vertigo.  Occasionally  a 
violent  diarrhcea  develops.  The  urine  is  normal,  save  that  it  contains  uric 
acid  in  excess.  The  heart  sounds  are  normal,  although  the  first  sound  may 
be  feeble,  and  anaemic  murmurs  can  occasionally  be  heard.  Retinal  hemor- 
rhages may  cause  blindness.  Hemiplegia  with  coma,  the  result  of  cerebral 
hemorrhage,  may  occur.  A  moderate  but  varying  febrile  movement  is  nearly 
always  present.  Occasionally  persistent  priapism,  probably  due  to  irrita- 
tion of  the  spinal  cells  by  anaemia,  is  present.    Sudden  death  may  take  place. 

In  cases  of  lymphatic  leukoemia  the  symptoms  complained  of  by  the 
patient  are  not  different  from  those  just  described,  but  the  spleen  is  not 
much  enlarged.  The  lymph  nodes  are,  however,  increased  in  size,  and 
so  the  appearance  of  the  patient  may  not  be  unlike  that  of  Hodgkin's 
disease. 

It  is  important  to  recall  the  fact  that  in  both  of  these  states  an 
irregular  febrile  movement  may  be  present  and  give  rise  to  the  belief 
that  some  one  of  the  acute  or  chronic  infections  characterized  by  fever 
are  present.  This  is  particularly  true  in  certain  cases  of  acute  lymphatic 
leukemia,  in  which  the  condition  of  the  patient  may  be  so  like  that  of 
typhoid  fever  that  an  examination  of  the  blood  is  required  to  determine 
the  exact  nature  of  the  illness.  The  condition  often  runs  its  course  in 
three  to  four  weeks;  fever  of  moderate  degree  is  present,  and  the  general  state 
is  asthenic.  Even  an  autopsy  may  not  reveal  the  real  cause  of  the  illness, 
because  the  lymph  nodes  in  the  solitary  and  agminated  glands  of  the  intes- 
tine are  infiltrated  as  in  typhoid  fever. 

Diagnosis. — The  pallor,  the  enlarged  spleen,  and  the  state  of  the  blood  are 
all  part  of  a  picture  which  cannot  be  mistaken  for  any  other  disease,  but  in 
doubtful  early  cases  repeated  blood  examinations  may  be  necessary  to  deter- 
mine the  diagnosis  positively. 

Prognosis. — The  prognosis  of  leukaemia,  like  that  of  pernicious  anaemia, 
is,  in  the  great  majority  of  cases,  fatal,  but  rare  instances  have  been  recorded 
in  which  recovery  has  taken  place.  Life  may  be  preserved  from  a  year  to 
three  years.  Unfavorable  prognostic  signs  are  marked  dyspnoea,  an  exces- 
sive number  of  leukocytes,  a  tendency  to  exhausting  diarrhoea  or  to  hemor- 
rhages, and  high  fever.  The  lymphatic  type  usually  runs  a  more  rapidly 
fatal  course  than  the  splenomedullary  form.  When  death  occurs,  the  cause 
is  usually  pulmonary  oedema,  pneumonia,  or  exhaustion. 


784  DISEASES  OF   THE  BLOOD 

Treatment. — ^The  treatment  of  leukaemia  in  both  its  forms  is  identical,  but, 
unfortunately,  it  is  by  no  means  successful,  for  the  disease  in  all  instances 
proceeds  by  a  more  or  less  rapid  course  to  a  fatal  ending.  There  can,  how- 
ever, be  no  doubt  that  the  administration  of  arsenic  in  ascending  doses  until 
the  point  of  intolerance  is  reached  seems  to  exercise  a  favorable  influence 
upon  the  malady,  at  least  in  so  far  that  it  delays  its  advance.  Cases  of 
leuksemia  not  subjected  to  treatment  not  infrequently  have  periods  of  remis- 
sion, in  which  temporary  improvement  may  take  place.  It  is,  therefore, 
difficult  to  determine  how  much  credit  should  be  given  to  arsenic  when  the 
remissions  occur  under  its  use.  Those  members  of  the  profession  who  have 
had  the  most  experience  in  the  treatment  of  leuksemia,  however,  regard 
arsenic  as  being  practically  the  only  remedy  of  any  value,  and  it  should 
always  be  tried,  preferably  in  the  form  of  Fowler's  solution.  The  begin- 
ning doses  should  be  3  drops  three  times  a  day,  rapidly  increased  until  the 
patient  has  some  puffiness  of  the  face  or  some  griping  of  the  bowels. 
Recently  several  clinicians  have  reported  "  cures"  of  this  disease  by  exposing 
the  patient  to  the  Roentgen  rays.  As  well  shown  by  Warthin  in  his  ex- 
haustive discussion  of  this  subject  the  final  outcome  of  most  if  not  all 
of  the  cases  thus  treated  is  relapse  and  death  from  the  disease.  Warthin's 
experimental  studies  indicate  a  possible  danger  from  the  absorption  of  sub- 
stances liberated  by  the  destruction  of  cells  brought  about  by  the  Roentgen- 
ray  exposures.  Further  investigations  will  be  necessary  to  place  this  pro- 
cedure upon  a  sound  therapeutic  basis,  as  it  deals  with  a  disease  that  is 
notoriously  resistant  to  ordinary  remedial  measures.  However,  the  question 
is  one  that  merits  careful  study. 


GHLOROMA. 

Under  the  name  chloroma  is  recognized  a  condition  characterized  by  the 
formation  of  greenish  lymphoid  tumors,  especially  in  the  cranial  bones  and 
periosteum,  and  the  occurrence  of  a  profound  anaemia  which  Dock  and 
Warthin  regard  as,  in  some  if  not  all  cases,  a  malignant  type  of  leuksemia. 
Exophthalmos  and  lymphoid  infiltration  of  the  cornea  and  of  the  conjunc- 
tiva may  be  present.  Later  the  periosteum  of  the  bones  of  the  spinal 
column  become  affected.  Localized  paralyses,  from  pressure  exerted  by 
these  growths  upon  nerve  trunks,  may  arise.  Another  characteristic  of 
chloroma  is  the  peculiar  green  hue  of  the  new-growths  ;  the  cause  of  this 
coloration  is  unknown. 

The  latest  study  of  this  remarkable  and  rare  disease  is  that  made  by 
Dock  and  Warthin.  These  investigators  conclude  that  the  disease  consists 
in  a  neoplastic  hyperplasia  of  the  parent  cells  of  the  leukocytes  which 
develops  primarily  in  the  red  bone-marrow  and  secondarily  affects  the  peri- 
osteum. Typical  and  atypical  leukocytes  are,  therefore,  developed,  set 
free  in  the  blood,  and  may  appear  as  large  lymphocytes  or  as  neutrophiles 
or  eosinophile  myelocytes.  On  the  other  hand,  it  is  not  essential  for  the 
diagnosis  of  chloroma  that  these  leukocytic  changes  be  present,  for  some- 
times they  fail  to    appear.    Chloroma  may,  therefore,  be  regarded  as  a 


PURPURA  785 


malady  lying  midway  between  leukaemia  and  lymphosarcoma.  The 
essential  point  of  differentiation  is  the  development  of  the  green  masses  of 
lymphoid  tissue  which  are  distinctly  neoplastic  in  character.  The  prog- 
nosis of  chloroma  is  invariably  fatal. 


AN.ffiMIA  INFANTUM. 

Definition. — Under  this  term  von  Jaksch  has  described  a  form  of  anaemia 
occurring  in  children  under  four  years  of  age  and  resembling  leukaemia  in 
many  respects,  in  that  there  is  great  enlargement  of  the  spleen,  marked 
leukocytosis,  some  increase  in  the  size  of  the  liver  and  of  the  lymph  nodes. 
Von  Jaksch  believes  that  this  malady  separates  itself  from  a  true  leukaemia 
of  infancy  by  the  fact  that  the  increase  in  the  white  cells  is  never  so  marked 
as  in  true  leukaemia,  that  children  often  recover,  and  because  there  is  never 
any  leukaemic  infiltration  of  the  viscera.    The  cause  is  not  known. 

The  red  cells  are  so  much  decreased  that  they  number  only  from  3,000,000 
to  1,500,000.  There  are  also  present  poikilocytes  and  usually  a  large  number 
of  nucleated  red  cells.  The  total  leukocytosis  rarely  exceeds  50,000,  the  chief 
increase  being  in  the  mononuclear  corpuscles.  Myelocytes  are  absent,  or 
not  present  in  sufficient  number  to  justify  a  diagnosis  of  leukaemia.  The 
liver  and  spleen  are  enlarged.  The  condition  is  usually  met  with  in  rachitic 
or  syphilitic  children  and  in  those  suffering  from  chronic  gastrointestinal 
catarrh. 

Treatment. — The  treatment  is  identical  with  that  of  leukaemia. 


PURPURA. 

Under  this  term  is  included  all  those  cases  in  which,  as  the  result  of  various 
causes,  extravasations  of  small  quantities  of  blood  take  place  into  the  skin. 
These  extravasations  are  multiple  and  often  very  widespread.  It  must  be 
borne  in  mind  that  under  no  condition  is  purpura  a  disease  in  itself.  It  is  a 
symptom  or  manifestation  of  some  disturbance  in  the  nutrition  of  the  smaller 
bloodvessels  or  of  the  blood  itself.  Thus,  it  occurs  as  a  manifestation  of 
severe  infections,  such  as  profound  septicaemia,  scarlet  fever,  typhus  fever, 
measles,  and  smallpox,  and  in  infections  not  so  well  understood,  in  which 
micro-organisms,  known  and  unknown,  are  manifestly  the  cause  of  the 
condition.  Various  investigators  have  isolated  from  cases  of  purpura  such 
micro-organisms  as  the  Streptococcus  pyogenes,  the  Staphylococcus  pyogenes 
aureus,  the  pneumococcus,  and  the  Bacillus  aerogenes  capsulatus.  The 
Bacillus  coli  communis  has  also  been  obtained  from  the  blood.  Again,  cer- 
tain poisons,  as  snake  venom  and  poisons  from  the  mineral  kingdom,  may 
cause  purpura.  A  large  number  of  cases  of  marked  purpura  have  developed 
in  persons  who  have  taken  iodide  of  potassium,  and  after  the  use  of  mercury, 
copaiba,  and  the  chlorate  of  potassium.  It  may  also  develop  as  the  result 
of  some  congenital  defect  in  the  blood,  as  in  haemophilia. 

Diseases  generally  called  diathetic,  such  as  scurvy,  tuberculosis,  Hodgkin's 
50 


786  DISEASES  OF   THE  BLOOD 

disease,  and  chronic  nephritis,  may  cause  this  s}Tiiptom.  Purpuric  extravasa- 
tions sometimes  develop  after  severe  neuralgic  seizures  in  locomotor  ataxia 
and  along  the  course  of  certain  nerves  in  hysterical  women. 

Some  writers  have  given  the  name  purpura  hsemorrhagica  to  that  form  of 
purpura  in  which,  in  addition  to  the  extravasations  into  the  skin,  there  are 
also  lesions  of  this  character  in  the  mucous  membrane  of  the  mouth. 

Under  the  name  ''purpura  rheumatica,"  or  " peliosis  rheumatica,"  a  form 
of  purpura  develops  in  which  there  is  a  distribution  of  the  spots  chiefly  about 
the  large  joints,  particularly  about  the  knees.  Associated  with  this  eruption 
there  is  swelling  of  the  tissues  about  the  joints  resembling  that  seen  in  rheu- 
matism. There  is  usually  no  fever  and  little  pain,  although  the  joints  appear 
stiffened  at  times.  It  was  this  arthritic  state  that  gave  the  name  "  purpura 
rheumatica  "  to  the  condition.  In  some  instances  the  joint  disorder  is  due 
to  acute  rheumatism  but  in  the  majority  it  is  some  other  form  of  infec- 
tion. 

Under  the  name  of  "Schonlein's  disease"  a  very  much  more  severe  t}^e  of 
this  condition  has  been  described.  Many  of  the  joints  are  affected,  so  that 
the  patient  is  bedridden,  and  the  extravasations  of  blood  into  the  submucous 
tissues  and  into  the  skin  are  so  copious  that  great  swelling  and  even  slough- 
ing may  result.  Some  years  ago  I  saw,  in  consultation  with  Dr.  "Wilson,  of 
Woodbury,  New  Jersey,  another  physician  who  not  only  had  the  joints  of 
the  extremities  greatly  affected,  but  the  inferior  maxillary  joint  was  also 
involved.  The  buccal  mucous  membrane  was  so  infiltrated  that  we  feared 
the  development  of  noma,  and  the  whole  face  was  much  distorted  by  the  in- 
filtration. Notwithstanding  the  severity  of  the  lesions  and  the  intense  pros- 
tration of  the  patient,  recovery  usually  takes  place.  Care  must  be  taken  that 
this  form  of  purpura  is  not  confused  with  scurvy  or  scorbutus  (which  see). 

"Henoch's  purpura  "  is  a  condition  affecting  children  and  characterized  by 
lesions  in  the  skin,  which  may  be  a  combination  of  purpura  and  erythema 
multiforma.  The  joints  may  or  may  not  be  affected,  and  bleeding  from  the 
gums  may  appear.  The  most  distinctive  symptom,  which  is  not  present  in 
all  cases,  but  which  may  be  present  when  the  others  are  absent,  is  gastro- 
intestinal crises,  in  which  the  child  is  seized  with  pain,  diarrhoea,  and 
vomiting.  All  these  symptoms  are  prone  to  recur  at  irregular  intervals. 
Recovery  usually  occurs,  except  in  those  cases  in  which  the  hemorrhagic  state 
affects  the  kidneys,  when  a  fatal  result  may  ensue. 

A  form  of  fulminating  purpura  sometimes  develops  in  young  girls  and 
causes  death  in  a  few  days,  the  patient  being  apparently  overwhelmed  by 
some  unknown  infection. 

There  are  three  hemorrhagic  affections  of  the  newborn  that  occasionally 
occur. 

In  children  with  inherited  syphilis,  hemorrhage  from  the  mucous  mem- 
branes and  from  the  navel,  with  intense  subcutaneous  extravasations,  may 
occur  and  cause  death.  The  autopsy  shows  hemorrhages  into  the  liver  and 
kidneys,  and  signs  of  inherited  syphilis  in  these  parts  as  well. 

Under  the  name  of  Winckel's  disease  a  condition  of  jaundice  develops 
within  a  week  of  birth,  followed  by  dyspnoea,  hsemoglobinuria,  and  deep 
cyanosis.     I  saw  a  case  some  years  ago  in  which  the  child  was  so  cyanotic 


HEMOPHILIA  787 

that  parts  of  its  body  were  blue-black.  The  autopsy  in  such  a  case  shows 
swelling  of  the  spleen  and  fatty  degeneration  of  the  liver  and  kidneys. 

A  third  state  called  "morbus  maculosus  neonatorum"  develops  in  new- 
born infants,  and  consists  in  hemorrhages  from  the  stomach,  intestines,  or 
from  the  navel.  It  is  rarely  seen  in  private  practice,  and  is  probably  due  to 
some  infection. 

Hayem  and  Bensaude  have  stated  that  in  purpura  haemorrhagica  the  blood, 
when  allowed  to  stand  in  a  vessel  for  twenty-four  hours,  slowly  clots,  but  the 
clot  does  not  contract  to  any  extent,  and  therefore  does  not  squeeze  out  the 
serum  as  it  does  in  normal  blood. 

Treatment. — The  treatment  of  all  forms  of  purpura  is  based  upon  the 
recollection  of  two  facts,  viz.,  first,  that  the  condition  is  due  in  most  cases  to 
an  infection  or  at  least  to  a  cause  which  has  impaired  the  health,  and  therefore 
every  means  to  aid  the  vital  resistance  of  the  body  must  be  resorted  to.  The 
food  should  be  easily  digested  and  nutritious;  the  patient,  if  able  to  travel, 
should  be  removed  to  some  place  where  he  can  bask  all  day  in  the  sunshine. 
Moderate  doses  of  tincture  of  the  chloride  of  iron  should  be  given  each  day 
to  combat  the  infection  and  the  ansemia. 

The  second  point  to  be  recalled  is  that  certain  drugs  may  be  employed 
to  increase  the  coagulability  of  the  blood.  Of  these,  the  only  ones  with  any 
real  claim  to  power  are  the  lactate  and  chloride  of  calcium,  which  may  be 
given  in  the  dose  of  20  grains  three  times  a  day  to  an  adult,  well  diluted 
with  water.  Certain  cases  seem  unable  to  absorb  calcium  salts  through  the 
alimentary  canal  and  these  should  be  treated  by  hypodermic  injection. 
The  solution  should  not  be  stronger  than  1  part  in  20  of  water  and  the 
lactate  should  be  used  because  the  chloride  is  too  irritating.  The  effect  of 
one  day's  dose  of  60  grains  lasts  three  or  four  days,  and  it  should  not  be  too 
frequently  repeated,  since,  if  this  is  done,  coagulabiHty  is  decreased.  Turpen- 
tine, oil  of  erigeron,  ergot,  and  sulphuric  acid  have  all  been  used.  Their 
employment  is  purely  empirical,  and  there  is  httle  reason  to  rely  on  them. 
Several  ounces  of  nutritious  food,  fresh  air,  and  a  day  in  the  bright  sunlight 
will  do  more  good  in  this  state  than  all  the  medicines  can  accomplish,  and 
this,  too,  without  damaging  the  stomach.  The  use  of  these  remedies  in  this 
state  is  putting  "  drugs  of  which  we  know  little  into  bodies  of  which  we  know 
less." 

HiEMOPHILIA. 

Definition. — Hsemophilia  is  a  condition  of  the  body  in  which  there  is  an 
inability  to  arrest  hemorrhage  by  the  normal  coagulation  of  the  blood,  or  in 
which  hemorrhage  arises  apparently  without  cause  and  persists  without  any 
attempt  being  made  by  nature  to  arrest  it.  The  disease  is  essentially  hered- 
itary in  most  cases,  and  it  is  an  extraordinary  fact  that  the  hemorrhagic 
tendency  is  transmitted  to  males  only  through  the  female  parent,  although 
the  mother  is  herself  usually  not  afflicted. 

Etiology. — The  cause  of  this  condition  is  entirely  unknown.  Virchow 
believed  it  to  be  dependent  upon  an  abnormal  thinness  and  narrowness  of 
the  arteries,  but  it  is  probably  due  to  some  deficiency  in  the  coagulability  of 


788  DISEASES  OF   THE  BLOOD 

the  blood  as  well.  Stengel  has  recorded  an  instance  in  which  the  hemor- 
rhagic tendency  was  Umited  to  one  part  of  the  body,  namely,  the  head,  and 
Osier  states  that  the  late  D.  Hayes  Agnew  described  to  him  a  similar  case. 

Pathology  and  Morbid  Anatomy. — There  are  no  changes  in  the  blood  cells 
that  account  for  this  condition;  indeed, no  peculiar  state  of  the  blood  is  found 
save  a  diminished  coagulability.  An  examination  of  the  tissues  of  the 
various  organs  is  also  practically  negative,  save  that  if  the  hemorrhage  has 
been  profuse  the  changes  always  met  with  in  marked  anaemia  are  present. 

Symptoms. — An  active  but  oozing  capillary  hemorrhage  is  the  form  in 
which  the  bleeding  usually  occurs,  and  it  follows  in  some  instances  very  slight 
injury.  Thus,  the  mere  blowing  of  the  nose  may  be  sufficient  to  rupture 
the  fine  vessels  of  the  nasal  mucous  membrane  and  cause  a  dangerous  loss 
of  blood,  and  epistaxis  is  the  most  common  form  in  which  this  condition 
manifests  itself.  Another  common  source  of  the  blood  is  from  the  gum 
after  tooth  extraction. 

In  some  cases  bloody  effusions  take  place  into  the  large  joints. 

Prognosis. — The  prognosis  depends  largely  upon  the  severity  of  the  loss 
of  blood  and  upon  the  abihty  of  the  patient  to  restore  the  quantity  lost  before 
the  next  bleeding  comes  on.  Fully  50  per  cent,  of  bleeders  die  before  the 
seventh  year,  but  some  live  to  old  age.  Although  girls  who  reach  puberty 
menstruate  with  their  entrance  upon  adult  life,  and  so  are  exposed  to  an 
excessive  loss  of  blood,  their  mortality  rate  in  this  disease  is  not  so  high  as 
that  of  boys'. 

Treatment. — The  treatment  consists  in  the  building  up  of  the  general 
health  by  out-door  life  and  exposure  to  sunshine,  and  in  the  use  of  small  tonic 
doses  of  iron  and  arsenic  if  anaemia  is  present.  If  a  special  tendency  to 
hemorrhage  exists  at  any  particular  time,  calcium  lactate  or  chloride  should 
be  given  in  doses  varying  from  10  to  20  grains  three  or  four  times  a  day,  well 
diluted,  to  increase  the  coagulability  of  the  blood,  but  this  must  not  be  used 
for  long  periods  without  intermission,  as  after  a  certain  amount  is  taken  the 
coagulability  of  the  blood  is  decreased  and  not  increased.  The  local  treatment 
consists  in  the  use  of  tampons  wet  with  adrenalin  chloride,  1 :  1000,  or  gelatin 
solution  of  the  consistency  of  thin  mucilage  may  be  used  for  the  same  pur- 
pose. When  adrenalin  cannot  be  obtained,  peroxide  of  hydrogen  may  be 
applied  in  the  same  manner  to  the  bleeding  spot.  When  the  hemorrhage 
is  from  the  gum,  a  compress  made  of  punk  may  be  used,  or  a  compress  wet 
with  a  saturated  solution  of  alum,  with  Monsel's  solution,  or  with  adrenalin 
chloride  solution,  1:1000. 


DISEASES  OE  NUTEITION. 


DIABETES  MELLITUS. 


Definition. — Diabetes  mellitus  is  a  disease  characterized  by  the  appearance 
in  the  urine  of  glucose,  and  the  development  of  polyuria,  thirst,  and  excessive 
appetite,  with  impairment  of  nutrition,  and  in  some  cases  progressive 
emaciation.  The  mere  presence  of  glucose  in  the  urine  does  not  necessarily 
indicate  that  diabetes  is  present.  The  glycosuria  must  be  associated  with 
other  morbid  processes  to  present  the  symptom-complex  of  the  disease. 

History. — Diabetes  mellitus  has  been  known  since  the  time  of  Christ, 
but  it  was  not  till  the  latter  part  of  the  seventeenth  century  that  WilHs,  in 
England,  noted  that  the  sweet  taste  of  the  urine  was  probably  due  to  sugar, 
and  not  until  1775  that  Dobson,  of  England,  actually  obtained  sugar  from  the 
urine.  Since  that  time  a  host  of  experimental  investigators  and  clinicians 
have  studied  the  disease  from  every  aspect  and  have  added  much  to  our 
knowledge  of  it,  but  no  one  has  as  yet  been  able  to  give  us  a  clear  conception 
of  the  causes  of  the  malady. 

Distribution  and  Frequency. — Diabetes  occurs  in  all  parts  of  the  civilized 
world,  but  is  much  more  common  in  Europe  than  in  the  United  States.  It 
is  frequently  met  with  in  France,  in  Sweden,  in  Italy,  in  India,  and  Ceylon, 
but  is  comparatively  rare  in  Russia,  Holland,  and  in  Brazil.  Negroes  rarely 
suffer  from  it,  but  Hebrews  are  so  frequently  affected  by  it  that  it  may  almost 
be  said  to  be  the  prevalent  disease  of  that  race.  Kiilz,  of  Germany,  found 
that  in  692  cases  of  diabetes  17.8  per  cent,  occurred  in  Jews,  which  is  all  the 
more  remarkable  when  we  consider  that  Hebrews  constitute  only  1.2  per  cent, 
of  the  population  of  that  country.  Frerichs  found  102  Jews  in  400  diabetic 
patients,  and  von  Noorden  252  Jews  in  650  patients  suffering  from  this  disease. 

It  is  a  disease  of  adult  life,  as  a  rule,  but  very  young  children  suffer  from 
it  occasionally,  and  even  nurslings  have  from  time  to  time  been  reported  as 
presenting  well-developed  cases  of  the  malady.  To  emphasize  its  rarity  in 
children.  Stern  may  be  quoted  in  his  assertion  that  only  thirteen  deaths  have 
been  reported  from  this  malady  as  occurring  in  children  under  five  years  of 
age  in  the  past  thirteen  years.  It  is  more  common  in  males  than  in  females 
in  the  proportion  of  3  to  2. 

The  statement  generally  made  that  diabetes  is  a  disease  of  cities  rather 
than  of  country  districts  is  not  altogether  true.  Some  years  ago  Purdy 
showed  that,  as  a  rule,  it  was  much  more  frequent  in  the  country  districts 
than  in  cities.  In  the  United  States  the  disease  is  much  less  frequent  in 
the  Gulf  and  South  Atlantic  States  than  anywhere  else. 

(789) 


ron 

1  1870  to  1880  . 

.  191 

n 

1880  to  1890  . 

.  280 

11 

1890  to  1900  . 

.  470 

790  DISEASES  OF  NUTRITION 

There  can  be  no  doubt  that  the  disease  is  becoming  very  much  more  fre- 
quent than  it  was  several  decades  ago.  I  showed  this  in  a  paper  pubhshed 
some  years  since,  based  upon  statistics  gathered  from  the  Jefferson  Medical 
College  Hospital  and  other  large  hospitals  here  and  abroad.  Since  then 
additional  statistics  have  been  collected  which  indicate  the  correctness  of 
these  earlier  conclusions. 

According  to  the  mortality  statistics  of  the  United  States  Census  Reports 
for  six  decades,  the  proportion  of  deaths  from  diabetes  mellitus  in  100,000 
deaths  from  all  known  causes  has  been  as  follows: 

From  1840  to  1850     .  .       72 

"      1850  to  1860     .  .       98 

"     1860  to  1870     .         .     170 

It  seems  scarcely  credible  that  so  great  an  increase  could  have  occurred, 
and  it  is  possible  that  greater  care  in  examining  patients  and  in  regard  to  cor- 
rect death  certificates  is  responsible  for  part  of  the  increase,  yet  the  records 
of  the  Massachusetts  General  Hospital  from  1824  to  1898  show  that  four 
times  as  many  cases  of  diabetes  were  admitted  to  the  hospital  during  the 
last  thirteen  years  of  that  period  as  during  the  first  fifteen  years.  On  the 
other  hand,  it  is  only  fair  to  state  that  the  statistics  of  L'Hotel  Dieu,  Lyons, 
for  seventeen  years,  which  were  collected  by  Alix,  for  Lupine,  who  attempted 
to  ascertain  if  diabetes  was  increasing  in  a  certain  district  of  France,  do  not 
show  any  increase  in  the  disease. 

Etiology. — ^The  causes  of  diabetes  are  not  known,  although  it  is  a  well- 
recognized  fact  that  lesions  in  certain  portions  of  the  nervous  system  are 
followed  by  glycosuria,  and  that  certain  alterations  in  the  islands  of  Lan- 
gerhans  in  the  pancreas  and  in  the  circulation  of  the  liver  are  also  followed 
by  the  same  symptom.  (See  Pathology.)  As  somewhat  indirect  causes 
we  recognize  severe  nervous  strain  and  errorrs  in  diet,  but  these  alone  are 
not  sufficient  to  cause  even  glycosuria,  much  less  true  diabetes,  in  the  vast 
majority  of  human  beings. 

There  is  some  evidence  to  indicate  that  the  disease  is  hereditary,  for 
sometimes  it  happens  that  several  members  of  the  same  family  suffer  from 
the  malady,  but  this  may  be  due  to  their  being  exposed  to  the  same  exciting 
causes,  whatever  they  may  be.  A  more  pronounced  factor  than  any  so 
far  named  seems  to  be  excessive  indulgence  in  rich  foods  and  sweet  wines, 
but  a  very  small  proportion  of  the  persons  who  commit  these  dietetic  errors 
suffer  from  diabetes. 

Pathology. — Of  the  pathology,  or  morbid  physiology,  of  diabetes  we  are 
very  ignorant,  although  an  immense  amount  of  skilled  research  has  been 
devoted  to  this  subject  for  years.  It  is  a  well-recognized  fact  that  in  all 
human  beings  glycogen  is  prepared  from  carbohydrate  foods,  and  even 
from  proteids  and  fats,  and  deposited  in  the  liver  and  in  the  muscles, 
where  it  lies  as  in  a  storehouse  as  reserve  food.  It  also  circulates  in  the 
healthy  blood  stream  in  the  proportion  of  about  1 :  1000,  and  so  is  carried 
to  various  parts  of  the  body  for  nutritional  purposes. 

There  are  many  conditions  which  produce  loss,  or  leakage,  of  this  sub- 
stance in  the  form  of  glucose  in  the  urine.     Thus,  glycosuria,  or  the  mere 


DIABETES  MELLITUS  791 

presence  of  sugar  in  the  urine,  may  follow  the  ingestion  of  an  excess  of  either 
cane-sugar  or  grape-sugar  or  an  excess  of  carbohydrate  food.  Under  these 
circumstances  it  is  simply  an  overflow  of  material  which  the  system  cannot 
utilize.  This  being  true,  it  is  readily  conceivable  that  in  certain  states  of 
disease  the  system  may  be  unable  to  utilize  the  ordinary  amount  of  glycogen, 
and  therefore  it  escapes  from  the  body.  This  view  receives  support  from 
the  theory  advanced  by  Loewi  and  Kolisch,  who  believe  that  there  is  in  the 
organism  a  body,  or  ferment,  or  agent,  which  binds  the  glycogen  in  the 
tissues  in  such  a  form  that  it  does  not  appear  in  the  blood  in  excess.  If  for 
any  reason  this  binding  body  (Bindekorper)  is  diminished  in  power,  an 
excess  of  glucose  passes  to  the  kidneys  and  so  escapes  from  the  body.  This 
view  explains  a  considerable  number  of  cases  of  glycosuria,  but  by  no  means 
all  of  them. 

It  is  a  well-known  fact  that  injury  or  disease  of  the  so-called  diabetic 
centre  of  Claude  Bernard  in  the  medulla  is  followed  by  glycosuria,  and 
that  this  glycosuria  is  directly  due  to  a  disorder  of  the  blood  supply  in  the 
capillaries  of  the  liver.  This  may  interfere  with  the  "binding"  of  the  gly- 
cogen in  that  organ.  Again,  the  administration  of  phloridzin  will  produce 
glycosuria,  but  this  condition  is  quite  different  in  its  causation  from  ordinary 
glycosuria,  in  that  the  drug  acts  upon  the  kidney  structure  in  such  a  way 
that  it  permits  a  leakage  of  the  normal  content  of  glycogen  from  the  blood. 
In  other  words,  in  this  state  the  fault  does  not  lie  in  an  inability  of  the  body 
to  use  its  glycogen,  but  in  the  inability  of  the  kidneys  to  prevent  its  escape 
from  the  body. 

We  find,  therefore,  that  glycosuria  and  diabetes  mellitus  are  by  no  means 
identical  conditions  necessarily,  although  glycosuria  is  the  predominant 
symptom  in  this  disease.  There  may  be  a  loss  of  sugar  in  the  urine  for 
many  years  without  any  impairment  of  health,  or  the  glycosuria  may  not 
be  constant,  but  recurrent  and  appear  only  when  nutritional  processes  are 
for  any  reason  jarred  or  disturbed.  In  true  diabetes  mellitus,  on  the  other 
hand,  there  are  associated  with  the  glycosuria  more  or  less  profound  impair- 
ment of  nutrition,  with  wasting,  emaciation,  and  the  development  in  the 
body  of  certain  poisons  which  act  very  deleteriously  and  may  cause  death. 

These  distinctions,  which  serve  to  separate  in  the  mind  of  the  student 
glycosuria  from  true  diabetes  mellitus,  however,  like  many  other  dis- 
tinctions, do  not  actually  hold  true  in  all  cases,  for  we  frequently  see  per- 
sons who  begin  with  the  leakage  of  sugar  into  the  urine  and  end  with  true 
diabetes;  and  we  meet  intermediate  cases  in  which  the  degree  of  emaciation, 
thirst,  and  polyphagia  is  so  mild  that  it  is  difficult  to  tell  whether  the  patient 
is  a  sufferer  from  an  inability  to  deal  with  carbohydrate  food  or  is  really 
diabetic. 

The  question  of  the  pathology  of  this  disease,  as  far  as  we  know  it  to-day, 
can  perhaps  be  summed  up  in  the  following  words:  In  certain  individuals 
there  exists,  as  a  result  of  a  congenital  or  acquired  defect  in  the  metabolic 
functions  of  the  body,  an  inability  to  utilize  for  the  purpose  of  nutrition  all 
the  carbohydrate  material  which  is  taken  as  food.  Such  persons  suffer 
from  simple  glycosuria.  If  the  defect  just  referred  to  becomes  more  marked 
they  gradually  lose  the  power  to  retain  and  utilize  any  noteworthy  quantity 


792  DISEASES  OF  NUTRITION 

of  the  carbohydrates  ingested,  and  when  this  condition  develops  they  speedily 
emaciate  and  lose  vital  resistance.  Finally,  by  reason  of  some  further 
defect  in  the  organs  whose  functions  govern  nutrition,  such  persons  actually 
convert  their  body  fat  and  proteid  tissues  into  sugar  and  pass  it  from  them 
in  the  urine,  in  which  cases  death  soon  closes  the  scene. 

Certain  factors  tend  to  produce  the  chain  of  disturbances  just  enumerated, 
and  all  these  agencies  may  cause  changes  which  may  be  mild  and  continue 
so,  or,  in  another  case,  become  severe  and  rapidly  fatal.  These  may  be 
mentioned  as  follows: 

1.  Heredity.  It  is  conceivable  that  the  parent  may  hand  down  to  the 
offspring  certain  defects  which  will  interfere  with  the  proper  utilization 
of  carbohydrates. 

2.  Errors  in  diet,  both  as  to  food  and  drink.  It  is  conceivable  that  errors 
of  this  character  can  so  pervert,  or  overwhelm,  the  processes  of  nutrition 
or  elimination  that  primary  glycosuria  followed  by  permanent  diabetes 
may  ensue.  Thus,  the  excessive  beer-drinkers  of  Bavaria  often  suffer  from 
this  disease,  probably  because  of  the  excess  of  fluid,  of  alcohol,  and  of 
carbohydrate  which  they  ingest.  These  factors  pervert  the  function  of  the 
liver,  of  the  pancreas,  and  of  the  kidney. 

3.  Profound  nervous  worry  and  mental  anxiety  are  undoubtedly  followed 
by  diabetes  in  some  persons  probably  because  the  nervous  mechanism  gov- 
erning nutritional  processes  is  perverted  in  function  by  the  stress  and  strain. 

4.  Certain  injuries  to  the  central  nervous  system  may  so  result,  for  severe 
trauma  of  the  head  or  the  growth  of  an  intracranial  tumor  may  produce 
diabetes. 

5.  Certain  infectious  diseases  may  produce  temporary  glycosuria,  which 
disappears  with  the  acute  disease  or  persists  and  becomes  true  diabetes, 
probably  because  the  acute  infection  has  damaged  beyond  repair  nervous 
centres  or  glands  whose  function  is  to  control  glycogenesis  and  the  utiliza- 
tion of  glycogen. 

6.  Diathetic  diseases  such  as  gout  undoubtedly  cause,  or  predispose  to, 
diabetes  in  some  cases,  but  whether  this  influence  is  direct  or  simply  a  sign 
of  general  perversion  of  metabolism  we  do  not  know. 

Finally,  it  must  be  recalled  that  of  all  the  organs  of  the  body  the  liver 
and  the  pancreas  are  the  viscera  which  show  the  greatest  morbid  changes 
in  true  diabetes.  Not  only  is  the  liver  the  organ  which  is  chiefly  concerned 
with  the  manufacture  and  storing  of  glycogen,  but  the  pancreas  undoubtedly 
exercises  a  very  powerful  influence  upon  the  glycogenic  processes;  for  not 
only  does  it  secrete  digestive  ferments  which  act  in  the  intestine,  but  also  a 
ferment  or  factor  which  enters  the  blood  stream  and  is  intimately  concerned 
with  the  utilization  of  glycogen.  Thus,  if  the  pancreas  is  extirpated  glyco- 
suria is  at  once  developed,  and  the  same  condition  ensues  if  the  gland  is 
totally  destroyed  by  disease.  It  would  appear  that  the  so-called  islands  of 
Langerhans  are  the  portion  of  the  gland  which  exercises  this  influence 
upon  the  processes  connected  with  the  utilization  of  glycogen,  and  in 
many  cases  these  islands  are  found  to  be  distinctly  diseased.  While  dis- 
ease of  the  pancreas  is  responsible  for  the  development  of  diabetes  in 
some  cases  of  the  malady,  it  is  also  a  fact  that  in  many  cases  of  very 


DIABETES  MELLITUS  793 

severe  diabetes  the  most  careful  examination  of  the  pancreas  after  death 
fails  to  discover  any  lesion  that  can  be  considered  in  any  way  responsible  for 
the  malady.  It  seems  evident,  therefore,  that  many  causes  may  so  pervert 
nutritional  processes  that  glycosuria  or  true  diabetes  may  result,  and  in  this 
sense  it  may  be  said  that  diabetes  is  not  a  primary  disease,  but  rather  a 
symptom  of  some  primary  lesion  which  we  do  not  at  present  understand. 

Morbid  Anatomy. — The  changes  found  in  the  islands  of  Langerhans  are 
various.  In  some  cases  they  manifest  capillary  engorgement  or  hemorrhagic ' 
extravasation.  In  others  there  is  found  a  pericapillary  or  peri-insular  scle- 
rosis, an  atrophy,  a  necrobiosis,  or  hyaline  degeneration.  The  latter  is 
probably  always  primary,  and  the  former  conditions  usually  secondary. 
Aside  from  changes  of  the  islands  of  Langerhans  in  the  pancreas,  the  most 
notable  changes  presented  postmortem  in  any  of  the  organs  of  the  body  are 
found  in  the  liver.  This  organ  is  usually  markedly  hypersemic  and  darker 
in  color  than  in  diseases  which  do  not  affect  its  functions.  Microscopically 
it  is  found  that  its  capillaries  are  congested,  and  that  the  liver  cells  are 
enlarged  and  show  a  tendency  to  coalesce.  These  changes  are  not,  how- 
ever, peculiar  to  the  disease,  being  found  in  other  states;  and  it  is  a  fact 
worthy  of  consideration  that  when  death  results  in  cases  of  severe  disease 
of  the  liver,  glycosuria  is  rather  an  unusual  symptom. 

There  is  a  form  of  diabetes,  associated  with  hepatic  cirrhosis  and 
bronzing  of  the  skin,  called  "bronzed  dialDetes,"  owing  to  the  color  of  the 
skin. 

The  structure  of  the  kidneys  is  diseased  in  a  very  large  number  of  diabetics. 
These  changes  are  not  in  any  way  a  part  of  the  disease  itself,  but  result  from 
the  increased  activity  of  these  organs  in  excreting  water  and  sugar,  and  by 
reason  of  the  effect  of  toxic  substances,  such  as  acetone,  diacetic  acid,  and 
oxybutyric  acid,  which,  as  they  are  eliminated,  damage  the  renal  tissues. 
The  constancy  of  renal  changes  in  diabetes  is  proved  by  the  frequency  with 
which  these  organs  are  found  diseased  at  autopsy  when  death  has  occurred 
from  this  disease.  Out  of  121  autopsies,  reported  by  Griesinger,  Dickinson, 
and  Seeger,  renal  changes  in  diabetes  were  found  in  77  cases,  and  Elliott  has 
collected  statistics  from  European  clinicians  which  show  that  albuminuria 
is  present  in  43.68  per  cent,  of  all  cases  of  diabetes.  The  renal  lesions  may 
be  divided  into  two  classes:  In  one  class,  which  is  usually  met  with  in 
chronic  cases,  an  ordinary  chronic  nephritis  develops  in  which  parenchy- 
matous and  interstitial  changes  both  occur.  In  the  second  form,  which  is 
really  toxic  in  origin,  there  is  a  hyaline  degeneration  of  the  tubular 
epithelium,  the  so-called  "cellular  necrosis  of  Ebstein."  A  so-called  gly- 
cogen degeneration  of  Henle's  loop  and  of  the  straight  uriniferous  tubules 
(Ehrhch's  lesion)  is  also  found,  but  it  cannot  be  claimed  that  these  changes 
are  pathognomonic. 

The  changes  in  the  nervous  system  are  usually  of  little  importance. 
Peripheral  neuritis  is  often  present.  Probably  this  is  purely  secondary. 
Distinct  changes  have,  however,  been  found  in  the  spinal  cord  in  cases 
of  diabetes  mellitus,  notably  by  Williamson.  Using  Van  Gieson's  method 
this  clinician  found  an  increase  in  connective  tissue  in  the  columns 
of   Goll   in    the    cervical    area.     There    was    also    a    diminution  in   size 


794  DISEASES  OF  NUTRITION 

of  the  nerve  fibres  in  these  columns,  and  the  myelin  sheaths  and  axis 
cylinders  were  also  diminished  in  size,  although  a  few  of  the  myelin 
sheaths  were  distended.  When  Marchi's  method  was  employed  degen- 
erated fibres  were  seen  in  Goll's  columns  in  the  cervical,  dorsal,  and 
lumbar  regions,  and  a  few  degenerated  fibres  were  present  in  Burdach's 
columns.  So,  too,  degeneration  was  found  in  the  intramedullary  course  of 
the  posterior  nerve  roots,  between  the  posterior  surface  of  the  cord  and  the 
posterior  horn  of  gray  matter,  and  to  the  median  side  of  the  posterior  horn. 
These  latter  changes  were  most  marked  in  the  lumbar  and  cervical  region. 
In  a  few  instances  degenerated  fibres  were  seen  in  the  posterior  roots  just 
outside  the  pia  mater.  These  changes  are  probably  secondary  and  due  to 
the  altered  condition  of  the  blood  in  diabetes. 

The  blood  is  not  only  unduly  rich  in  glucose,  but  sometimes  contains  an 
excess  of  fat-globules  to  such  an  extent  that  it  may  form  a  cream-like  layer 
on  the  clot  when  it  stands  after  withdrawal.  Fraser  has  recorded  a  case  in 
which  an  analysis  of  the  blood  showed  that  it  contained  16.5  per  cent,  of 
fat  and  the  pleural  fluid  20  per  cent. 

The  blood  in  some  cases  of  diabetes  mellitus  is  of  a  pale  salmon  color 
which  has  been  thought  to  be  due  to  the  presence  of  fat,  and  for  this  reason 
this  condition  has  been  called  lipsemia.  Futcher,  however,  has  shown  that 
this  appearance  is  not  entirely  due  to  fat,  for  it  is  not  possible  to  remove  it 
from  drawn  blood  by  the  use  of  ether,  and  the  granules  do  not  stain  black 
with  osmic  acid.  He  suggests  that  these  granules  are  in  part  albuminous. 
More  recently  Cole,  in  testing  the  blood  in  a  case  for  Hale  ^Vliite,  reaches 
the  conclusion  that  true  fat  is  not  present,  but  that  the  foreign  material 
seems  to  be  an  ester  of  cholesterine  with  one  of  the  higher  fatty  acids.  Heyl 
showed  in  1880  that  this  state  of  the  blood  could  be  demonstrated  in  the 
retinal  vessels,  and  Hale  White  has  more  recently  recorded  a  beautiful  case 
of  the  same  character. 

The  lungs  are  often  found  to  contain  tuberculous  foci,  and  may  show  well- 
developed  bronchopneumonia  or  croupous  pneumonia,  but  these  are  the 
result  of  terminal  infections  and  not  part  of  the  primary  disease.  Arterio- 
sclerosis and  its  train  of  associated  lesions  are  of  frequent  occurrence  in 
diabetes  mellitus. 

Symptoms. — The  symptoms  of  diabetes  vary  very  greatly  in  their  severity  in 
different  cases,  so  greatly  that  it  is  almost  impossible  to  detail  any  array  of 
symptoms  which  are  common  to  all  cases.  In  many  instances  the  glycosuria 
exists  for  a  considerable  period  of  time  before  the  patient  suffers  from 
symptoms  which  lead  him  to  think  he  is  not  well.  A  very  well-known 
medical  writer  in  London,  some  years  ago,  first  discovered  he  was  diabetic 
by  observing  that  flies  were  unduly  attracted  to  the  vessel  in  which  he  urin- 
ated, and  later  by  noticing  that  a  few  drops  of  urine  which  accidentally  fell 
on  his  black  trousers  left  a  white  stain  on  drying.  Later  on,  all  the  diabetic 
manifestations  developed,  and  he  died  of  diabetic  gangrene  of  the  foot. 

As  a  rule,  as  the  disease  progresses  the  patient  notices  that  he  passes 
water  more  frequently  and  in  larger  quantity  than  is  normal,  he  develops 
more  or  less  thirst,  and  loses  sexual  desire  and  power.  Later  on  he  begins 
to  feel  languid  and  inert;  he  is  usually  constipated  because  of  his  polyuria, 


DIABETES  MELLITUS  795 

and  he  may  develop  an  inordinate  appetite  in  the  endeavor  to  compensate 
for  the  loss'of  nutriment  through  his  urine.  The  thirst,  the  polyphagia,  and 
the  loss  of  strength  and  flesh  are  usually  in  direct  proportion  to  the  polyuria 
and  the  quantity  of  sugar  excreted.  When  the  polyuria  is  marked  the 
tongue  becomes  glazed,  dry  and  raw  in  appearance,  and  attacks  of  stomatitis 
or  thrush  may  develop.  The  skin  is  also  dry  and  harsh,  and  the  hair  lustre- 
less and  brittle.    The  pulse  is  feeble  and  the  temperature  subnormal. 

Although  the  disease  is  often  characterized  by  excessive  emaciation,  this 
symptom  is  subject  to  extraordinary  variations  in  different  patients. 
Marked  loss  of  flesh  is  almost  constant  in  all  persons  under  twenty-five  years 
of  age,  but  after  this  time  it  is  by  no  means  uncommon  to  meet  with  patients 
who  maintain  their  weight  for  years.  This  holds  true  in  direct  proportion 
to  the  years  of  age  and  the  degree  of  polyuria  and  loss  of  sugar.  Where  the 
tissues  are  freely  drained  of  fluid  or  starved  beyond  repair  the  weight  of 
course  suffers. 

The  urine  in  diabetes  mellitus  is  not  only  abnormal  in  that  it  contains  sugar, 
but  it  not  uncommonly  contains  albumin  as  well.  (See  Complications.) 
Its  specific  gravity  is  high  and  ranges  from  1.025  to  1.045,  and  one  instance 
of  1.074  is  recorded  by  Trousseau.  Such  a  specific  gravity,  however,  is 
exceedingly  rare.  Notwithstanding  its  high  specific  gravity,  however,  the 
urine  is  usually  exceedingly  limpid  and  clear,  it  has  a  sweet  odor,  and  is  acid 
in  reaction. 

The  quantity  of  sugar  present  varies  over  wide  ranges.  Sometimes  it  is 
found  in  as  small  an  amount  as  1  to  3  per  cent.;  in  others  it  is  found  to  be 
present  in  the  proportion  of  10  per  cent.  The  total  quantity  passed  in 
twenty-four  hours  may  be  from  one  ounce,  or  less,  to  a  pound  and  a  half. 
Very  rarely  even  more  escapes.  Dickinson  reports  a  case  that  passed  the 
incredible  amount  of  fifty  ounces  of  sugar  a  day. 

The  quantity  of  urine  is  also  very  great  in  some  cases,  while  in  others  it 
may  not  be  much  above  the  normal  quantity.  As  much  as  six  to  twelve  pints 
are  often  passed  in  each  twenty-four  hours,  and  cases  are  recorded  in  which 
as  much  as  thirty  pints  were  passed  in  this  time. 

Complications  and  Sequelae. — The  complications  and  sequelae  of  diabetes 
mellitus  are  important,  and  so  constantly  present  that  they  may  aid  mate- 
rially in  the  diagnosis  of  the  disease.  Many  of  them  are  dependent  upon 
the  fact  that  the  constant  loss  of  sugar  lowers  nutrition  and  so  decreases 
vital  resistance  to  the  various  infections,  or  they  result  from  perverted 
metabolic  processes  closely  associated  with  the  inability  of  the  body  to 
properly  control  the  functions  governing  glycogenesis  and  the  proper 
utilization  of  glucose  in  the  economy. 

Sweet  has  demonstrated  that  for  certain  organisms  the  blood  loses  its 
bactericidal  power  in  diabetes. 

It  not  infrequently  happens  that  the  first  symptom  presented  by  a  diabetic 
patient  is  repeated  crops  of  boils  or  carbuncles.  When  the  urine  is  examined 
sugar  is  found,  and  it  becomes  evident  that  the  lowered  vitality  caused  by 
diabetes  mellitus  has  permitted  infection  of  the  skin  to  occur.  Sometimes  the 
carbuncle  becomes  malignant  and  speedily  destroys  the  patient.  In  still  other 
instances,  which  are  not  as  common  as  has  been  thought,  diabetic  gangrene 


796  DISEASES   OF  NUTRITION 

occurs,  the  primary  lesion  being  some  break  in  the  skin  of  a  finger  or  toe 
resulting  from  the  blister  made  by  an  ill-fitting  shoe,  or  by  wounding  a  corn. 
Through  this  lesion  infection  takes  place,  and  vital  resistance  is  so  low  that 
the  micro-organism  speedily  causes  the  local  death  of  the  part,  and  almost 
equally  rapidly  may  involve  the  blood  in  a  diabetic  septicsemia.  In  such 
cases  the  gangrene  is  moist.  In  another  class  of  cases,  which  depend  upon 
secondary  vascular  changes  not  due  to  direct  infection,  the  gangrene  is  dry 
and  of  the  so-called  senile  type. 

Elliott's  statistics,  abeady  quoted,  show  that  albuminuria  is  present  in 
about  43.68  per  cent,  of  diabetics.  This  albuminuria  may  at  times  possess 
grave  significance,  and  is  worthy  of  careful  consideration.  It  may  be  said  to 
arise  from  three  causes,  namely,  from  renal  congestion,  due  to  cardiac  feeble- 
ness and  impairment  of  the  circulation ;  from  degeneration  of  the  kidney,  due 
to  true  nephritis,  and,  finally,  to  severe  irritation  or  inflammation  of  the  renal 
tissues  by  the  poisons  of  the  disease.  The  first  type  can  usually  be  relieved 
by  careful  treatment  of  the  heart,  and  the  second  type,  with  casts  in  the  urine, 
is  to  be  regarded  as  a  complicating  condition  of  gravity  superimposed  upon 
one  already  exceedingly  severe.  The  third  or  toxic  type  is,  however,  the  form 
which  presents  the  most  grave  and  alarming  aspect,  for  its  onset  is  usually 
acute;  it  comes  on  when  the  patient  is  already  profoundly  ill,  and  it  often 
betokens  the  rapid  approach  of  diabetic  coma,  which  in  such  a  case  may 
be  said  to  be  partly  due  to  the  renal  lesions.  Many  clinicians  consider 
that  coma  never  comes  on  without  this  associated  symptom.  The  kidney 
condition  is  therefore  to  be  studied  carefully  in  these  cases,  as  it  may  give 
warning  of  approaching  coma. 

Dyspeptic  symptoms  are  often  very  annoying.  They  depend  upon 
the  excessive  eating  and  drinking,  to  which  many  diabetics  are  forced  by 
their  thirst  and  hunger,  the  feebleness  of  the  digestion  arising  from  the  failure 
in  vital  power,  or  to  perversion  of  the  digestive  functions  by  the  toxsemic 
state  often  developed  as  the  disease  advances.  Extreme  constipation  is  often 
a  very  troublesome  symptom. 

Pulmonary  complications,  such  as  bronchopneumonia  or  tuberculosis, 
are  very  frequently  met  with  in  diabetics,  owing  to  the  lowered  vital  resist- 
ance which  permits  infection.  Such  complications  are  very  often  the  cause 
of  death,  particularly  tuberculosis. 

Although  albuminuria  is  quite  a  common  symptom,  particularly  in  those 
patients  who  have  arteriosclerosis,  general  dropsy  is  rare,  notwithstanding 
the  enfeeblement  of  the  heart  and  the  impaired  state  of  the  kidneys,  because 
the  urinary  flow  is  so  profuse  that  the  body  is  rapidly  drained  of  fluid. 

Callian  has  especially  studied  the  influence  of  diabetes  on  the  female 
genitals;  pruritus  vulvae  is  verycommon;  menstrual  disturbances  are  common; 
the  atrophy  of  uterus  and  ovaries,  he  thinks,  depends  on  the  associated 
sclerosis  of  their  nutritive  vessels. 

Diabetes  occurs  in  a  certain  percentage  of  cases  of  acromegaly  and 
exophthalmic  goitre. 

The  nervous  complications  of  diabetes  mellitus  may  be  divided  into  the 
acute  and  chronic.  The  acute  complications  are  very  serious  from  a  prog- 
nostic point  of  view,  and  consist  chiefly  of  diabetic  coma.     Many  theories 


DIABETES  MELLITUS  797 

have  been  advanced  as  to  its  direct  cause.  It  is  undoubtedly  toxic  in  origin, 
and  seems  to  be  chiefly  associated  with  a  state  of  acidiosis,  or  the  presence 
of  one  or  more  abnormal  acids  in  the  blood,  of  which  one  is  called  /?-oxy- 
butyric  acid.  The  idea  that  acetone  and  diacetic  acid  are  the  causes  has 
been  cast  aside.  In  some  instances  the  onset  of  the  coma  (sometimes  called 
"Kussmaul's  coma")  is  sudden,  but  it  may  be  gradual,  although,  even  in  the 
gradual  cases,  it  is  a  matter  of  a  few  hours  at  the  most,  as  a  rule. 

Diabetic  coma  may  be  said  to  appear  in  three  types :  The  first,  and  most 
common,  is  often  met  with  in  young  persons,  and  develops  with  suddenness 
in  many  instances;  that  is  to  say,  its  onset  lasts  but  a  few  hours  at  the  most. 
The  early  symptoms  are  those  of  disorders  of  digestion,  with  abdominal  pain, 
vomiting,  muscular  weakness,  and  drowsiness,  which  soon  ends  in  coma.  The 
breathingin  this  coma  is  often  slow  and  deep,  very  much  as  it  is  in  the  second 
stage  of  opium  poisoning.  At  other  times  it  is  sighing.  To  the  respiratory 
state  in  this  condition  Kussmaul  applied  the  descriptive  word  "Lufthunger." 
The  second  form  often  comes  on  after  fatigue,  particularly  in  elderly  persons, 
and  the  symptoms  may  be  those  of  profound  collapse.  In  the  third  form  the 
early  symptoms  are  those  of  ataxia  and  confusion  of  speech. 

Sometimes  the  unconsciousness  is  preceded  by  great  restlessness  and 
irritability,  while  in  other  instances  the  onset  of  the  comatose  state  is  gentle. 

Of  the  ocular  complications,  cataract,  optic  nerve  atrophy,  and  diabetic 
retinitis  are  to  be  remembered.  Sudden  blindness  due  to  optic  nerve  or 
retinal  changes  occasionally  ensues  and  palsies  of  the  ocular  muscles  may 
take  place. 

Diabetics  are  also  subject  to  apoplexy. 

Of  the  subacute  nervous  symptoms  we  find  painful  neuritis,  and  not  infre- 
quently a  pseudotabes  due  to  this  cause,  with  loss  of  knee-jerk,  Romberg's 
symptom,  and  even  the  Argyll-Eobertson  pupil.  Sometimes  a  true  tabes 
dorsalis  seems  to  develop. 

Diagnosis. — ^The  diagnosis  of  diabetes  mellitus  is  easily  made  if  the  physi- 
cian will  carefully  examine  the  urine  and  will  bear  in  mind  the  fact  that  he  is 
not  justified  in  deciding  that  the  well-developed  disease  is  present  unless  some 
symptoms  which  are  characteristic  are  associated  with  the  glycosuria.  It 
may  be  said  that  he  who  has  constant  glycosuria  is  in  the  early  stages 
of  diabetes  mellitus,  and  this  is  particularly  true  if  this  symptom  be 
constant  in  a  young  person.  On  the  other  hand,  it  not  infrequently  hap- 
pens that  a  person  of  fifty-five  or  sixty  years  develops  a  mild  glycosuria 
which  lasts  for  years,  and  does  not  materially  impair  the  health  for  a  long 
period  of  time.  Even  these  cases,  however,  often  develop  into  the  true 
disease.  In  other  words,  we  may  say  that  while  glycosuria  is  not  diabetes, 
it  is  a  state  that  indicates  a  tendency  to  this  disease  or  the  presence  of  its 
early  stages.  The  separation  of  the  polyuria  of  diabetes  insipidus  from  that 
of  diabetes  mellitus  is  made  by  the  low  specific  gravity  of  the  urine  in  the 
former  disease,  and  the  fact  that  sugar  is  present  in  the  latter  malady. 

It  not  infrequently  happens  that  diabetes  mellitus  is  overlooked  because 
the  patient  does  not  complain  either  of  thirst  or  of  excessive  urination,  and  the 
physician  fails  to  examine  the  urine  as  a  matter  of  routine.  But  patients  often 
present  symptoms  which,  while  not  distinctly  urinary,  should  at  once  call 


798  DISEASES  OF  NUTRITION 

the  attention  of  the  physician  to  the  possibiHty  of  diabetes  being  present. 
Thus,  any  patient  who  suffers  from  marked  loss  of  flesh  and  increasing  weak- 
ness should  always  be  suspected  of  having  diabetes,  even  if  signs  of  tubercu- 
losis are  present,  for  not  infrequently  the  tuberculosis  is  secondary  to  the 
diabetes.  So,  too,  women  will  sometimes  complain  of  pruritus  of  the  vulva 
or  eczema  of  the  genitals,  or  men  will  state  that  they  are  becoming  impotent, 
in  all  of  which  cases  the  urine  should  be  examined,  since  diabetes  often  pro- 
duces these  signs.  So,  too,  defects  of  vision,  due  to  diabetic  cataract,  or,  more 
rarely,  to  retinal  changes,  may  be  the  first  symptoms  manifest  to  the  patient, 
and  still  others  complain  of  numbness  or  tingling  in  the  extremities  and 
present  the  symptoms  of  locomotor  ataxia.  On  the  other  hand,  as  already 
pointed  out,  physicians  not  infrequently  are  so  careless  as  to  examine  the 
urine  only  once,  and  when  they  discover  sugar  consider  that  the  case  is  one 
of  diabetes ;  or  they  obtain  a  reaction  with  Fehling's  test,  because  of  the  pres- 
ence of  some  sugar-reducing  substance,  as  when  the  patient  is  taking  chloral; 
or,  again,  they  mistake  physiological  glycosuria  for  true  diabetes.  It  is 
evident  that  most  of  these  mistakes  in  the  diagnosis  of  diabetes  depend  upon 
lack  of  urinary  examination  or  imperfect  methods  of  testing  this  secre- 
tion. 

As  an  illustration  of  how  necessary  it  is  to  examine  a  number  of  samples 
of  urine  before  determining  that  the  patient  has  or  has  not  diabetes,  it  may 
be  recalled  that  urine  passed  during  the  night  or  before  breakfast  is  often 
free  from  sugar;  while  that  passed  after  breakfast  and  during  the  day  may 
contain  much  of  it. 

The  condition  of  diabetic  coma  is  separated  from  the  unconsciousness  of 
uraemia  by  the  cider-like  odor  of  the  breath,  the  presence  of  glycosuria  and 
acetonuria,  and  the  absence  of  the  high  arterial  tension  usually  met  with  in 
renal  disease,  for  in  this  state  the  pulse  is  feeble  and  of  low  tension.  At  the 
same  time,  it  is  to  be*  recalled  that  uraemia  may  complicate  diabetes.  The 
patient  lies  in  a  condition  which  resembles  profound  alcoholic  intoxication. 
Deeply  unconscious,  with  half-opened  eyeHds,  wandering  eyeballs,  and 
dilated  pupils,  he  breathes  in.  a  panting  manner,  a  deep  inspiration  being 
followed  by  a  quick  expiration.  The  respiratory  rate  may  not  be  greatly 
different  from  the  normal,  but  sometimes  it  is  hurried,  and  then  forms 
"diabetic  dyspnoea,"  with  a  gradually  increasing  cyanosis.  The  tempera- 
ture is  usually  normal  or  below  normal.  This  state  almost  invariably  ends 
in  from  one  to  two  days  in  death. 

Blood  Tests. — In  1896  Williamson,  of  Manchester,  England,  introduced  a 
modification  and  improvement  upon  Bremer's  method  of  distinguishing  dia- 
betic from  non-diabetic  blood,  which  is  of  practical  clinical  value  in  cases  of 
temporary  disappearance  of  sugar  from  the  urine.  This  test,  which  is  based 
upon  the  fact  that  glucose,  even  in  minute  quantity,  decolorizes  warm  alka- 
line solutions  of  methylene  blue,  is  performed  as  follows:  20  c.mm.  of  the 
suspected  blood  are  added  to  40  c.mm.  of  distilled  water  contained  in  a  test- 
tube.  Then  1  c.c.  of  a  1 :  6000  watery  solution  of  methylene  blue  and  40  c.mm. 
of  liquor  potassse  are  added  to  the  mixture.  The  contents  of  the  tube  are  then 
well  mixed  by  shaking.  A  control  experiment  is  made  by  preparing  the 
same  quantities  of  normal  blood  and  reagents  in  another  tube.    Both  tubes 


DIABETES  MELLITUS  799 

are  placed  in  a  beaker  of  water,  which  is  brought  to  the  boihng  point  over 
a  spirit  lamp  and  then  allowed  to  boil  for  four  minutes.  By  the  end  of 
this  time  the  fluid  containing  the  diabetic  blood  will  have  turned  to  a 
dirty  pale-yellow  color. 

In  diabetes  mellitus  the  erythrocytes  do  not  stain  at  all  or  stain  only  faintly 
with  certain  aniline  dyes.  This  has  been  proposed  as  a  means  of  diagnosis, 
but  as  the  same  phenomenon  has  been  observed  in  cases  of  exophthalmic 
goitre,  leukaemia,  and  Hodgkin's  disease,  it  cannot  be  regarded  as  of  practi- 
cal value.  Diabetic  blood  stains  with  biebrich-scarlet,  while  normal  blood 
does  not. 

Urinary  Tests. — For  many  years  the  most  popular  tests  for  the  deter- 
mination of  the  presence  of  sugar  in  the  urine  have  been  those  which  depend 
upon  the  fact  that  strongly  alkaline  solutions  of  grape-sugar  reduce  copper 
oxide  to  lower  grades  of  oxidation.  The  most  frequently  employed  of  these 
tests  is  that  which  is  made  by  means  of  Fehling's  solution.  This  is  best 
made  in  the  following  manner: 

Copper  sulphate,  34.64  gm.,  with  water  enough  to  make  500  c.c.  Mix 
and  keep  in  a  bottle  by  itself.  Pure  Rochelle  salts,  173  gm.;  solution  of 
sodium  hydrate,  specific  gravity  1.330,  100  c.c,  and  water  enough  to  make 
500  c.c.  For  use  mix  equal  volumes  of  these  two  solutions,  thereby  forming 
Fehling's  solution.  About  one  drachm  of  this  solution  is  placed  in  an 
ordinary  test-tube  and  boiled.  If  the  solution  does  not  remain  clear,  it  is 
unsuitable  for  use.  If,  on  the  other  hand,  it  does  remain  clear  on  boiling 
the  suspected  urine  is  to  be  added  to  it  a  few  drops  at  a  time,  and  the 
boiling  continued,  when,  if  sugar  is  present,  the  solution  becomes  opaque 
and  yellow  in  hue,  and  soon  a  dense,  yellowish-red  sediment  falls  to  the 
bottom.  Should  the  quantity  of  sugar  present  be  exceedingly  small,  it 
may  be  necessary  to  add  urine  until  the  volume  of  urine  and  the  volume 
of  Fehling's  solution  are  equal.  But  the  volume  of  urine  must  never  exceed 
that  of  the  Fehling  solution. 

Trommer's  test  is  performed  in  the  following  manner: 

A  drachm  of  urine  is  placed  in  an  ordinary  test-tube,  and  is  treated  with 
sufficient  quantity  of  sulphate  of  copper  solution  to  render  the  fluid  a  light- 
green  color.  An  equal  volume  of  liquor  potassse  is  then  added.  This  results 
in  a  blue  precipitate  of  hydrated  copper  protoxide,  which  dissolves  upon 
shaking  the  tube,  so  that  a  clear-blue  solution  remains.  If  the  test-tube  be 
allowed  to  stand  for  some  time  the  copper  is  gradually  reduced,  and  precipi- 
tation of  the  yellowish-red  suboxide  of  copper  occurs.  If  the  solution  is 
heated,  the  tests  act  more  promptly.  Care  must  be  taken  that  the  fluid  is 
not  boiled  actively,  as  under  these  circumstances  precipitation  may  take 
place  without  sugar  being  present. 

It  is  hardly  necessary  to  add  that  in  making  these  tests  the  greatest  possible 
cleanliness  in  the  test-tubes  and  bottles  should  be  maintained. 

Occasionally  the  urine  in  cases  of  diabetes  mellitus  contains  acetone  in 
excess  and  diacetic  and  oxybutyric  acids.  The  appearance  of  acetone  in 
amounts  greater  than  normal  (0.008  to  0.027)  is  always  to  be  considered  a 
signal  of  danger  of  diabetic  coma.  The  test  for  the  presence  of  acetone 
consists  in  distilling  the  urine  and  adding  to  several  cubic  centimetres  of  the 


goo  DISEASES  OF  NUTRITION 

distillate  a  few  drops  of  liquor  potassse,  to  render  it  alkaline.  Several  drops 
of  Lugol's  solution  are  now  added,  when,  if  acetone  is  present,  the  fluid 
becomes  turbid,  and  iodoform  is  precipitated  in  crystals.  If  this  fluid  is 
now  heated,  the  odor  of  iodoform  is  noticeable. 

Gerhardt's  test  consists  in  adding  tincture  of  chloride  of  iron  to  the  urine, 
when,  if  acetone  is  present  in  large  amount,  the  fluid  becomes  a  deep  red. 

Prognosis. — The  prognosis  of  diabetes  is  largely  influenced  by  a  number 
of  factors.  In  the  first  place,  as  a  rule,  but  by  no  means  always,  the  outlook 
is  favorable  for  long  life  in  direct  proportion  to  the  age  of  the  patient.  Thus, 
it  not  infrequently  happens  that  men  and  women  who  develop  the  disease 
after  fifty  or  sixty  years  of  age  live  the  full  length  of  years  usually  credited 
to  human  beings  of  that  age.  Even  in  these  cases,  however,  the  possibility 
of  some  intercurrent  infection,  like  pneumonia,  is  to  be  borne  in  mind  as  a 
constant  threat  against  hfe.  Conversely,  the  disease  is  rapidly  fatal  in  pro- 
portion to  the  youth  of  the  patient.  In  young  persons  it  runs  a  rapid  course 
and  may  destroy  life  in  a  few  weeks.  Great  emaciation  usually  develops  in 
these  cases;  whereas,  older  persons  may  maintain  their  weight.  The  mere 
presence  of  glycosuria  is  not  justification  for  as  grave  a  prognosis,  even  if 
the  amount  of  sugar  be  marked,  as  is  the  presence  of  glycosuria  with  associated 
thirst,  hunger,  and  loss  of  flesh.  For  the  first  state  is  a  leakage,  while  the 
second  shows  that  nutritional  changes  are  marked,  and  that  true  complete 
diabetes  mellitus  is  present. 

The  prognosis  also  depends  somewhat  upon  the  manner  in  which  the 
patient  responds  to  the  regulation  of  his  diet.  Thus,  if  on  the  gradual  with- 
drawal of  carbohydrates  and  the  use  of  proteid  and  fatty  food  the  sugar  is 
no  longer  found  in  the  urine,  and  the  urine  gives  no  reaction  with  perchloride 
of  iron  for  acetone,  the  condition  may  be  considered  as  a  mild  form  of  the 
disease.  If,  on  the  other  hand,  the  quantity  of  sugar  diminishes,  but  does 
not  disappear,  and  the  urine  gives  any  reaction  with  perchloride  of  iron,  the 
case  should  be  considered  as  one  of  moderate  severity.  Again,  if  the  gradual 
decrease  in  starchy  foods,  until  the  patient  is  taking  no  carbohydrates,  fails  to 
diminish  the  sugar  excretion,  and  if  a  perchloride  of  iron  test  gives  a  Bur- 
gundy or  port-wine  coloration,  showing  the  presence  of  acetone  in  excess, 
then  the  disease  is  to  be  considered  as  severe. 

The  cause  of  death  in  diabetes  mellitus  is  usually  one  of  the  acute  infec- 
tions, such  as  pneumonia,  tuberculosis,  or  septicaemia,  with  or  without 
carbuncle.  Diabetic  coma  is  another  common  cause  of  death.  Frerichs 
found  that  150  out  of  250  deaths  in  diabetes  were  caused  by  coma. 
Of  43  fatal  cases  observed  by  Taylor,  death  resulted  from  coma  in  26. 
Mackenzie  found  19  deaths  from  coma  in  87  fatal  cases. 

Mandel  and  Lusk  have  recently  stated  the  following  proposition  as  to 
prognosis:  If  a  diabetic  be  put  on  a  meat-fat  diet  (rich  cream,  meat,  butter, 
and  eggs),  and  the  twenty-four-hour  urine  of  the  second  day  be  properly 
collected,^  the  discovery  of  3.65  grams  of  dextrose  to  1  gram  of  nitrogen 

1  "  The  urine  should  he  collected  so  that  an  early  morning  hour  (hefore  breakfast)  terminates  the  period 
for  one  day.  This  is  necessary,  because  the  sugar  formed  from  eaten  proteid  is  eliminated  hefore  the 
nitrogen  belonging  to  the  same.  The  long  period  between  the  evening  meal  and  breakfast  allows  for 
the  elimination  of  both  constituents." 


DIABETES  MELLITUS  801 

signifies  a  complete  intolerance  for  carbohydrates,  and  probably  a  quickly 
fatal  outcome.     They  have  called  this  the  fatal  ratio. 

It  may  be  laid  down  as  a  rule,  that  true  diabetes  mellitus  never  gets  w^ell, 
but  that  temporary  glycosuria  often  does  so  under  proper  treatment.  Diabetes 
may,  however,  be  controlled  and  life  prolonged  very  materially  by  resort  to 
suitable  diet  and  remedial  agents. 

Treatment. — By  treatment  much  can  be  done  for  the  control  of  this  dis- 
ease. As  already  stated,  simple  glycosuria  can  usually  be  entirely  relieved 
by  proper  attention  to  exercise,  the  regulation  of  the  diet,  so  that  the  patient 
does  not  overeat  or  overdrink,  and  particularly  by  the  limitation  of  the 
amount  of  carbohydrate  food  which  he  ingests.  In  these  cases  the  appearance 
of  sugar  in  the  urine  is  to  be  regarded  as  evidence  of  the  inability  of  the  patient 
to  properly  utilize  these  substances  in  the  body.  If  there  is  reason  to  believe 
tliat  he  is  too  sedentary  in  his  habits,  it  sometimes  happens  that  a  moderate 
amount  of  exercise  causes  a  disappearance  of  the  glucose.  Again,  if  he  is  a 
thin,  spare  individual,  who  naturally  worries  much  about  business  or  pro- 
fessional duties,  absolute  rest  from  these  causes  of  stress  must  be  insisted 
upon,  in  order  that  the  nervous  system  may  recover  its  equipoise. 

When  true  diabetes  mellitus  is  present,  it  is  even  more  essential  that  these 
etiological  factors  should  be  controlled.  Indeed,  it  may  be  well  said  that  to 
attempt  treatment  by  a  diet  and  drugs  is  useless  in  a  case  of  diabetes  mellitus, 
unless  the  patient  can  be  properly  controlled  in  regard  to  his  manner  of  life, 
provided  that  manner  of  life  is  deleterious.  In  other  words,  it  is  futile,  in  the 
majority  of  instances,  to  regulate  the  diet  and  to  give  drugs  if  the  patient  is 
to  be  continually  exposed  to  causes  which  are  more  potent  for  evil  than  the 
remedies  are  for  good. 

There  can  be  no  doubt  that  the  dietetic  treatment  of  diabetes  is  far  more 
important  than  that  by  drugs,  and  it  is  essential  that  this  fact  be  borne  in 
mind,  since  physicians  are  often  careless  in  regard  to  the  question  of  dietetics, 
and  patients  are  still  more  so,  even  after  the  importance  of  a  proper  diet  has 
been  conveyed  to  them.  Quite  frequently  they  follow  the  directions  of  the 
physician  for  a  short  time,  and  then,  wearying  of  being  deprived  of  favorite 
articles  of  food,  take  these  articles  surreptitiously,  or  openly  declare  that 
whether  it  does  them  harm  or  good  they  do  not  intend  to  be  deprived  of 
things  of  which  they  are  fond.  For  these  reasons  the  dietetic  treatment  of 
diabetes  is  much  the  more  difficult  part  of  the  care  of  these  cases. 

As  diabetes  is  a  condition  in  which  the  body  is  unable  to  properly  utilize 
carbohydrates  and  their  educts,  it  is  manifest  at  once  that  an  excess  of  carbo- 
hydrates must  be  forbidden;  but  what  is  an  excess  to  one  individual  may  not 
be  an  excess  to  another,  for  an  excess  is  that  quantity  which  is  more  than  the 
body  can  use.  For  this  reason  it  is  usually  wise,  when  placing  a  patient 
upon  an  antidiabetic  diet,  to  diminish  the  quantity  of  carbohydrates  which 
he  receives,  by  a  very  gradual  process,  and  to  watch  the  quantity  of  sugar  in 
the  urine  from  day  to  day,  since  by  this  means  the  quantity  of  carbohydrate 
material  which  he  can  utilize  may  perhaps  be  approximated.  A  second 
reason  for  carrying  out  this  gradual  diminution  in  the  quantity  of  starchy 
food  lies  in  the  important  fact  that  not  infrequently  cases  of  diabetes  are 
plunged  into  diabetic  coma  by  the  institution  of  a  diet  practically  free  from 
51 


802  DISEASES  OF  NUTRITION 

carbohydrates,  perhaps  because  the  system  is  in  such  a  condition  that  no 
sudden  variations  in  the  character  of  the  food  can  be  permitted.  Not  only 
is  it  a  cHnical  fact  that  coma  may  be  precipitated  in  this  manner,  but  we  also 
know  that  the  quantity  of  acetone  in  the  urine  is  greatly  increased  by  severe 
restrictions  of  carbohydrates.  For  this  reason  the  physician,  when  restrict- 
ing diet,  should  always  examine  the  urine,  not  only  as  to  its  content  of  sugar, 
but  as  to  content  of  acetone  as  well,  and  if  this  latter  ingredient  is  present  in 
an  amount  in  excess  of  that  which  may  be  considered  normal,  for  a  minute 
trace  is  sometimes  present  in  non-diabetic  persons,  it  is  absolutely  essential 
that  he  shall  at  once  restore  the  full  carbohydrate  diet,  since  by  so  doing  the 
quantity  of  acetone  is  diminished  and  the  condition  of  acidiosis  which  pro- 
duces coma  is  diminished.  (See  Treatment  of  Coma.)  The  elimination  of 
more  than  one  gram  of  acetone  in  twenty-four  hours  is  to  be  considered  an 
excess. 

Thirdly,  patients  will  often  resent  the  total  removal  of  carbohydrates  from 
their  diet  list,  and  yet  yield  to  their  gradual  removal.  On  the  other  hand,  it 
is  not  to  be  forgotten  that  in  some  diabetics  a  certain  amount  of  carbo- 
hydrate food  seems  to  be  essential,  in  order  that  they  may  not  manufacture 
glucose  from  other  articles  of  food,  or  from  the  proteids  of  their  own  bodies, 
and  in  order  that  acidiosis  be  not  produced.  That  is  to  say,  the  administra- 
tion of  starch  in  moderate  quantity  may  compensate  for  their  loss  of  glucose. 

Sugars  should  always  be  excluded.  They  are  unnecessary  articles  of  diet, 
and,  aside  from  the  fact  that  the  body  is  unable  to  utilize  them,  they  are  apt 
to  disturb  digestion. 

Because  carbohydrate  food  cannot  be  utilized,  it  has  come  to  be  well 
recognized  that  the  patient  must  subsist  largely  upon  the  different  forms 
of  meat,  both  salt  and  fresh,  excepting  liver,  which  contains  glycogen,  and 
which,  therefore,  ought  not  to  be  given.  So,  too,  butter,  cheese,  and  the 
various  oils  and  fats  may  be  used. 

It  has  already  been  pointed  out  that  diabetic  patients  whose  supply  of 
carbohydrate  material  has  been  cut  down  should  be  provided  with  an  amount 
of  fat  over  and  above  that  usually  ingested,  provided,  of  course,  that  the 
individual  can  digest  and  assimilate  fats.  It  is  evident,  however,  from  a 
series  of  investigations  made  by  von  Noorden  and  others,  that  butter,  when 
taken  in  excess  of  five  ounces  a  day,  may  cause  an  increase  in  the  quantity  of 
oxybutyric  acid  in  the  blood.  Von  Noorden  has  pointed  out,  however,  that 
this  deleterious  effect  of  large  amounts  of  butter  can  be  diminished  if  the 
butter  is  first  washed  with  cold  water  in  a  most  thorough  manner,  since  by 
this  means  we  remove  the  lower  fatty  acids  which  are  chiefly  concerned  in  the 
production  of  acidiosis.  Under  these  circumstances,  von  Noorden  tells  us 
that  as  much  as  seven  ounces  of  butter  can  be  taken  daily  without  difficulty. 

Most  of  the  shell-fish  are  useful,  but  contain  too  much  glycogen. 

In  the  way  of  fresh  vegetables,  the  patient  may  receive  the  various  greens, 
such  as  lettuce,  spinach,  dandelion,  cabbage,  cauliflower,  Brussels  sprouts, 
string-beans,  celery,  watercress,  tomatoes,  onions,  cucumbers,  olives,  and 
the  various  kinds  of  pickles,  and  practically  all  of  the  nuts  which  are  com- 
monly employed  as  foods,  except  chestnuts,  which  contain  too  large  a  pro- 
portion of  starch. 


DIABETICS  MELLITUS  803 

Not  rarely  the  patient  does  best  when  he  is  placed  upon  a  diet  which  varies 
in  carbohydrates  from  week  to  week;  that  is  to  say,  he  is  given  a  very  small 
quantity  of  carbohydrate  one  week,  and  a  fairly  large  quantity  of  it  the  next. 
In  those  instances  in  which  the  acetone  reaction  persists  in  the  urine,  whether 
carbohydrates  are  removed  or  allowed,  von  Noorden  has  strongly  recom- 
mended what  he  calls  "the  oatmeal  cure."  In  this  cure  the  patient  eats  noth- 
ing but  oatmeal  gruel  for  from  one  to  two  weeks,  save  that  in  addition  to  the 
eight  ounces  of  oatmeal  he  is  given  a  similar  quantity  of  butter  and  some 
vegetable  albumin.  Often  this  mixture  is  administered  as  frequently  as  every 
two  hours.  Von  Noorden  asserts  that  on  this  diet  the  excretion  of  sugar  falls 
to  a  point  far  below  that  excreted  on  a  mixed  diet  from  which  all  carbo- 
hydrate has  been  removed.  At  the  end  of  a  week  or  two  it  is  always  neces- 
sary to  return  to  other  foods  temporarily,  as  otherwise  the  patient  rebels 
against  the  pursuance  of  a  pure  oatmeal  diet;  but  even  with  these  frequent 
returns  to  an  ordinary  diet,  excellent  results  are  said  to  be  reached. 

Tea,  coffee,  and  cocoa  may  be  employed,  provided  they  are  not  sweetened  by 
cane-sugar,  but  by  saccharin.  Dry  wines  which  contain  little  sugar  may  be 
given  to  those  who  are  accustomed  to  alcoholic  drinks,  although  Scotch 
whiskey,  rye  whiskey,  and  dry  gin  are  better  than  most  wines.  The  various 
simple  mineral  waters  may  also  be  given,  and  of  these  both  the  natural  and 
artificial  Vichy  waters  are  excellent,  because  of  the  quantity  of  bicarbonate 
of  sodium  which  they  contain.  The  old  idea  that  because  the  patient  urinates 
in  excess  he  should  be  deprived  of  water  is  no  longer  followed.  These  patients 
should  be  allowed  water  freely,  in  order  that  the  system  may  be  flushed 
of  toxic  materials.  When  constipation  is  present,  the  mild  saline  purgative 
waters  may  be  given,  varying  from  Apenta,  Carlsbad,  and  Hathorn  water, 
to  the  more  powerful  saline  purges. 

Theoretically,  gluten  provides  a  source  of  nourishment  for  diabetic 
patients,  but  practically  it  is  almost  impossible  to  obtain  a  satisfactory  gluten 
bread  which  does  not  contain  a  very  considerable  quantity  of  starch.  There 
are  upon  the  market  a  few  samples  of  biscuits  made  from  gluten  flour  which 
probably  contain  a  very  small  percentage  of  starch,  and  these  may  be  freely 
given  to  these  patients.  The  diflSculty  in  the  majority  of  instances  is  that 
patients  get  exceedingly  tired  of  a  diet  from  which  all  forms  of  bread  are 
excluded,  and  for  this  reason  it  may  be  impossible  to  entirely  exclude  bread 
from  the  diet  list.  Most  of  the  biscuits  which  are  made  from  substitutes  for 
wheat  flour,  such  as  that  of  the  soya  bean,  are  so  oily  that  patients  find  it 
difficult  to  digest  them.  Almond  meal,  which  also  contains  a  very  large 
percentage  of  oil  and  no  starch,  may  be  given.  But  here,  again,  the  difiiculty 
in  digesting  the  fats  it  contains  is  often  marked.  Perhaps  the  most  satisfac- 
tory bread  is  that  which  is  known  as  aleuronat,  and  which  has  been  highly 
recommended  by  von  Noorden.  Williamson  gives  the  following  formula  for 
its  preparation:  Mix  two  ounces  (62  gm.)  of  desiccated  cocoanut  powder 
with  a  little  water  containing  a  small  quantity  of  German  yeast.  Make  the 
mass  into  a  sort  of  paste,  and  put  in  a  warm  place  for  half  an  hour  or  longer. 
The  small  amount  of  sugar  contained  in  the  cocoanut  is  almost  entirely 
decomposed  by  the  fermentation  produced  by  the  yeast,  and  the  cocoanut 
paste  becomes  spongy.    Add  two  ounces  (62  gm.)  of  aleuronat,  one  beaten 


804  DISEASES  OF  NUTRITION 

egg,  and  a  small  quantity  of  water,  in  which  a  little  saccharin  has  been  dis- 
solved, and  mix  well  until  a  dough  is  formed.  Divide  into  cakes  and  bake  in 
a  moderate  oven  for  twenty  or  thirty  minutes.  The  great  difficulty  is  to 
obtain  cocoanut  fibres  sufficiently  desiccated  and  powdered. 

Among  the  articles  which  are  to  be  carefully  avoided  are  all  the  sweet  fruits, 
such  as  melons,  grapes,  peaches,  and  those  vegetables  which  contain  a  very 
large  amount  of  starch  and  sugar,  such  as  rice,  sweet  potatoes,  beets,  beans, 
peas,  and  carrots. 

Although  potatoes  are  eminently  a  starchy  food,  recent  investigations 
indicate  that  it  is  perhaps  the  best  form  of  starch  which  can  be  taken  by  the 
diabetic. 

The  medicinal  treatment  of  diabetes  mellitus  has  narrow  limits.  It  is 
true  that  a  host  of  drugs  have  been  recommended  by  various  clinicians  at 
various  times,  the  statement  being  made  that  they  were  capable  of  materially 
decreasing  the  quantity  of  sugar  which  was  lost  in  the  urine,  but  further 
experience  has  almost  universally  proved  that  they  possess  little  power. 
Furthermore,  very  few  of  them  have  been  shown  to  possess  any  influence 
upon  the  symptoms  associated  with  the  glycosuria.  In  other  words,  at 
the  best  they  affect  only  the  one  symptom  of  loss  of  sugar,  and  in  no  way 
correct  the  underlying  cause  of  the  malady. 

Without  doubt  opium  is  the  most  valuable  drug  in  the  treatment  of 
diabetes  mellitus  in  the  majority  of  cases,  for  it  exercises  a  more  potent 
influence  in  diminishing  the  elimination  of  sugar  in  the  urine  than  any 
other  drug.  Its  alkaloids,  morphine  and  codeine,  are  also  exceedingly 
valuable,  and  may  be  employed  when  they  prove  capable  of  controlling  the 
glycosuria  and  when  the  opium  increases  the  constipation,  but  neither  of 
these  alkaloids  is  the  equal  of  the  crude  drug. 

There  are  several  important  points  in  regard  to  the  employment  of  opium, 
or  its  derivatives,  in  diabetes:  First,  patients  of  all  ages  seem  to  be  able  to 
take  large  quantities  of  opium  in  this  disease  without  developing  the  evil 
manifestations  of  the  opium  habit.  Second,  these  patients  usually  have 
to  take  ascending  doses  of  the  drug  until  they  reach  a  dose  which  controls 
the  glycosuria  more  or  less  completely.  Third,  opiates  possess  the  advan- 
tage that  they  diminish  to  a  large  extent  nervous  irritation  and  stress.  Not 
only  do  they  protect  the  nervous  system  from  external  causes  of  irritation, 
but  by  producing  mental  quiet  and  diminishing  worry  they  indirectly  cause 
good  results.  An  endeavor  should  be  made  from  time  to  time  to  diminish, 
at  least  temporarily,  the  quantity  of  the  drug  which  is  taken.  Ordinary 
deodorized  opium  is  the  best  preparation.  Patients  may  start  on  |  grain 
once,  twice,  or  thrice  a  day,  and  gradually  increase  it,  if  necessary.  Or, 
I  to  J  grain  of  morphine  may  be  given  at  these  intervals.  In  other  instances 
^  to  1  grain  of  codeine  may  be  used  as  a  beginning  dose.  Some  patients 
get  so  much  comfort  and  such  a  diminution  of  glycosuria  under  moderate 
doses  of  these  drugs  that  the  size  of  the  dose  does  not  have  to  be  increased. 
Thus,  I  have  had  under  my  care  for  nearly  twelve  years  a  woman  who  has 
taken  but  3  grains  of  codeine  a  day  during  all  that  time.  She  has  never  had 
any  desire  to  increase  the  dose  beyond  this  amount,  and  it  has  kept  her 
glycosuria  within  bounds,  besides  giving  her  a  great  deal  of  comfort. 


DIABETES  MELLITUS  805 

In  cases  which  do  not  possess  marked  nervous  symptoms,  but  which  are 
rather  phlegmatic  in  type,  and  have  a  gouty  tendency,  the  sahcylate  of 
sodium  or  sahcylate  of  strontium  may  be  given  in  full  doses  varying  from 
10  to  20  grains  three  or  four  times  a  day;  or,  in  their  place,  we  may  employ 
some  of  the  new  coal-tar  products,  such  as  antipyrin,  acetanilid,  and  phena- 
cetin.  These  drugs,  however,  must  be  given  in  full  doses  to  have  any  effect, 
and  they  so  greatly  increase  the  susceptibility  of  the  patient  to  cold  that  they 
must  be  used  with  great  caution.  In  cases  which  have  a  syphilitic  history,  or 
which  seem  to  be  gouty,  the  iodide  of  potassium,  in  the  dose  of  10  to  30  grains 
or  more  three  or  four  times  a  day,  often  does  good.  When  the  patient  can 
digest  it,  cod-liver  oil  is  an  exceedingly  valuable  alterative  and  nutrient. 

With  the  idea  that  the  alkalies  aid  oxidation  processes  in  the  body  and  so 
help  to  burn  up  sugar,  various  alkalies,  as  the  potassium  and  sodium  salts, 
have  been  largely  employed.  Thus,  potassium  or  sodium  bicarbonate  may 
be  given  in  10,  15,  or  20  grain  doses  three  or  four  times  a  day. 

Another  remedy  which  is  of  value  in  some  cases,  particularly  if  ancemia 
is  present,  is  Fowler's  solution  in  doses  varying  from  1  to  3  minims  three 
times  a  day.    With  some  clinicians  it  has  a  great  reputation  in  this  disease. 

In  the  treatment  of  the  various  complications  of  diabetes  we  must  first 
consider  diabetic  coma.  After  coma  is  once  established,  we  have  no  method 
of  treatment  which  promises  permanent  recovery.  I  have  several  times 
seen  a  temporary  return  to  consciousness  follow  the  intravenous  injection 
of  one  quart  of  normal  saline  solution,  and  Continental  clinicians  have 
employed  and  strongly  recommended  the  injection  of  carbonate  of  sodium 
in  solution.     (See  page  806.) 

When  the  presence  of  acetone  in  the  urine  or  of  the  early  symptoms  of 
intoxication  indicate  that  diabetic  coma  is  not  far  distant,  two  plans  of 
treatment  should  be  promptly  instituted.  One  of  these  is  directed  to  the 
prevention  of  the  further  formation  of  acidiosis,  due  to  acetone-producing 
substances,  and  the  oxidation  of  those  already  found.  The  other  is  designed 
to  deprive  these  substances  of  their  poisonous  properties.  As  already  pointed 
out,  the  addition  of  moderate  amounts  of  starchy  foods  to  the  diet  results  in 
the  decrease  or  disappearance  of  acetone  from  the  urine — acetone  being  the 
symbol  of  intoxication.  If  this  cannot  be  done  by  the  use  of  remedies  by 
the  mouth,  because  the  stomach  is  unfit  to  deal  with  food,  then  one  of  the 
monosaccharids,  such  as  levulose  or  dextrose,  should  be  dissolved  in  sterile 
salt  solution  and  injected  subcutaneously  or  into  a  vein.  Ordinary  sugars 
(disaccharids)  cannot  be  used  in  this  way,  because  they  require  the  action  of 
the  digestive  juices  to  be  disintegrated.  The  quantity  of  fluid  used  should 
be  a  quart  with  10  per  cent,  of  dextrose.  Not  less  than  50  to  100  grams 
of  levulose  should  be  given  a  day  by  the  mouth.  If  neither  of  these  can  be 
had,  glycerin  may  be  given  by  the  mouth.  Another  point  of  importance  is  to 
cut  down  the  fats  given  to  these  patients,  who  before  the  onset  of  these  symp- 
toms have  been  subsisting  largely  upon  fats  and  proteids,  because  the 
poisons  of  coma  are  derived  from  fats  and  fatty  acids. 

For  the  diminution  of  the  poisonous  properties  of  the  toxic  substances 
already  formed  everyone  is  in  accord  that  alkalies  should  be  freely  admin- 
istered.    Vichy  water  should  be  taken  in  large  quantities,  and  20  or  30 


806  DISEASES  OF  NUTRITION 

grains  of  bicarbonate  of  sodium  may  be  given  every  two  or  three  hours  dis- 
solved in  Vichy  water,  thereby  fortifying  it.  Stadelmann  has  advised  the 
intravenous  injection  of  carbonate  of  sodium  in  order  that  it  may  combine 
with  the  acids  in  the  blood,  diminish  acidiosis,  and  aid  in  their  elimination. 
For  this  reason  the  quantity  of  acetone  in  the  urine  may  be  temporarily 
increased  by  this  plan  of  treatment.  Naunyn  uses  35  to  40  grams  of  car- 
bonate of  sodium  (not  bicarbonate)  dissolved  in  a  quart  of  water.  This  must 
be  given  very  slowly  by  intravenous  injection.  Even  this  plan,  if  instituted 
after  coma  is  present,  rarely  does  more  than  restore  consciousness  temporarily. 
If  the  bowels  are  confined  they  should  be  opened  by  some  saline  purge,  but 
active  purgation  should  not  be  resorted  to,  since  by  this  means  concentration 
of  the  poison  may  take  place  if  the  bowel  is  not  active  in  the  process  of 
eliminating  poisons  from  the  blood. 


DIABETES  INSIPIDUS. 

Definition. — Diabetes  insipidus  is  a  condition  in  which  a  person  passes 
excessive  quantities  of  urine  containing  no  abnormal  constituents  and  of 
a  low  specific  gravity.  This  term  is  sometimes  applied  erroneously  to  a 
fleeting  attack  of  polyuria  due  to  nervousness  or  fright  and  to  profuse  diu- 
resis following  the  ingestion  of  excessive  amounts  of  water.  It  is  also  to  be 
separated  from  the  constant  polyuria  sometimes  seen  in  hysterical  women. 

Etiology. — Diabetes  insipidus  is  most  commonly  met  with  in  persons 
under  thirty  years  of  age  and  may  occur  in  early  childhood.  It  is  more 
common  in  males  than  in  females.  Very  rarely  it  is  definitely  hereditary, 
and  occasionally  there  is  in  the  history  of  the  patient  a  statement  that  it 
developed  after  some  severe  injury,  as  a  railroad  accident  or  fall.  In  some 
instances  this  may  be  due  to  damage  of  the  central  nervous  system,  in 
others  to  local  nervous  lesions.  It  has  also  followed  sunstroke  and  pro- 
longed fevers  of  an  infectious  type,  and  it  has  been  met  with  as  a  symptom 
in  cases  of  brain  tumor. 

The  cause  is  unknown,  but  it  is  probably  due  to  some  condition  of  relaxa- 
tion of  the  bloodvessels  supplying  the  Malpighian  tufts,  with  the  result  that 
an  excessive  quantity  of  fluid  passes  downward  from  these  tufts  through 
the  tubules. 

Morbid  Anatomy. — No  distinct  lesions  have  been  found  constantly  in 
cases  of  this  character  at  autopsy,  and  nothing  has  been  learned  of  the 
pathology  of  the  malady  by  dead-room  investigation.  Sometimes  the  kid- 
neys are  found  to  be  swollen  and  congested,  but  no  real  renal  lesion  explain- 
ing the  polyuria  has  as  yet  been  described. 

Symptoms. — The  dominant  symptom  of  diabetes  insipidus  is,  of  course, 
a  profuse  urinary  flow.  Next  to  this  symptom  is  the  constant  thirst  suffered 
by  the  patient,  who  no  sooner  provides  his  system  with  fluid  by  drink- 
ing than  it  escapes  from  the  kidneys.  The  third  symptom  of  importance 
is  the  annoyance  caused  by  the  necessity  of  emptying  the  bladder  many 
times  a  day  and  the  loss  of  rest  at  night  by  reason  of  the  same  condition. 
Closel}'^  related  to  these  symptoms  in  its  causation  is  dryness  of  the  mouth 


DIABETES  INSIPIDUS  807 

and  excessive  dryness  of  the  skin.  Partly  because  of  the  fact  that  the  condi- 
tion develops  usually  in  nervous  patients,  or  in  those  whose  nerves  have 
been  shattered  by  accident,  persons  suffering  from  diabetes  insipidus  are 
often  very  irritable  and  peevish,  an  irritability  which  is  maintained  by  the 
necessity  of  frequent  micturition.  The  body  temperature  may  be  normal 
or  subnormal.  Tyson  states  that  some  cases  can  take  inordinate  quantities 
of  alcohol  without  intoxication,  but  that  others  are  unduly  susceptible  to 
the  cerebral  effects  of  this  drug. 

The  quantity  of  urine  passed  by  some  cases  of  diabetes  insipidus  quite 
equals  that  passed  by  well-advanced  cases  of  diabetes  mellitus  with  free 
polyuria.  As  much  as  eighty  and  ninety  pints  a  day  have  been  excreted 
but  the  usual  quantity  is  rarely  above  ten  or  twelve  pints.  The  specific 
gravity  is  almost  as  low  as  ordinary  water,  and  rarely  exceeds  1.003  or  1.005, 
owing  to  the  fact  that  the  normal  urinary  solids  are  dissolved  in  such  an 
exceedingly  large  quantity  of  fluid;  but  a  high  specific  gravity  alone  does 
not  indicate  glycosuria,  since  diabetic  urine  may  not  be  over  1.012  or 
1.015.  At  times  the  total  urea  is  greatly  in  excess  of  that  normally 
excreted.     Albumin  is  never  present  except  in  very  small  amount. 

Diagnosis. — Before  deciding  that  a  patient  has  true  diabetes  insipidus 
it  must  be  determined  that  the  condition  is  not  a  fleeting  polyuria,  but  a 
constant  state.  Tests  as  to  specific  gravity  of  the  urine  and  for  sugar  will 
reveal  diabetes  mellitus.  The  state  of  the  cardiovascular  system  and  the 
eye-grounds  may  reveal  chronic  contracted  kidney. 

Prognosis. — Prognosis  so  far  as  life  is  concerned  is  good.  Recovery  is 
by  no  means  rare,  and  even  if  it  does  not  take  place  death  from  the  malady 
rarely,  if  ever,  occurs.  The  celebrated  case  of  Willis  lived  fifty  years  with 
this  condition  present.  It  is  only  when  the  diabetes  insipidus  depends  upon 
a  serious  nervous  lesion  that  the  prognosis  is  bad,  and  then  because  of  the 
lesion  and  not  because  of  the  polyuria. 

Treatment. — No  treatment  for  diabetes  insipidus  which  has  yet  been 
instituted  has  proved  satisfactory.  It  is  quite  true  that  a  large  number  of 
remedies  have  been  spoken  of  in  terms  of  praise  by  various  practitioners, 
but  the  very  number  of  them  indicates  that  no  one  of  them  gives  results 
which  are  definitely  curative.  The  use  of  vegetable  astringents,  such  as  gallic 
acid,  with  the  idea  that  by  this  means  a  diminution  in  the  secretion  of  urine 
may  be  brought  about,  sometimes  produces  favorable  results.  The  dose 
must  be  large,  from  5  to  20  grains  three  or  four  times  a  day;  but  even  when 
such  large  doses  are  used  as  to  disorder  the  stomach,  it  not  infrequently 
happens  that  no  decrease  in  the  quantity  of  urine  is  brought  about.  In 
other  instances  good  results  are  said  to  accrue  from  the  employment  of  an 
active  fluid  extract  of  ergot  given  in  the  dose  of  20  to  30  minims  three  or 
four  times  a  day,  alone  or  with  the  bromide  of  sodium  in  the  dose 
of  20  grains.  The  ergot  is  supposed  to  act  by  contracting  the  capillaries 
in  the  Malpighian  tufts.  When  the  polyuria  causes  much  restlessness 
and  insomnia,  the  remedies  already  named  may  be  aided  by  the  simul- 
taneous administration  of  codeine,  which  will  probably  not  decrease  the 
quantity  of  urine,  but  which  usually  acts  as  a  nervous  sedative  with  suffi- 
cient power  to  prevent  the  bladder  from  waking    the    patient  more  fre- 


808  DISEASES  OF  NUTRITION 

quently  than  is  absolutely  necessary.  The  bromides  may  also  be  used  for 
this  purpose.  In  those  cases  which  are  associated  with  neurasthenia  or  which 
follow  prolonged  nervous  strain,  the  "Rest  Cure  "  or  a  vacation  where  the 
patient  is  not  annoyed  by  business  or  family  cares  will  probably  give  better 
results  than  will  drugs. 

GOUT. 

Definition. — Gout  is  a  disease  which  depends  for  its  existence  upon  a 
disorder  of  metaboHsm,  as  a  result  of  which  deposits  of  biurate  of  sodium 
take  place  in  the  joints  and  in  the  fibrous  tissues  surrounding  them.  It  is 
characterized  by  associated  changes  of  a  fibroid  and  calcareous  character 
in  other  parts  of  the  body  in  many  instances,  and  in  its  acute  exacerbations 
it  frequently  causes  severe  inflammation  and  pain  in  one  or  more  joints. 
The  joint  of  the  big  toe  is  very  commonly  the  chief  seat  of  the  articular  dis- 
order.    Gout  is  sometimes  called  "  podagra." 

Etiology. — ^The  precise  cause  of  gout  is  unknown,  but  certain  etiological 
factors  in  its  development  are  universally  recognized  as  being  active.  The 
first  of  these  is  undoubtedly  heredity,  but  while  it  is  true  that  the  tendency 
to  the  disease  is  often  inherited  it  is  also  true  that  the  descendants  of  gouty 
persons  often  fail  to  develop  the  disease,  and  that  other  persons  who  have 
no  gout  in  their  family  history  suffer  from  the  malady.  It  is  interesting  in 
this  connection  to  note  that  younger  children  of  gouty  persons  more  fre- 
quently fall  victims  to  gout  than  the  children  of  their  earlier  years,  probably 
because  the  gouty  diathesis  is  better  developed  in  advanced  years  in  the 
parents  than  in  youth. 

A  second  factor  in  the  production  of  gout  is  mode  of  life  as  to  exercise 
and  mental  labor.  There  is  universal  accord  that  great  mental  and  nervous 
stress  with  little  physical  exercise  frequently  produces  a  gouty  diathesis 
and  often  precipitates  an  acute  attack  of  the  malady  in  those  already  gouty. 
Duckworth  states  that  political  life  in  England  is  notoriously  conducive  to 
gout,  and  that  lawyers  are  very  prone  to  it.  In  the  case  of  the  country  squire 
who  is  so  often  gouty,  high  living  and  drinking,  with  a  long  heritage  of 
dietetic  indiscretion,  probably  overcomes  all  the  good  effects  of  an  active 
out-door  existence.  In  those  who  live  chiefly  out-of-doors,  as  farmers, 
soldiers,  and  sailors,  the  disease  is  rare. 

A  third  factor  of  some  importance  is  age.  While  cases  of  well-developed 
gout  are  met  with  in  young  children  and,  very  rarely,  even  in  infancy,  the 
malady  commonly  does  not  develop  till  after  the  thirtieth  year,  but  rarely 
waits  till  the  fifth  decade  of  life  before  at  least  beginning  its  early  manifesta- 
tions. 

A  fourth  factor  is  the  abuse  of  alcohol,  not  in  the  sense  of  going  on  sprees, 
but  in  such  a  manner  that  the  system  is  all  the  time  engaged  in  oxidizing  or 
destroying  this  drug.  Ales  and  beers — that  is,  malt  liquors — are  more  prone 
to  cause  gout  than  are  whiskies  and  other  distilled  liquors.  Sweet  and  sour 
wines  are  also  provocative  of  this  disorder,  particularly  champagne. 

A  fifth  factor  is  overeating.  There  is  an  increasing  number  of  persons 
in  America  who  do  not  eat  to  live,  but  live  to  eat,  and  who  stimulate  the 


GOUT  809 

digestive  organs  to  greater  activity  by  the  use  of  highly  seasoned  dishes, 
with  the  result  that  they  ingest  and  absorb  more  food  than  the  system  can 
use,  stifling  oxidation  and  clogging  elimination. 

Finally,  a  very  powerful  factor  in  producing  gout,  in  those  who  are  exposed 
to  the  metal,  is  lead  poisoning  of  the  chronic  type. 

We  find,  then,  that  the  chief  causes  of  gout  are  heredity,  lack  of  exercise, 
nervous  stress,  and  the  ingestion  of  more  food  or  drink  than  the  body  can 
properly  deal  with. 

Frequency. — True  gout  in  its  frank  forms  is  far  less  common  in  England 
than  it  was  in  the  early  part  of  the  last  century  or  in  the  eighteenth  century. 
In  America  it  is  certainly  very  rare.  On  the  other  hand,  both  in  England 
and  in  this  country  "lurking,"  "lateral,"  or  masked  gout  is  certainly  greatly 
on  the  increase.    The  disease  is  more  common  in  men  than  in  women. 

Pathology. — When  we  come  to  a  study  of  this  disease  from  the  standpoint 
of  perverted  physiology  or  pathology,  we  encounter  a  task  over  which  the 
profession  has  toiled  unceasingly  year  after  year  with  little  advance  in  our 
understanding  of  gout,  but  great  advance  in  our  knowledge  of  the  meta- 
bolic changes  in  the  body.  When  Sydenham  wrote,  after  being  a  sufferer 
from  gout  for  years,  that  it  is  due  to  "the  impaired  concoction  of  matters 
both  in  the  parts  and  juices  of  the  body,"  he  expressed  himself  as  clearly 
and  correctly  as  do  many  modern  writers  on  this  subject. 

The  pages  of  a  text-book  are  not  suitable  for  a  discourse  in  which  a  multi- 
tude of  researches  are  analyzed  and  judged,  yet  it  is  proper  to  take  note  of 
several  theories  as  to  the  cause  of  gout  that  have  been  strongly  advocated  by 
one  or  more  investigators,  with  some  basis  for  their  views. 

One  theory  is  that  when  the  blood  and  lymph  are  saturated  with  uric  acid 
the  urates  are  precipitated  by  a  slight  lowering  of  the  temperature,  such  as 
is  apt  to  occur  in  an  exposed  joint.  This  theory  is  not  adequate  to  explain 
the  disease,  because  it  has  been  proved  that  the  fluids  are  not  saturated  with 
uric  acid  or  urates  in  cases  of  gout,  and  the  disease  affects  parts  which  are 
not  chilled. 

Again,  Kolisch  advanced  the  view  that  the  so-called  xanthin  bases  are  the 
cause  of  gout.  This  investigator  believes  that  the  nucleinic  bodies  are  broken 
up  into  xanthin  and  hypoxanthin,  and  that  in  the  healthy  kidneys  these  are 
in  turn  changed  into  uric  acid.  In  gout  he  thinks  that  the  kidneys  fail  to  per- 
form their  function  properly,  that  the  xanthins  are  not  transformed  into  uric 
acid,  and  that  this  results  in  the  retention  of  xanthins,  which  straightway 
proceed  to  cause  gout.  This  view  has  been  impaired  by  the  fact  that  his 
methods  of  research  were  faulty  and  by  the  fact  that  other  investigators, 
using  more  accurate  methods,  get  different  results. 

His  believes  that  the  uric  acid  of  the  gouty  is  a  product  of  the  disease,  and 
that  it  is  capable  of  causing  evil  effects  in  the  body.  It  is  not  the  prime 
factor,  in  other  words,  but  a  secondary  factor,  just  as  the  bacillus  of  diph- 
theria is  the  prime  factor,  and  the  toxins  which  it  produces  cause  wide- 
spread lesions  as  secondary  factors.  In  the  normal  body  uric  acid  is  in 
large  part  destroyed;  whereas,  in  gout  it  is  permitted  to  exist  and  induce 
secondary  evil  effects.  Any  cause  which  prevents  the  destruction  of 
uric  acid  predisposes  the  patient  to  its  deleterious  influences,  and  these 


810  DISEASES  OF  NUTRITION 

causes  may  be  inherited,  acquired,  or  due  to  poisons,  such  as  lead.  Here, 
again,  we  are  met  by  the  contradictory  fact  that  in  a  number  of  dis- 
eases an  excess  of  uric  acid  develops  without  any  signs  of  gout  appearing. 
Thus,  in  leukaemia,  pneumonia,  and  chronic  kidney  disease  this  acid  cir- 
culates in  the  blood  in  excess,  but  no  gout  is  produced. 

The  view  of  Ebstein  is  that  there  is  a  primary  nutritional  disturbance  in 
the  affected  joints,  and  in  other  tissues,  which  results  in  tissue  death  within 
those  parts,  and  that  in  these  devitalized  areas  urates  are  deposited.  Finally, 
von  Noorden  believes  that  a  special  ferment  acts  to  produce  these  local 
nutritional  changes  and  that  the  deposit  of  urates  then  ensues. 

The  most  popular  theory  as  to  the  cause  of  the  symptoms  has  been  that 
there  is  present  in  the  body  an  excess  of  uric  acid.  This  is  the  theory  of 
Garrod,  and  in  more  recent' times  has  had  its  most  enthusiastic  advocate  in 
Haig.  Garrod's  theory  that  the  decrease  of  uric  acid  in  the  urine  at  the  time 
of  an  attack  is  due  to  its  retention  in  the  body,  and  that  this  retention  causes 
an  outbreak,  is  now  held  to  be  erroneous,  or  at  least  is  regarded  with  grave 
doubt,  as  is  also  his  view  that  a  decreased  alkalinity  of  the  blood  causes  a 
precipitation  of  the  urates,  for  Magnus-Levy,  Luff,  and  W.  His,  Jr.,  have 
all  proved  that  the  quantity  of  uric  acid  in  the  blood  is  not  increased  during 
or  before  an  attack,  nor  is  the  alkalinity  of  the  blood  decreased.  Still  others 
have  shown  that  the  decrease  in  the  excretion  of  uric  acid  just  before  an 
attack  of  gout  is  due,  in  part  at  least,  to  a  decreased  ingestion  of  food.  These 
researches  do  not  prove,  however,  that  uric  acid  producing  substances  are 
not  present  in  excess,  and  it  is  entirely  possible  that  the  scanty  elimination 
of  uric  acid  in  many  of  these  patients  in  the  interval  between  attacks  is  due 
to  the  failure  of  the  body  to  change  them  into  uric  acid,  with  the  result  that 
they  cause  an  attack,  at  which  time  the  percentage  of  uric  acid  excreted 
often  temporarily  rises.  I  confess  that  this  view  seems  the  more  attractive. 
When  we  consider  that  the  injection  of  uric  acid  into  the  blood  does  not  cause 
gout,  that  it  is  present  in  leukaemia,  pneumonia,  and  nephritis  without  causing 
gout,  and  that  no  excess  of  uric  acid  is  found  in  the  blood  in  gout,  it  is  hard 
to  believe  that  uric  acid  causes  gout.  While  Kolisch's  theory  may  be  imper- 
fect in  detail,  and  while  the  kidney  may  not  transform  xanthin  into  uric  acid, 
it  is  entirely  possible  that  an  excess  of  xanthin  may  be  present  in  gout.  This 
view  is  supported  by  several  facts,  which  indicate  that  uric  acid  is  an  end- 
product  derived  from  nuclein  breakdown,  and  that  it  is  not  this  healthy  end- 
product,  but  by-products  which  are  morbid  in  effect.  From  nuclein  we  can 
obtain  albumin  and  nucleinic  acid ;  from  nucleinic  acid  we  can  obtain  phos- 
phoric acid  and  a  substance  which  in  turn  may  be  split  up  into  xanthin  bases 
and  uric  acid.  If  oxidation  is  complete,  uric  acid  is  the  chief  end-product, 
if  it  is  incomplete,  then  xanthin  is  the  chief  product.  Bain  and  Futcher  have 
both  shown  that  when  there  is  an  increase  in  uric  acid  excretion  there  is  an 
increase  in  phosphoric  acid  secretion,  and  they  believe  that  this  throws  a  side 
light  upon  the  relation  of  uric  acid  and  xanthin  to  gout.  Thus,  in  one  of 
Futcher's  cases  there  was  a  marked  fall  in  both  phosphoric  acid  and  uric 
acid  immediately  before  an  attack,  followed  by  a  very  great  increase  at  the 
time  of  the  attack,  and  this  again  by  a  fall.  The  phosphoric  acid  curve  was 
far  greater  than  the  uric  acid  curve. 


GOUT  811 

It  would  seem,  therefore,  that  the  destruction  of  nucleinic  bodies  may  be 
perverted  in  gout,  and  this  is  all  that  Futcher's  study  proves,  namely,  that 
as  phosphoric  acid  and  uric  acid  are  both  derived  from  nucl^in,  and  as  they 
are  greatly  disturbed  in  amount  in  relation  to  the  attack,  it  is  fair  to  assume 
that  some  relation  exists  between  nucleinic  bodies,  their  derivatives,  and 
gout. 

At  the  present  time  it  would  seem  probable  that  we  may  divide  this  ques- 
tion of  the  pathology  of  gout  into  two  sub-questions,  viz. : 

1.  Is  there  present  in  the  body  at  the  time  of  an  attack  of  gout  an  excess 
of  uric  acid,  or,  rather,  of  material  capable  of  producing  uric  acid?  The 
answer  is  "Yes." 

2.  What  is  the  reason  that  this  condition  develops  ?  The  answer  is  that  we 
do  not  know,  but  that  it  is  dependent  upon  a  perversion  of  metabolism  not 
yet  understood,  whereby  in  health  uric  acid,  a  primarily  harmless  body,  is 
produced,  and  in  disease  a  by-product  is  found,  which  causes  an  attack  dur- 
ing, or  before,  which  urate  of  sodium  is  deposited  in  the  tissues. 

Morbid  Anatomy .^ — Gout  may  produce  morbid  changes  in  every  tissue  of 
the  body,  even  to  the  hair  and  nails,  but  the  parts  which  are  most  frequently 
impaired  by  its  existence  are  the  heart  and  the  bloodvessels,  the  kidneys 
and  the  joints.  From  the  standpoint  of  outward  manifestations  and  early 
discomfort,  the  joint  changes  are,  of  course,  the  most  important,  but  from 
the  standpoint  of  the  physician,  whose  duty  it  is  to  prolong  Hfe,  the  cardio- 
vascular and  renal  changes  are  the  factors  which  deserve  most  attention. 
Because  of  the  wide  distribution  of  gout  in  the  body,  Sydenham  wrote: 
"Totum  corpus  est  podagra.'' 

The  lesions  in  the  joints  are  characteristic;  the  ligaments,  tendons,  and 
bursse  all  become  affected,  and  even  the  articular  cartilages  are  involved. 
In  all  these  tissues  deposits  of  biurate  of  sodium  take  place,  and  they  may  be 
so  copious  that  the  parts  are  deformed  and  incapacitated  by  roughening  of 
the  cartilaginous  surfaces,  or  by  thickening  of  the  sheaths  of  the  tendons  and 
joints.  In  typical  cases  the  disease  first  attacks  the  joint  of  the  big  toe,  then 
the  finger  joints,  after  this  the  metacarpal  and  metatarsal  joints,  and  still  later, 
but  much  more  rarely,  the  large  joints.  When  these  are  affected,  the  wrist, 
elbow,  and  knee  are  the  parts  usually  involved.  The  ball-and-socket  joints 
(hip  and  shoulder)  are  very  rarely  involved  in  gout,  and  the  upper  extremities 
are  much  less  frequently  affected  than  the  lower  ones.  When  the  disease  is 
well  advanced  there  is  so  great  a  deposit  of  biurate  of  sodium  that  it  lies 
under  the  skin  in  a  white  knob,  or  pea-shaped  mass,  which  looks  white  and 
chalky.  If  the  skin  covering  such  a  deposit  is  injured,  it  not  rarely  undergoes 
necrosis,  and  biurate  of  sodium  exudes  from  the  part,  looking  like  wet  chalk. 
Sometimes  on  the  fingers,  near  the  base  of  the  finger-nails,  or  about  the  first 
phalangeal  joint,  there  develop  small,  hard,  uratic  masses  called  "crabs'  eyes." 
It  is  a  remarkable  fact  that  these  deposits  often  take  place  without  any  other 
manifestation  of  gout  being  present  and  without  any  pain,  so  that  attention 
may  be  called  to  them  only  by  reason  of  the  disfiguration  produced.  Gouty 
deposits  about  the  base  of  the  finger  or  at  the  second  joint  are,  however, 
usually  part  of  a  general  gouty  outbreak. 

When  the  articulating  cartilages  are  affected  two  conditions  may  be  pre- 


812  DISEASES  OF  NUTRITION 

sented.  If  no  injury  has  occurred,  and  if  no  cause  of  irritation  has  existed 
other  than  the  gout,  the  articulating  surface  is  seen  to  be  smeared  or  plas- 
tered, to  use  Duckworth's  expression,  with  a  uratic  deposit  looking  as  white 
and  smooth  as  fresh  white  lead  (Fig.  105).  When  irritation  has  been  present 
the  articular  cartilage  may  be  eroded.  In  this  latter  form  there  is  often 
overgrowth  of  connective  or  fibrous  tissue  in  the  surrounding  parts  along  with 
the  deposit  of  urates,  as  already  described,  and  stiffening  or  distortion  of  the 
joint.  The  changes  in  the  bursa  are  often  noteworthy.  I  have  a  case  now  under 
treatment  in  which  there  is  a  bursa  swollen  to  the  size  of  a  bantam's  egg  on 
the  heel  at  the  insertion  of  the  tendo  Achillis.  It  is  a  very  dusky  red  and  is 
exquisitely  sensitive,  but  contains  nothing  but  fluid.  It  has  often  developed 
before,  and  under  active  treatment  for  gout  has  always  disappeared  and  left 
no  trace  behind  it. 

Fig.  105 


Showing  urate  of  sodium  deposited  on  an  articulating  surface.     (Graupner  and  Zimmerman.) 

The  cardiovascular  changes  caused  by  gout  do  not  result  from  the  deposition 
of  biurate  of  sodium  in  the  heart-valves  or  in  the  bloodvessel  walls.  Indeed, 
it  is  rare  for  such  deposits  to  be  found,  although  cases  are  recorded  in  which 
the  cardiac  valves  and  the  intima  of  the  aorta  have  contained  the  biurate  of 
sodium.  But  while  it  is  true  that  biurate  of  sodium  is  not  deposited  in  the 
vascular  system,  as  it  is  in  the  joints,  it  is  also  true  that  gout  causes  first 
arterial  spasm,  then  arteriocapillary  fibrosis,  and,  finally,  advanced  calcare- 
ous changes  in  the  vessels.  The  result  of  this  is  cardiac  hypertrophy  on  the 
left  side  of  the  heart  in  particular.  The  endocardium  is  never  the  seat  of 
acute  endocarditis  as  a  result  of  true  gout.  The  only  endocardial  changes 
are  those  common  to  ordinary  cases  of  general  atheromatous  degeneration, 
in  that  sclerotic  changes  take  place  in  the  valves,  particularly  those  guard- 


GOUT  813 

ing  the  aortic  and  mitral  orifices.  The  chorda  tendinea  are  also  shortened 
by  a  similar  process  and  rendered  inelastic. 

The  pericardium  is  very  rarely  affected. 

The  venous  system  is  prone  to  varicosities  and  calcareous  plates  may  be 
present  in  the  walls  of  the  veins.  These  in  turn  may  result  in  thrombosis 
and  phlebitis. 

Gout,  cardiovascular  disease,  and  angina  pectoris  are  a  wicked  trio  that 
bring  many  a  noble  man  to  death. 

Whatever  the  gouty  poison  may  be  which  causes  changes  in  the  general 
vascular  system,  that  poison  also  damages  the  renal  tissues  as  well.  The 
bloodvessels  of  the  kidneys  are,  of  course,  involved  in  the  general  vascular 
fibrosis,  and  we  have  the  small,  contracted  kidney  often  called  a  *'  gouty  kidney," 
because  it  is  often  the  result  of  gout.  Many  years  ago  Ord  and  Greenfield 
showed  that  in  two-thirds  of  all  cases  examined  at  autopsy  in  which  there  was 
gout  in  the  great  toe  there  was  chronic  granular  kidney,  and  in  the  remaining 
one-third  a  condition  allied  to  it.  While  it  is  quite  true  that  deposits  of 
biurate  of  sodium  are  sometimes  found  in  the  kidney  structure  in  the  region 
of  the  papillae,  and  extending  outward  along  the  pyi'amids  toward  the 
periphery  of  the  organ  in  whitish  streaks,  such  cases  are  very  rare  when 
we  consider  the  number  of  cases  of  gout  and  the  number  of  cases  of  renal 
disease  complicating  its  existence. 

Symptoms. — These  are  best  studied  in  three  divisions :  the  acute,  the 
chronic,  and  the  aberrant  types. 

Acute  Gout. — In  this  form  the  fully  developed  symptoms  are  often  pre- 
ceded by  several  hours  or  days  of  nervous  irritability,  of  insomnia,  or  of  general 
wretchedness  not  easily  described.  In  some  cases  pruritus  ani  is  present,  or 
itching  elsewhere  may  annoy  the  patient  and  keep  him  restless  at  night. 
The  urinary  secretion  is  often  scanty  and  the  bladder  may  be  irritable.  In 
other  cases  these  symptoms  are  entirely  absent  and  the  patient  will  recall, 
during  his  hours  of  suffering,  that  he  has  seldom  felt  as  well  as  he  felt  for  a 
day  or  two  before  the  attack  came  on. 

The  attack  itself  usually  consists  in  the  sudden  onset  of  sharp  pain  and 
inflammation  in  the  ball  of  the  great  toe.  The  pain  is  very  severe  and  stab- 
bing in  character,  often  extending  upward  into  the  foot.  A  swelling  develops 
with  surprising  rapidity  and  the  skin  over  it  is  red,  hot,  and  burnished.  In 
addition,  the  part  affected  is  exquisitely  sensitive,  so  that  the  pressure  of  the 
bed-clothes,  much  less  that  of  a  shoe,  is  insupportable.  Not  rarely  a  distinct 
febrile  condition  is  present,  the  temperature  reaching  102°  or  more.  After 
a  few  hours  the  agony  diminishes,  the  swelling  decreases,  and  the  patient 
is  more  comfortable,  but  within  the  next  twenty-four  hours  the  malady  may 
return  with  fresh  severity.  This  may  persist  for  several  days,  but  at  the  end 
of  that  time  the  patient  is  not  only  soon  on  the  road  to  recovery,  but  feels 
better  than  for  a  considerable  time  before  the  attack,  although  the  ball  of 
the  toe  may  be  swollen  and  inflamed  for  some  days  longer. 

There  are  three  noteworthy  peculiarities  about  these  seizures,  namely, 
that  they  usually  develop  after  midnight,  waking  the  patient  from  sleep; 
that  although  the  inflammatory  process  in  and  about  the  joint  seems  furious 
in  its  severity,  the  part  never  goes  on  to  suppuration,  and  the  onset  and 


814  DISEASES  OF  NUTRITION 

disappearance  of  the  attack  is  followed  by  little  if  any  disability  in  the 
affected  part.  Only  when  repeated  attacks  take  place  is  there  developed 
much  deformity  of  the  area  involved  in  the  gouty  manifestation. 

Acute  gout  is  nearly  always  recurrent.  Sometimes  it  attacks  the  patient 
every  few  weeks,  in  other  cases  every  few  months,  and  in  others  every  few 
years. 

This  form  of  gout  is  very  rare  in  the  United  States,  but  frequent  in 
England,  although  less  so  than  it  was  many  years  ago. 

Chronic  Gout. — Chronic  gout  as  a  distinct  condition  from  acute  gout 
does  not  really  exist;  that  is  to  say,  no  sharp  line  separates  this  type  from 
the  acute  form.  Two  types  of  it  may  be  recognized.  In  one,  repeated 
attacks  of  acute  gout  are  connected  with  one  another  by  modified  gouty 
manifestations,  such  as  stiffness  and  soreness  in  various  parts,  as  in  the  wrists 
and  elbows,  or  the  maintenance  of  a  certain  degree  of  low-grade  inflamma- 
tion in  the  joint  of  the  big  toe.  In  the  other  form  there  are  no  acute  out- 
breaks such  as  have  just  been  described,  but  a  gradual  process  of  gouty 
thickening  of  fibrous  tissues  and  an  equally  gradual  deposition  of  biurate  of 
sodium  about  the  tendons,  the  joints,  and  in  the  articular  cartilages.  Similar 
deposits  called  tophi  are  found  in  the  edges  of  the  ears,  and  the  "crab's  eye" 
formations  in  the  fingers  already  referred  to  are  found. 

The  urine  is  scanty,  the  arterial  tension  is  usually  high,  and  the  aortic 
second  sound  accentuated.     (See  Morbid  Anatomy.) 

In  some  instances  sudden  inflammatory  attacks  of  moderate  severity, 
as  compared  to  the  acute  attacks  in  the  big  toe,  develop  in  one  or  several 
of  the  large  joints,  as  the  elbow  and  knee,  and  may  give  rise  to  the  belief 
that  acute  articular  rheumatism  is  present,  particularly  as  a  rise  of  two  or 
three  degrees  of  fever  may  take  place.  I  have  seen  a  patient  with  severe 
nodular  gout  of  the  hands  develop  an  attack  of  universal  articular  gout 
after  having  his  hands  baked  in  a  hot-air  apparatus,  probably  because  the 
treatment  caused  the  distribution  of  a  mass  of  gouty  material  in  his  body. 
The  alterations  in  the  appearance  of  the  joints  in  these  attacks  has  already 
been  described  when  writing  of  the  morbid  anatomy  of  this  disease.  They 
may  resemble  very  closely  that  malady  called  arthritis  deformans. 

After  this  type  of  gout  continues  for  years  the  patient  comes  to  his  death 
as  a  result  of  renal  or  cardiovascular  disease,  or  by  some  acute  infection,  such 
as  pneumonia,  which  finds  a  ready  victim  in  one  whose  vital  organs  are 
already  impaired.     In  other  words,  death  is  due  to  a  terminal  infection. 

Not  rarely  patients  with  this  type  of  gout  are  intellectually  brilliant  up  to 
the  moment  of  their  final  illness.  The  presence  of  the  disease  seems  to  be 
a  spur  to  mental  activity. 

Irregular  Gout. — Without  this  division  of  gout  some  modern  physicians 
would  be  sadly  at  sea  in  diagnosis.  It  affords  a  loophole  of  escape  when  a 
patient  insists  on  a  diagnosis,  and  Haig  deserves  the  gratitude  of  many  prac- 
titioners for  having  popularized  the  idea  of  "uric  acid  as  a  factor  in  dis- 
ease." There  can  be  no  doubt  that  many  patients  do  present  symptoms  of 
aberrant  or  modified  gout,  but  they  are  by  no  means  as  numerous  as  they 
are  thought  to  be.  The  gouty  poison  is  capable  of  producing  almost  as 
many  symptoms  and  ailments  as  is  hysteria,  but  not  all  the  symptoms  which 


GOUT  815 

are  credited  to  it,  and  it  is  unfortunate  that  "uric  acid"  is  so  often  a  cloak 
to  ignorance  which  so  pacifies  the  physician  and  patient  that  a  search 
for  a  true  cause  is  discontinued.  Uric  acid  is,  as  already  stated,  in  all 
probability  not  the  cause  even  in  the  true  gouty  cases  of  many  of  the  symp- 
toms presented,  but  rather  the  result  of  the  metabolic  disorders  underlying 
the  illness. 

There  can  be  no  doubt,  on  the  other  hand,  that  gout  really  is  responsible 
in  many  cases  for  the  presence  of  a  very  large  number  of  disorders  in  widely 
different  organs  of  the  body,  such  as  eczema  and  other  forms  of  inflamma- 
tory or  irritative  changes  in  the  skin,  notably  pruritus.  Duckworth  speaks 
of  a  painful  induration  of  the  ala  of  the  nose  in  some  gouty  persons.  In 
the  circulatory  system  the  changes  caused  by  gout,  even  in  those  who  have 
no  outward  manifestation  of  the  disease,  may  be  very  notable,  as  already 
pointed  out. 

In  the  article  on  gonorrhoea!  infection  it  has  already  been  stated  that  a 
suppurative  urethritis  may  be  due  to  gout,  and  irritability  of  the  bladder 
and  renal  stone  may  arise  from  this  cause.  So,  too,  it  is  not  infrequent  for 
diabetes  mellitus  to  develop  in  gouty  persons  and  to  be  modified  in  its  course 
by  anti-gout  remedies. 

Albuminuria  is  also  frequently  present  as  a  result  of  the  high  arterial 
tension  or  of  the  nephritis  produced  by  the  gouty  poison. 

Gouty  persons  often  suffer  from  sudden  and  severe  attacks  of  acute  pharyn- 
gitis or  laryngitis,  and  from  acid  dyspepsia,  and  ophthalmologists  con- 
stantly meet  with  iritis,  conjunctivitis,  and  other  inflammatory  processes 
in  the  eye  due  to  this  cause.  So,  too,  it  often  happens  that  a  thickening  of 
the  tympanic  membrane,  which  causes  deafness,  has  its  origin  in  this  malady. 

Finally,  and  by  no  means  least  important,  gout  or  gouty  tendencies  often 
cause  furious  attacks  of  neuralgia  and  of  migraine.  Not  rarely  after  such  a 
seizure  of  pain  the  patient  feels  unusually  well,  just  as  he  does  after  a  frank 
attack  of  gout. 

Retrocedent  gout  is  a  condition  in  which  the  gouty  process  suddenly  leaves 
the  toe  or  other  joint  and  attacks  some  one  of  the  internal  viscera,  pro- 
ducing, it  may  be,  violent  purging  and  vomiting  or  precipitating  an  attack 
of  angina  pectoris.  In  other  cases  the  patient  suffers  from  an  asthmatic 
seizure.  Sometimes  a  sudden  uraemia  makes  it  appear  that  a  retrocedent 
gout  has  gone  to  the  brain.  As  a  matter  of  fact  retrocedent  gout  is  not  often 
seen.  A  letter  of  inquiry  sent  by  me  to  several  eminent  English  physicians 
brought  replies  that  they  had  rarely  seen  this  accident  occui",  although  they 
have  frequently  met  with  cases,  as  we  all  have,  in  which  a  man  subject  to 
acute  gout  of  the  toe  has  had  a  gouty  angina  pectoris  after  prolonged  free- 
dom from  trouble  in  the  toe. 

Diagnosis. — The  diagnosis  of  gout  when  it  affects  the  big  toe  is  a  simple 
matter.  When  present  in  the  form  of  dermal,  ocular,  otic,  or  muscular  gout, 
the  history  of  the  patient  and  the  character  of  the  attack  render  a  diagnosis 
possible;  but  when  the  polyarticular  form  of  gout  with  fever  develops,  only 
careful  study  and  the  absence  of  heart  changes  will  enable  us  to  separate 
the  conditions  if  we  can  find  no  gouty  history  and  no  gouty  signs,  as  in  tophi 
in  the  ears.    Again,  there  may  be  some  hesitancy  in  separating  gout  from 


gl6  DISEASES  OF  NUTRITION 

chalky  deposits  and  fixation  of  joints  of  arthritis  deformans  in  which  the 
articular  process  is  somewhat  inflammatory  and  painful,  and  in  which 
fibroid  changes  in  the  connective  tissue  about  a  joint  are  present.  Arthritis 
deformans  is,  however,  a  more  surely  progressive  malady;  it  causes  greater 
crippling  of  the  patient;  it  is  not  characterized  by  chalky  crab's  eyes  and 
tophi  in  the  ears,  nor  by  inflammatory  attacks  in  the  eyes  or  the  great  toe, 
nor  in  the  tendons  and  bursse. 

Many  of  the  cases  of  masked  gout  can  only  be  diagnosticated  by  the 
improvement  which  is  produced  by  proper  dietetic  measures  and  the  use 
of  therapeutic  measures  known  to  be  beneficial  to  gouty  persons. 

As  stated  at  the  beginning  of  the  discussion  of  irregular  gout,  remarkably 
various  symptoms  can  be  caused  by  this  malady,  but  all  curious  symptoms 
should  not  be  credited  to  it.  As  Duckworth  well  says:  "Without  doubt 
many  morbid  states  have  often  been  flippantly  or  erroneously  set  down  to 
irregular  gout  which  owned  no  such  designation,  and  thus  a  cloak  for  igno- 
rance has  always  been  at  hand  to  throw  over  careless  observation,  ignorance, 
or  wilful  misinterpretation  of  symptoms.  As  a  consequence  of  such  errors, 
some  have  come  to  regard  even  truly  gouty  manifestations,  when  not  articu- 
lar, as  actually  non-existent,  and  to  deny  the  dependence  of  such  upon  a 
gouty  habit.  The  latter  error  is  no  more  to  be  condoned  than  the  former, 
and  it  may  be  fraught  with  mischief  to  the  sufferer." 

Prognosis. — The  prognosis  of  gout  is  better  when  it  develops  after  forty 
than  if  it  appears  after  thirty  years  of  age.  In  many  cases  of  frank  gout 
the  prognosis  as  to  life  is  better  than  in  the  insidious  form,  for  the  latter  often 
attacks  the  circulatory  and  renal  tissues.  Much  depends  upon  the  vascu- 
lar system.  If  it  is  fibroid  the  outlook  is  bad,  and  if  it  is  not  the  mere 
existence  of  gout  need  not  shorten  life  unless  alcohol  is  abused.  Gouty 
persons,  however,  are  not  good  "risks"  in  life  insurance,  as  has  been  proved 
by  several  sets  of  statistics. 

Treatment. — ^The  treatment  of  gout  is  hygienic,  dietetic,  and  medicinal. 
A  further  subdivision  of  the  subject  may  be  made  into  that  which  is  devoted 
to  the  treatment  of  an  acute  attack  and  into  those  measures  which  are  taken 
for  the  relief  of  the  more  subacute  or  irregular  manifestations.  The  hygienic 
measures  which  are  to  be  employed  in  the  treatment  of  a  person  suffering 
from  either  gout  with  acute  exacerbations,  or  suppressed  gout,  consist  in 
such  exercise  as  can  be  taken  in  the  open  air  without  at  any  time  producing 
more  than  healthy  fatigue.  Exercise  taken  to  the  point  of  exhaustion  is  of 
course  always  deleterious,  and  particularly  in  those  who  are  gouty,  as  it  is 
prone  to  produce  an  acute  attack  or  reduce  vital  resistance  to  such  a  degree 
that  intercurrent  maladies  may  develop.  Golf,  horseback  exercise,  and 
similar  out-door  pursuits  are  therefore  exceedingly  advantageous,  but  are 
not  to  be  carried  to  an  excess.  These  patients  should  also  be  directed  to 
drink  water  in  as  large  a  quantity  as  may  be  taken  without  overloading  the 
stomach  at  any  one  time.  Many  persons  can  take  half  a  glass  of  water 
every  hour  without  producing  gastric  discomfort  or  interfering  with  diges- 
tion ;  whereas,  if  they  are  content  to  drink  only  at  meal  times,  but  small  quan- 
tities of  liquid  may  be  ingested.  Water  aids  in  producing  a  profuse  urinary 
flow,  and  so  helps  to  eliminate  impurities  from  the  body.    If  the  heart  is  not 


GOUT  817 

feeble,  hot  baths  or  hot  Turkish  baths  may  be  taken  two  or  three  times  a 
week  with  advantage.  Often  such  patients  are  greatly  benefited  by  going 
to  some  of  the  health  resorts  where  hot  springs  exist. 

The  dietetic  treatment  of  gout  consists  in  the  exclusion  of  all  sweet  wines 
and  of  fatty  or  rich  foods,  and  in  the  ingestion  of  meals  which  are  sufficiently 
varied  in  character  to  maintain  the  appetite  and  adequate  to  maintain 
nutrition.  The  patient  should,  however,  be  particularly  w^arned  against 
an  excessive  quantity  of  food.  In  many  instances  gouty  persons  will  be 
found  to  take  quantities  of  food  which  are  far  in  excess  of  those  which  are 
required  to  provide  the  patient  with  the  2500  to  3C00  calories  per  day  which 
he  requires  for  healthy  existence.  All  wines  and  beers  are  also  disadvan- 
tageous for  this  class  of  patients,  but  sweet  and  sour  wines  and  champagnes 
are  peculiarly  so.  In  regard  to  individual  articles  of  food,  it  has  been  held 
in  the  past  that  red  meats  were  distinctly  more  harmful  than  white  meats; 
but,  as  has  been  pointed  out  in  discussing  the  dietetics  of  Bright's  disease, 
this  view  of  the  relative  harmfulness  of  red  and  white  meat  is  becoming 
obsolete.  Chemical  analysis  fails  to  reveal  any  material  difference  between 
them.  The  point  of  importance  is  that  the  patient  shall  not  eat  an  excessive 
quantity  of  meat,  or  meats,  which  is  prepared  in  such  a  way  that  it  is  diffi- 
cult of  digestion,  as,  for  example,  larded  game  birds  or  larded  beef.  Of 
the  various  beverages  cocoa  is  perhaps  the  best,  but  rich  chocolates  are 
harmful.  Coffee  is  usually  considered  much  better  than  tea.  Indeed,  Dr. 
Haig  is  quite  confident  that  tea  is  an  abomination  for  the  gouty. 

In  the  way  of  treatment  by  drugs,  there  are  only  three  which  can  be  con- 
sidered as  exercising  an  approximately  specific  influence,  namely,  colchicum, 
iodine  in  its  various  forms,  and  the  salicylates.  Of  these  the  iodides  and 
salicylates  are  most  useful  for  the  subacute  or  irregular  forms  of  gout,  while 
the  colchicum  is  of  most  value  for  the  purpose  of  combating  an  acute  par- 
oxysm. Most  patients  with  constant,  irregular,  gouty  manifestations  do 
well  if  they  take  continuously,  over  a  long  period  of  time,  10  to  15  grains 
of  salicylate  of  strontium  three  or  four  times  a  day,  or  5  or  10  grains  of 
iodide  of  potash  or  iodide  of  sodium  at  similar  intervals.  By  this  means 
gouty  sore  throat,  gouty  iritis  and  conjunctivitis,  gouty  stiff  ness  of  the  various 
muscles,  and  gouty  neuralgia  and  migraine  may  be  modified  or  entirely 
relieved.  If  there  is  any  tendency  to  acidity  of  the  urine  full  doses  of  citrate 
or  acetate  of  potash,  10  or  15  grains  three  times  a  day,  should  be  given, 
well  diluted  with  water.  In  some  instances  the  urine  is  alkaline,  and  when 
it  is  so  the  patient  feels  heavy  and  depressed.  These  symptoms  can  often 
be  modified  by  the  use  of  10  to  20  grains  of  benzoate  of  sodium  in  capsule 
three  or  four  times  a  day. 

Acute  paroxysms  of  gout  are  to  be  treated  by  the  administration  of  full 
doses  of  the  wine  of  colchicum  root,  repeated  in  from  six  to  twelve  hours, 
the  dose  varying  from  20  to  40  minims  according  to  the  irritability  of  the 
stomach  and  the  idiosyncrasies  of  the  patient  to  the  drug.  Not  infre- 
quently much  better  results  will  be  obtained  if  before  the  colchicum  a 
moderate  dose  of  the  compound  extract  of  colocynth,  such  as  10  to  20 
grains  with  1  or  2  grains  of  extract  of  hyoscyamus,  is  given  to  unload  the 
bowels.  Colocynth  is  chosen  because  experience  has  shown  that  it  seems 
52 


813  DISEASES  OF  NUTRITION 

to  exercise  a  more  beneficial  influence  in  gout  than  any  other  purgative, 
and  the  hyoscyamus  is  used  because  it  prevents  the  colocynth  from  pro- 
ducing griping  pain.  Not  infrequently  some  relief  may  be  obtained  if  the 
inflamed  joint  is  wrapped  with  hnt  laden  with  a  50  per  cent,  ichthyol  oint- 
ment. Luff  has  strongly  recommended  the  following  apphcation  for  the 
same  purpose:  The  entire  foot  is  surrounded  by  a  warm  pack  consisting 
of  cotton-wool  saturated  with  the  soothing  lotion,  and  then  Ughtly  covered 
with  oiled  silk.    The  following  lotion  may  be  employed: 

U — Sodium  bicarbonate  .  .  .  .  .  •  .  Jiv. 

Linimentum  belladonnas  .  .  .  .  .  .  i  J  iv. 

Tincture  of  opium      .  .  =  .  •  .  •  f  3  iss. 

Water      .          .          .  .  .  »  .  .  •  f^viij 

Equal  portions  of  this  lotion  and  hot  water  should  be  used  to  saturate 
the  wool  which  has  been  rolled  around  the  joint,  and  the  dressing  should 
be  changed  every  four  hours. 

It  is  important  to  remember  that  no  local  depleting  measures  are  to  be 
instituted  under  any  circumstances.  Blisters,  leeches,  and  other  forms  of 
bloodletting  are  not  only  valueless,  but  dangerous,  as  they  afford  oppor- 
tunities for  infection. 

Many  cases  of  acute  and  chronic  gout  are  also  benefited  if  from  time  to 
time  they  receive  moderate  doses  of  calomel  or  blue  pill,  such  as  3  or  4 
grains  of  blue  pill  or  a  grain  of  calomel  in  broken  doses.  Many  physicians 
at  the  present  time  also  prefer  the  active  principle  of  colchicum,  colchicine, 
to  the  wine  of  colchicum  root.  It  may  be  given  in  the  dose  of  y^  to  gV  of 
a  grain  every  two  or  three  hours  in  a  case  of  acute  gout,  or  four  or  five  times 
a  day  in  the  subacute  varieties. 

Although  the  various  salts  of  lithium  are  largely  employed  by  some 
practitioners  for  the  purposes  of  combating  the  various  aberrant  forms  of 
gout,  it  is  to  be  remembered  that  the  popularity  of  these  salts  depends  more 
upon  the  skilful  advertising  of  tablet  manufacturers  than  upon  the  actual 
experience  of  the  profession.  Those  who  know  most  about  these  salts  have 
found  that  the  lithium  preparations  do  not  act  as  well  in  gout  as  do  the 
salicylates  of  sodium  or  potassium,  and  the  idea  that  lithium  has  a  peculiar 
affinity  for  the  uric  acid  is,  to  a  large  extent,  blasted  by  the  knowledge  that 
lithium  has  a  greater  affinity  for  the  acid  sodium  phosphate  in  the  blood 
than  it  has  for  uric  acid;  beautiful  test-tube  experiments  to  the  contrary 
notwithstanding. 

ARTHRITIS  DEFORMANS. 

Definition. — Arthritis  deformans  is  a  chronic  disease  affecting  the  joints, 
and  characterized  by  trophic  disturbances  in  their  cartilages,  in  the  ends  of 
the  bones,  and  in  the  synovial  membranes.  It  is  to  be  distinctly  separated 
from  acute  rheumatism  and  from  true  gout,  although  in  some  cases  it  appears 
to  be  a  sequel  of  acute  rheumatic  infection.  Sometimes  arthritis  deformans 
is  called  "  rheumatoid  arthritis,"  or  "  osteoarthritis." 


ARTHRITIS  DEFORMANS  819 

Etiology. — Much  discussion  has  arisen  as  to  the  cause  of  this  malady, 
some  adhering  to  the  view  that  it  is  due  to  nervous  lesions  which  result  in 
changes  in  the  joints,  and  others  asserting  that  it  is  the  result  of  an  infection. 
Within  recent  years  the  former  view  has  lost  in  popularity  and  the  latter 
opinion  is  now  in  the  ascendant,  although  as  yet  no  one  has  succeeded  in 
isolating  the  responsible  micro-organism. 

In  support  of  the  nervous  theory  we  find  that  trophic  changes  take  place 
not  alone  in  the  joints,  but  in  the  muscles  and  skin  near  the  joints  affected; 
that  pain  is  often  present  in  the  nerve  trunks,  as  in  neuritis,  and  that  dis- 
eases of  the  central  nervous  system  not  rarely  produce  lesions  in  the  joints 
which  resemble  those  found  in  arthritis  deformans.  Certain  French  clin- 
icians have  claimed  that  definite  lesions  are  demonstrable  in  the  spinal  cord, 
in  the  columns  of  Goll  in  the  cervical  level,  and  in  the  posterior  nerve  roots 
as  well.  The  difficulty  in  accepting  the  neural  theory  is  that  there  is  no 
proof  that  these  changes  are  primary  and  not  secondary,  for  it  is  well  known 
that  many  joint  affections  are  fallowed  by  similar  lesions,  at  least  in  the 
nerves,  skin,  and  muscles. 

Those  who  argue  in  favor  of  the  infectious  nature  of  the  malady  point  to 
the  fact  that  the  nearby  lymph  nodes  are  often  enlarged,  as  if  combating 
infection ;  that  infection  of  the  joints  by  various  micro-organisms  is  the  usual 
cause  of  arthritis,  and  that  a  considerable  portion  of  the  cases  of  arthritis 
deformans  have  had  at  some  previous  time  gonorrhoea  or  other  disease  which 
is  prone  to  cause  secondary  arthritic  lesions.  Ballantyne,  Wohlmann,  and 
Bloxall  have  isolated  a  bacillus,  of  dumb-bell  shape,  which  stains  with 
fuchsin  or  methylene  blue,  but  not  by  Gram's  method.  Other  investigators 
have  failed  to  find  it;  Chauffard  and  Ramond  have  isolated  a  diplobacillus 
that  they  think  is  the  cause.  Organisms  have  also  been  found  by  Charrin, 
Le  Roux,  and  Bouchard.  Poynton  and  Payne  have  isolated  a  diplococcus 
from  the  synovial  membranes  in  chronic  arthritis,  and  by  inoculation  have 
produced  the  joint  lesions  of  rheumatoid  arthritis  in  animals. 

Most  clinicians  divide  the  cases  of  this  disease  into  two  classes :  the  primary, 
in  which  the  arthritic  state  develops  without  any  preceding  joint  affection, 
and  the  secondary,  in  which  there  is  a  history  of  such  an  infection.  The 
primary  cases  are  those  in  which  the  disease  develops  after  a  prolonged 
nervous  stress  or  severe  physical  strain,  as  in  frequent  childbearing.  The 
secondary  form  follows  acute  articular  rheumatism  and  occasionally  develops 
after  injury  to  a  single  joint,  although  in  this  case  the  relationship  of  cause 
and  effect  is  very  doubtful.  Even  in  the  cases  in  which  acute  rheumatism 
has  preceded  the  malady  this  relationship  is  in  doubt,  and  there  is  nothing 
to  prove  that  there  exists  any  closer  tie  between  them  than  sequence  by 
coincidence.  To  sum  up  our  knowledge  of  the  etiology  of  arthritis  defor- 
mans, we  may  say  that  we  really  know  but  little  of  it. 

Statistics  as  to  the  frequency  of  arthritis  deformans  in  the  two  sexes  differ 
greatly.  In  Garrod's  statistics  the  disease  affected  411  women  out  of  500 
cases.  Stewart  has  recorded  40  cases,  of  which  20  were  in  women;  and 
more  recently  McCrae  has  reported  110  cases,  of  which  55  were  women  and 
55  were  men.  My  own  experience  at  the  Jefferson  Medical  College  Hospital 
has  been  that  nearly  all  are  women. 


820  DISEASES  OF  NUTRITION 

The  greatest  prevalence  of  the  disease  is  between  twenty  and  fifty  years 
of  age,  but  Moncorvo  has  collected  48  cases  of  polyarthritis  deformans  in 
patients  under  fourteen  years. 

The  disease  is  very  rare  in  the  negro  race.  In  a  clinic  rich  in  negroes 
McCrae  only  met  with  this  disease  in  negroes  four  times  in  110  cases,  which 
is  all  the  more  noteworthy  because  negroes  are  peculiarly  subject  to  other 
arthritic  changes. 

Morbid  Anatomy. — What  the  changes  are  in  the  early  stages  of  this  malady 
is  not  known,  because  patients  rarely  come  to  autopsy  until  after  the  dis- 
ease has  existed  for  a  long  period.  What  little  information  we  have  indi- 
cates that  the  process  is  primarily  inflammatory,  in  that  the  synovial 
membranes  are  injected  and  hypersemic.  This  is  follovt^ed  by  the  develop- 
ment of  fibrous  tissue,  and  this  again  by  the  absorption  of  the  cartilaginous 
coverings  of  the  ends  of  the  bones.  By  these  means  cartilages  become 
eroded  and  the  ends  of  the  bones  become  eburnated.  Finally,  there  develops 
from  the  periosteum  covering  the  ends  of  the  bones,  bony  growths  or  knobs 
which  lock  the  joints  and  because  of  the  thickened  membranes  and  rough- 
ened cartilages  increase  the  tendency  to  immobility  already  present.  These 
osteophytes  are  called  "Hay garth's  nodosities."  Associated  with  these 
changes  there  is  marked  wasting  of  the  muscles  which  govern  the  move- 
ments of  the  joint,  a  wasting  not  rarely  met  with  in  all  serious  joint  affec- 
tions, a  glossiness  of  the  skin  covering  the  affected  joints  due  to  atrophy  of 
the  glands  in  its  deeper  layers  and  to  changes  in  the  epiderm,  and  not  infre- 
quently trophic  changes  in  the  nails  which  may  be  greatly  thinned,  ridged, 
or  very  brittle. 

The  changes  in  the  vertebrse  consist  in  overgrowth  of  the  articular  car- 
tilages, followed  by  ossification.  The  ligaments  also  become  thickened 
or  atrophied.  Bony  formations  may  appear  on  the  edges  of  the  vertebrae, 
particularly  on  their  anterior  surfaces,  and  finally  in  this  way  the  whole 
vertebral  column  becomes  an  inflexible  pillar  composed  of  vertebral  bodies 
welded  together. 

Symptoms. — The  symptoms  vary  considerably  in  the  manner  of  their 
onset  and  in  the  course  of  the  disease  in  different  cases.  The  mode  of  onset 
may  take  two  forms :  the  slow  progressive  or  gradual  type  and  that  type 
in  which  a  series  of  attacks  of  articular  distress  occur  which  leave  behind 
them  more  and  more  chronic  change  in  the  joints.  In  some  patients  the  first 
complaint  consists  in  a  sensation  of  roughness  in  the  knee-joint;  the  part 
feels  stiff  after  it  has  been  in  one  position  for  any  length  of  time,  and  "  cracks  " 
when  it  is  moved.  Not  rarely  this  is  first  noticed  in  going  up  or  down  stairs 
or  in  rising  from  a  chair.  If  the  joint  is  flexed  by  the  physician  who  holds 
the  limb,  the  cracking  can  be  felt  by  him.  The  sensation  is  one  of  distress 
more  than  of  pain. 

The  tissues  about  the  joint  are  often  swollen,  but  rarely  if  ever  reddened. 
Usually  after  one  joint  is  affected  another  becomes  involved,  and,  as  the 
process  gradually  develops,  the  patient  becomes  more  and  more  incapaci- 
tated owing  to  the  advancing  changes  in  the  joints  and  the  new  areas  affected. 

The  atrophy  of  the  muscles  also  increases  the  inability  to  move  about  with 
ease. 


ARTHRITIS  DEFORMANS  821 

Finally,  the  disease  involves  all  the  articulations,  large  and  small,  even 
the  vertebral  joints  being  affected,  and  the  patient  is  as  completely  par- 
alyzed from  fixation  as  if  suffering  from  a  widespread  multiple  neuritis. 
Such  a  result,  however,  does  not  occur  in  most  instances,  the  malady  being 
less  widely  distributed. 

It  is  a  noteworthy  fact,  for  which  patients  with  this  disease  have  cause 
to  be  devoutly  thankful,  that  in  the  cases  with  greatest  fixation  of  the 
large  joints  the  small  joints  of  the  hand  often  escape,  and  when  the 
hands  are  severely  affected  it  often  happens  that  the  large  joints  are  not 
involved.  In  still  other  cases  the  disease  after  incapacitating  one  part 
ceases  to  be  progressive.  The  frequency  with  which  pain  occurs  in  these 
cases  is  very  variable.  In  some  there  is  none,  in  others  it  appears  only  when 
the  parts  are  used,  as  in  piano-playing,  and  in  others  the  pain  is  severe  and 
like  that  of  neuritis. 

Free  sweating  of  the  palms  of  the  hands  and  finger-tips  often  is  present. 

Because  of  the  fact  that  the  manifestations  of  the  disease  are  often  limited 
to  one  part  of  the  body  or  to  one  kind  of  joints,  it  has  been  customary  to 
divide  the  cases  into  those  with  only  one  joint  affected,  the  monoarticular 
form;  those  in  which  several  joints  are  chiefly  affected,  the  polyarticular 
type;  and  those  in  which  the  spinal  column  is  the  chief  seat  of  the  disease, 
the  so-called  spondylitis  type.  When  the  joints  of  the  fingers  are  chiefly 
affected,  so  that  they  are  locked  by  the  growth  of  small,  bony  knobs  on  the 
sides,  these  growths  are  called  "Heberden's  nodes."  An  important  differ- 
ence between  these  nodes  and  those  due  to  the  deposit  of  urates,  as  in  cases 
of  gout,  is  that  they  are  true  bony  growths,  and  not  due  to  the  deposition  of 
urate  of  sodium  in  the  fibrous  tissues.  It  is  easy  to  see  that  this  classifica- 
tion is  purely  one  of  convenience,  and  has  no  real  pathological  reason  for  its 
existence. 

When  the  large  joints  are  involved,  with  associated  fixation  of  spine, 
the  patient  lies  in  bed  helpless,  with  the  knees  flexed  and  the  back  so  stiff 
that  it  has  been  called  "  poker  back." 

Under  the  name  of  spondylitis  deformans  von  Bechterew  has  described 
a  state  of  spinal  fixation  in  which  there  is  pain,  compression  of  the  spinal 
nerve  roots,  and  muscular  atrophy.  Ascending  spinal-cord  degeneration 
is  also  present.  It  is  questionable  if  this  can  be  considered  a  part  of  true 
arthritis  deformans.  So,  too,  under  the  name  spondylitis  rhizomelique, 
otherwise  known  as  the  Striimpell-Marie  type  of  spinal  fixation,  the  muscles 
of  the  shoulder  and  hip  joints  are  involved,  but  severe  nervous  lesions  such 
as  those  just  detailed  do  not  develop.  Osier  believes  that  both  of  these 
affections  are  forms  of  arthritis  deformans.  This  may  be  a  correct  view, 
but,  if  so,  they  do  not  present  any  symptoms  common  to  arthritis  deformans 
as  it  is  generally  met  with. 

A  form  of  general  arthritis  without  exostosis,  but  with  considerable  swell- 
ing of  the  joints,  is  sometimes  met  with  in  children.  The  lymphatic  glands 
are  distinctly  enlarged,  the  mobility  of  the  joints  greatly  impaired,  and  the 
atrophy  of  the  muscles  well  marked.  Not  only  the  lymph  nodes  nearest 
the  joints,  but  all  the  lymphatics  may  be  swollen.  Anaemia  is  marked. 
To  this  condition  the  name  "Still's  disease"  has  been  applied,  because  it 


822  DISEASES  OF  NUTRITION 

has  been  carefully  studied  by  Dr.  Still.  Children  may  also  have  the  poly- 
articular form  of  arthritis  deformans  as  it  occurs  in  adults. 

Attention  must  be  called  to  that  type  of  arthritis  deformans  in  which 
the  vertebrae  suffer  alone.  In  such  instances  the  spine  is  fixed  and  immov- 
able, the  ankylosis  producing  so  much  rigidity  that  the  patient  in  stooping 
can  only  bend  at  the  hips.  When  in  addition  to  fixation  deformity  takes 
place,  the  spinal  column  may  be  deflected  laterally  or  posteriorly,  and  the 
arching  of  the  back  may  be  so  great  that  the  head  is  bowed  till  the  chin 
nearly  touches  the  chest  and  the  patient  can  only  see  a  short  distance  ahead 
by  rotating  the  eyes  upward.  Lateral  rotation  of  the  head  in  such  a  case 
is  often  impossible.  Associated  with  this  form  of  vertebral  arthritis  there 
is  often  a  good  deal  of  pain,  which  may  be  felt  not  only  in  the  back,  but  in 
the  hips  and  even  down  the  course  of  the  sciatic  nerves.  In  those  cases  in 
which  the  disease  is  limited  to  a  small  portion  of  the  spinal  column  the  case 
may  be  considered  as  one  of  tuberculous  disease,  and  the  only  means  by 
which  a  positive  diagnosis  can  be  reached  is  by  the  use  of  tuberculin,  if  no 
changes  in  other  joints  point  to  the  malady  now  under  consideration. 

Diagnosis. — When  a  well-developed,  bedridden  case  of  arthritis  deformans 
is  met  with,  the  patient  being  "fixed,"  and  the  bony  knobs  locking  the  joints, 
the  diagnosis  is  not  difficult.  The  difficulty  lies  in  the  cases  which  are  in 
the  early  stages  of  the  malady.  This  is  particularly  true  of  the  cases  which 
are  of  the  subacute  type,  and  which  are  ushered  in  by  a  somewhat  abrupt 
onset,  with  soreness,  stiffness,  and  pain  in  the  affected  parts.  The  differ- 
entiation of  such  cases  in  the  first  attack  from  a  subacute  form  of  true  artic- 
ular rheumatism  may  be  practically  impossible.  If  an  endocarditis  develops, 
the  disease  is  probably  rheumatism,  for  the  endocardium  usually  escapes 
in  rheumatoid  arthritis.  Another  point  of  differentiation  lies  in  the  fact 
that  acute  articular  rheumatism  passes  from  joint  to  joint,  often  diminishing 
in  the  first  joints  as  the  others  are  involved.  This  is  also  true  of  arthritis 
deformans,  save  that  the  joints  first  affected  do  not  get  well.  The  pain  of 
rheumatism  is  greater  and  the  parts  affected  are  more  tender  to  touch. 
Finally,  if  the  articular  difficulty  persists  week  after  week,  in  the  face  of  the 
salicylates  freely  given,  if  the  temperature  creeps  along  at  about  99°,  and 
if  there  is  crackling  in  the  joints  on  flexion,  the  diagnosis  of  arthritis  defor- 
mans is  probably  correct. 

Rheumatoid  arthritis  also  must  be  differentiated  from  the  arthritic  changes 
due  to  gonorrhoeal  infection  and  those  of  locomotor  ataxia. 

Prognosis. — A  well-developed  case  of  arthritis  deformans  is  absolutely 
incurable,  and  the  outlook  is  gloomy  as  to  freedom  of  movement.  The  fact 
that  the  disease  is  often  characterized  by  very  slow  progress  and  by  periods 
of  arrest  is  the  most  encouraging  feature  of  these  cases. 

Treatment. — From  the  stage  of  onset  the  treatment  consists  in  the  use  of 
gentle  massage  of  the  joints  with  50  per  cent,  ichthyol  ointment,  this  oint- 
ment being  also  thickly  smeared  over  the  part  between  the  times  at  which 
the  rubbing  occurs.  If  pain  is  present  acetanilid  or  antipyrin  may  be  used. 
If  much  stiffness  is  present  the  joint  should  be  baked  in  a  hot-air  apparatus 
every  day  or  two. 

It  is  a  vital  mistake  to  give  these  joints  rest  as  a  part  of  treatment.    Barring 


CHRONIC  RHEUMATISM  823 

use  to  the  point  of  fatigue  the  patient  should  be  told  to  move  the  affected 
parts  as  frequently  as  possible. 

Fresh  air  and  sunshine  are  essential  factors  in  controlling  the  anaemia 
often  present.  A  valuable  remedy,  probably  the  best  we  have,  is  syrup  of 
the  iodide  of  iron  in  30  or  60  drop  doses  three  or  four  times  a  day  well 
diluted  with  water  and  taken  two  hours  after  meals. 

When  deformity  which  interferes  with  movement  is  present  it  may  be  wise 
to  cut  contracted  tendons,  but  this  does  not  increase  mobility  of  the  joint,  for 
obvious  reasons. 

Many  patients  resort  to  hot  springs  and  hydrotherapeutic  institutes  for 
relief  from  this  disease.  Such  a  plan  of  treatment  is  good  for  the  general 
health  and  may  seem  to  arrest  the  process,  but  it  cannot  cause  a  cure,  and 
if  the  patient's  means  are  limited  it  is  useless  to  let  him  waste  them  in  a 
futile  search  for  health. 


CHRONIC  RHEUMATISM. 

Definition. — Chronic  rheumatism  is  a  condition  characterized  by  a  chronic 
low-grade  inflammatory  process  in  the  synovial  membranes  and  fibrous 
tissues  about  the  larger  joints  which  results  in  stiffness,  soreness,  and  dis- 
ability.   It  may  or  may  not  be  a  sequence  of  acute  articular  rheumatism. 

Etiology. — The  causes  of  this  state  are  unknown.  In  many  cases  it  seems 
to  be  part  of  the  general  fibrous  change  which  occurs  in  other  parts  of  the 
body  due  to  old  age.  Exposure  to  cold  and  wet,  as  in  the  case  of  soldiers, 
firemen,  and  policemen,  seems  to  be  productive  of  the  affection.  The 
malady  is  very  common  among  old  negroes.    It  often  causes  great  crippling. 

Morbid  Anatomy. — The  chief  change  consists  in  thickening  of  the  fibrous 
tissues  about  the  joints,  but  there  is  little  effusion,  as  a  rule,  and  no  deformity 
aside  from  inmobility  or  fixation  in  an  awkward  position  until  secondary 
muscular  atrophy  ensues,  as  it  usually  does  in  all  chronic  joint  affections. 
Occasionally  the  articular  cartilages  undergo  changes  and  some  crepitus 
can  be  felt  on  motion. 

Symptoms. — Stiffness  and  inability  to  move  readily  are  the  chief  symp- 
toms complained  of.  These  are  worse  when  there  is  a  threatened  change 
of  weather.  If  sudden  movement  is  attempted  pain  is  caused.  Rest  increases 
the  stiffness  and  exercise  greatly  decreases  it,  but,  on  the  other  hand,  suffi- 
cient exercise  to  limber  the  joints  is  often  very  painful,  either  at  once  or 
because  of  the  exaggerated  degree  of  stiffness  that  may  develop.  Occasionally 
these  patients,  particularly  if  they  be  women,  become  exceedingly  obese. 

Treatment. — Unlike  arthritis  deformans,  this  malady  gives  us  the  best 
therapeutic  results,  in  many  cases,  if  the  patient  can  be  subjected  to  the 
salutary  influence  of  the  Hot  Springs  of  Arkansas,  Virginia,  South  Dakota, 
Banff,  in  Canada,  or  at  Bath,  in  England.  The  various  sulphur  springs 
are  useful  in  many  cases.  When  these  springs  cannot  be  resorted  to  the 
patient  should  have  the  affected  joints  baked  in  a  hot-air  apparatus, or  should 
take  a  Turkish  bath  several  times  weekly.  A  well-constructed  Turkish  bath 
cabinet,  such  as  is  widely  sold  at  present,  may  be  used  at  home.    A  50  per 


824  DISEASES  OF  NUTRITION 

cent,  ichthyol  ointment  should  be  well  rubbed  into  the  joints  twice  a  day. 
This  may  be  alternated  with  chloroform  liniment  containing  4  drachms  of 
tincture  of  belladonna  and  2  drachms  of  tincture  of  aconite  in  8  ounces. 
In  other  instances  iodine  ointment  diluted  one-half  with  lanolin  may  be 
used. 

The  use  of  drugs  internally  is  not  very  satisfactory  as  to  results.  Pain 
may  be  decreased  by  acetanilid  or  antipyrin.  The  salicylates  are  rarely 
useful,  but  the  iodides  often  cause  great  improvement.  There  is  little  use 
in  dieting  these  patients.  If  they  eat  and  drink  sensible  things  the  ordi- 
nary diet  of  health  is  the  best.  Alcohol  should  of  course  be  used  but  little, 
if  at  all. 

Warm  flannel  should  be  kept  next  the  skin,  and  cold  winds  avoided  if 
possible  by  residence  in  a  balmy  climate  in  the  winter  months. 


MUSCULAR  RHEUMATISM. 

Under  the  name  of  muscular  rheumatism  there  exists  a  condition  in  which 
a  patient  experiences  pain  and  stiffness  when  attempting  to  move  certain 
muscles.  This  condition  is  most  frequently  met  with  in  patients  who  become 
chilled  after  severe  exercise.  It  sometimes  develops  when  certain  portions 
of  the  body  have  been  exposed  to  cold  and  wet,  as,  for  example,  the  stiff 
neck  which  follows  sitting  in  a  draught  of  cool  air  or  the  lumbago  which 
follows  exposure  to  a  storm. 

The  exact  cause  of  muscular  rheumatism  is  not  well  understood.  It  has 
been  claimed  by  some  persons  that  the  liquids  of  the  body  contain  so  large 
a  quantity  of  toxic  materials,  produced  by  perverted  metabolism,  that  when 
a  part  is  exposed  to  cold  precipitation  of  these  toxic  materials  takes  place, 
either  in  crystalline  or  amorphous  form,  and  this  causes  stiffness  and  pain. 

Treatment. — ^The  treatment  of  muscular  rheumatism  depends  somewhat 
upon  the  condition  which  has  produced  it.  If  it  has  followed  exposure  to 
cold,  a  very  hot  bath,  a  Turkish  bath,  or  a  hot  pack  will  often  serve  to  dis- 
sipate the  pain  and  stiffness,  particularly  if  after  the  bath  active  massage  of 
the  part  affected  is  practised.  In  still  other  instances,  particularly  if  the 
onset  of  the  condition  has  been  very  acute,  relief  is  obtained  by  acupuncture. 
This  consists  in  introducing  into  the  substance  of  the  affected  muscle  a  long 
needle,  which  does  good,  it  may  be,  by  relieving  tension  in  the  sheath  of  the 
muscle,  and  allowing  some  of  the  serum  to  escape.  In  many  cases  relief  is 
obtained  by  rubbing  the  affected  part  with  chloroform  liniment,  to  which 
may  be  added  tincture  of  aconite,  tincture  of  belladonna,  and  tincture  of 
opium.  Equal  parts  of  chloral  and  camphor,  which  deliquesce  when  they 
are  mixed,  may  be  rubbed  over  the  painful  area.  Before  giving  medicines 
internally,  the  urine  should  be  examined.  If  it  is  distinctly  acid,  the 
patient  should  receive  from  10  to  20  grains  of  bicarbonate  of  potassium 
in  water  three  or  four  times  a  day.  In  other  instances  similar  doses  of 
bicarbonate  of  sodium  will  prove  equally  efficacious.  In  still  others  it 
may  be  necessary  to  administer  one  of  the  salicylates.  Thus,  much 
benefit  will  often  follow  the  use  of  10  or  15  grains  of  strontium  saHcylate 


RICKETS  825 

given  three  times  a  day.  Often  it  is  advantageous  to  combine  with  this 
4  grains  of  acetanilid  or  the  same  quantity  of  phenacetin  or  antipyrin. 
In  obstinate  cases,  or  in  those  in  which  the  symptoms  frequently  occur, 
the  use  of  iodide  of  potassium  or  iodide  of  strontium  in  the  dose  of  5  or  10 
grains  three  times  a  day  is  advantageous,  and  sometimes  the  patient  requires 
the  additional  use  of  yw  of  a  grain  of  colchicine  three  or  four  times  daily. 
It  is  not  to  be  forgotten  that  some  of  these  patients,  particularly  those  that 
suffer  from  lumbago,  owe  their  condition  to  autointoxication  from  the  ali- 
mentary canal,  which  is  due  to  constipation,  and  in  such  patients  permanent 
relief  will  not  be  obtained  until  the  bowels  are  thoroughly  moved  each  dav. 
In  some  cases  the  use  of  one  of  the  saline  purgatives  is  all  that  is  necessary. 


RICKETS. 

Definition.  —  Rickets,  or  rachitis,  is  a  nutritional  disease  of  childhood, 
consisting  in  a  general  perversion  of  the  processes  by  which  normal  growth 
takes  place.  It  is  chiefly  characterized  by  imperfect  osteogenesis.  The  ends 
of  the  bones  are  often  larger  than  normal,  and  there  is  faulty  growth  in  the 
cartilages,  muscles,  and  tendons. 

Etiology. — Two  factors  are  chiefly  concerned  in  the  production  of  rickets, 
namely,  dietetic  faults  and  bad  hygienic  surroundings.  Of  these  the  most 
important  are  errors  in  diet.  On  the  other  hand,  it  would  seem  that  in  some 
cases  at  least  the  diet  may  be  correct,  yet  the  faults  in  nutrition  exist  because 
the  system  cannot  utilize  the  materials  which  are  ordinarily  employed  in 
the  production  of  normal  tissues  The  majority  of  children  suffering  from 
rickets  improve  as  soon  as  their  food  is  properly  adjusted. 

In  the  article  on  Scurvy  attention  has  been  called  to  the  fact  that  while 
rickets  affects  both  rich  and  poor,  it  is  chiefly  seen  in  the  latter  class,  whereas 
scurvy  in  infancy  is  frequently  a  disease  of  the  well-to-do.  In  many  cases, 
however,  scurvy  and  rickets  exist  simultaneously. 

The  most  common  fault  with  the  diet  consists  in  the  use  of  proprietary 
foods  for  infants,  in  the  use  of  condensed  milk,  and  in  the  carrying  on  of 
lactation  until  the  period  is  past  when  the  child  can  obtain  sufficient  nutri- 
ment from  a  breast  which  is  secreting  a  poor  quality  of  milk. 

It  is  interesting  to  note  in  this  connection  that  valuable  observations  have 
been  made  upon  young  animals  as  to  the  effect  of  depriving  them  of  ordinary 
diet  and  providing  them  with  one  not  suited  to  their  needs.  Thus,  Bland 
Sutton  fed  lion  cubs  with  raw  meat  and  rickets  developed.  When  a  diet  of 
milk,  cod-liver  oil,  and  powdered  bones  was  given  them  they  speedily  got 
well.    Experiments  made  upon  other  animals  have  given  like  results. 

Edlessen  holds  that  the  disease  is  of  infective  origin.  INIendel  thinks  it 
depends  on  some  change  (atrophy)  in  the  thymus  and  has  formulated  a 
system  of  treatment  based  on  the  thymic  origin  of  the  malady.  Spillman 
rejects  the  chemical  theory  and  holds  that  the  deficiency  in  lime-salts  is  a 
result  and  not  the  cause  of  rickets.  There  has  been  much  unprofitable  dis- 
cussion as  to  the  congenital  origin  of  the  disease.  Fede  and  Finizio  found, 
among  975  newborn,  4  that  might  have  been  called  cases  of  fetal  rickets; 


826  DISEASES  OF  NUTRITION 

but  most  of  the  cases  of  so-called  fetal  rickets  are  instances  of  achondro- 
plasia. 

Age  and  nationality  are  factors  of  some  importance  in  the  causation  of 
the  disease.  Holt  states  that  it  is  very  common  in  the  children  of  the  poorer 
class  of  Italians  found  in  all  our  large  cities,  and  it  is  certainly  very  common 
in  negro  children.  In  both  of  these  classes  the  race  has  not  so  much 
influence  as  poor  food  and  poor  surroundings. 

The  disease  is  rarely  met  with  in  children  over  three  years  of  age,  but  the 
signs  of  its  existence  often  persist  in  the  shape  of  bony  deformities  all  through 
life.  Cases  of  rickets  have  been  reported  in  children  at  the  time  of  birth 
and  as  old  as  twelve  years.    Both  sexes  suffer  equally  severely  from  it. 

Diseases  which  impair  nutrition  may  predispose  the  child  to  the  devel- 
opment of  rickets,  but  they  do  not  produce  it.  Thus,  congenital  syphilis 
may  act  as  a  cause,  but  is  not  directly  responsible. 

Fie.  106  Fig.  107 


Rachitic  epiphysitis,  showing  proliferated  cells  in  the  Syphilitic  epiphysitis, 

epiphysis.    (Graupner  and  Zimmerman.) 

Morbid  Anatomy. — While  it  is  true  that  we  know  little  of  the  underlying 
cause  of  rickets,  we  have  very  clear  and  definite  knowledge  of  its  morbid 
anatomy.  In  healthy  children  the  bones  grow  longitudinally  by  the  devel- 
opment of  bony  materials  at  the  space  between  the  diaphysis  and  the 
epiphysis,  and  in  breadth  by  the  deposition  of  bony  materials  by  the  inner 
layers  of  the  periosteum.  The  medullary  canal  is  increased  in  diameter 
by  the  gradual  absorption  of  the  adjacent  bone.  In  rickets  the  process 
is  abnormal  in  that  although  the  development  of  cells  at  the  points  of 
growth  may  be  carried  on  to  excess,  the  deposition  of  mineral  matter  to  form 
bone  is  inadequate.  The  resulting  structure  is  softer  in  texture  and  more 
vascular  than  normal,  that  is  the  osteoid  tissue  is  perverted  (Fig.  106).  It 
happens,  therefore,  that  while  the  length  and  breadth  of  the  bone  is  being 
abnormally  developed,  the  lemallse  adjacent  to  the  medullary  cavity  are 
being  absorbed,  thus  leading  to  structural  weakness.     Under  these  condi- 


RICKETS  827 

tions  it  is  not  difficult  to  understand  why  it  is  that  the  bones  are  unable  to 
bear  the  normal  stress  and  rapidly  become  deformed  if  any  strain  is  placed 
upon  them. 

Again,  the  process  of  development  may  be  so  abnormal  that  areas  of  bone 
are  found  in  the  midst  of  cartilage  and  far  in  advance  of  the  edge  of  the 
normal  bone  growth,  or  the  reverse  holds  true,  and  in  the  midst  of  bone 
there  may  be  a  cartilaginous  mass  with  little  mineral  matter  in  it. 

Histologically  there  is  excessive  proliferation  of  the  cartilages  preliminary ' 
to  ossification  with  irregular  distribution  of  the  columns  of  cells,  excessive 
vascularity,  and  imperfect  calcification.  These  enlargements  seem  particu- 
larly marked  at  the  ends  of  the  long  bones  and  at  the  costal  ends  of  the  ribs 
and  consist  of  this  bone-like  (osteoid)  tissue,  which  later  solidifies  and 
perpetuates  deformities  of  which  it  was  originally  the  cause. 

In  addition  to  the  deformity  of  the  long  bones  produced  in  this  manner 
we  find  similar  changes  occurring  in  the  bones  of  the  head  and  pelvis.  Not 
only  do  the  fontanelles  remain  open  for  a  longer  time  than  is  normal,  but 
in  addition  the  surfaces  of  the  bones  are  found  to  be  soft  and  porous  and 
unduly  vascular.  In  some  places  the  occipital  bone  may  be  irregularly 
developed  and  spaces  exist  which  are  closed  by  membrane  alone.  This 
condition  is  called  "  craniotabes."  The  frontal  bones  are  often  large  and 
bulging,  forming  the  so-called  "bossy  frontals"  described  by  the  English 
clinicians. 

The  actual  deformities  which  result  are  bending  of  the  long  bones,  par- 
ticularly in  the  legs;  the  development  of  pigeon-breast,  with  an  increase  in 
the  anteroposterior  depth  of  the  chest,  and  the  production  of  spinal  curva- 
ture. A  very  constant  state  is  the  presence  of  swellings  or  enlargements  of 
the  ends  of  the  ribs  where  they  join  the  cartilages,  producing  the  knobs  or 
the  so-called  "  rachitic"  rosary.  The  spleen  and  liver  are  increased  in  size 
and  Mendel  thinks  this  is  compensatory  for  the  loss  of  thymic  function. 
Mettenheimer  and  Friedleben  describe  atrophy  of  the  thymus  in  rickets. 

Symptoms. — The  symptoms  of  rickets,  when  the  condition  is  well  devel- 
oped, are  very  characteristic  and  can  scarcely  be  overlooked  even  by  the  most 
careless  observer.  In  the  earlier  stages,  however,  the  manifestations  of  the 
disease  are  not  so  evident,  and  yet  they  are  important  in  that  they  should 
place  the  physician  in  a  position  in  which  he  can  prevent  further  advance 
of  the  malady.  These  early  symptoms  consist  in  sweating  of  the  head,  so 
that  the  child's  pillow  is  wet  with  the  perspiration,  and  restless  sleep,  with 
grinding  of  the  teeth.  Partly  because  of  the  wet  pillow  and  partly  because 
of  lowered  vitality,  rachitic  children  are  very  prone  to  colds  and  often  suffer 
from  constant  catarrh  of  various  mucous  surfaces.  Constipation  is  usually 
a  marked  symptom. 

In  addition  to  these  symptoms  a  physical  examination  of  the  patient  will 
reveal  in  some  cases  in  the  early  stages  heading  of  the  ribs,  that  is,  enlarge- 
ment of  the  junctures  of  the  costal  cartilages  and  ribs,  the  so-called  "rachitic 
rosary."  The  forehead  may  be  full  and  large  from  the  bulging  of  the  frontal 
bones,  the  so-called  "bossy  frontals,"  already  referred  to,  and  the  belly  is 
bulging  and   tumid. 

If  the  condition  is  far  advanced  all  these  signs  are  more  marked,  and  in 


828  DISEASES  OF  NUTRITION 

addition  there  may  be  found  wide-open  fontanelles  and  soft  spots  in  the 
skull  due  to  craniotabes.  This  state  of  craniotabes  is  much  more  marked 
in  those  cases  which  suffer  from  syphiHs,  and  some  observers  have  asserted 
that  it  only  occurs  in  children  who  have  inherited  this  malady.  Auscultation 
over  the  open  fontanelles  may  reveal  a  humming  murmur  synchronous 
with  cardiac  systole.     Anaemia  may  or  may  not  be  a  marked  symptom. 

The  nervous  sijmptoms  consist  in  laryngeal  spasm  (spasmodic  croup)  and 
great  irritabiUty.    Epileptoid  fits  or  tetany  may  develop. 

The  shape  of  the  thorax  is  also  modified  so  that  the  lateral  diameter  is 
decreased  and  the  anteroposterior  diameter  increased.  This  gives  it  a 
somewhat  bulging  or  "chicken-breast"  appearance.  In  the  neighborhood 
of  the  ensiform  cartilage  there  is  seen,  in  some  cases,  a  shallow  depres- 
sion of  the  costal  cartilages  and  ribs,  which  extends  outward  and  upward 
toward  the  axilla  on  both  sides.  This  depression  covers  the  space  of  from 
one  to  three  ribs  and  is  called  "Harrison's  groove."  It  is  chiefly  due  to 
protrusion  of  the  lower  ribs,  which  are  pushed  outward  by  the  bulging  of 
the  abdominal  wall.  This  deformity  is  most  marked  in  children  who  suffer 
from  spasmodic  croup  and  obstruction  of  the  upper  respiratory  passages. 
Palpation  of  the  chest  wall  may  reveal  the  fact  that  it  is  abnormally  pliable 
or  yielding. 

If  the  child  is  old  enough  to  walk  the  long  bones  become  deformed  because 
they  bend  under  the  weight  of  the  body.  For  this  reason  the  hones  of  the 
legs  may  be  bent  and  badly  curved  anteriorly  or  laterally.  There  may  be 
posterior  curvature  of  the  spine. 

Dentition  in  rachitic  children  is  usually  considerably  delayed,  and  is 
accompanied  by  gastrointestinal  disorders,  chiefly  because  a  tendency  to 
catarrh  of  these  parts  is  always  present.  The  teeth  when  cut  are  usually 
fairly  well  developed  and  do  not  readily  decay.  This  is  in  contrast  to  the 
history  of  syphilitic  infants,  who  often  cut  their  teeth  abnormally  early  and 
then  promptly  suffer  dental  decay. 

Several  of  the  symptoms  described,  while  often  found  when  rickets  is 
present,  are  by  no  means  characteristic  of  this  disease,  and  occur  frequently 
in  other  conditions.  These  are  the  craniotabes  of  syphilis,  the  laryngeal 
spasms,  the  systolic  cranial  murmur,  restless  sleep,  and  grinding  of  the 
teeth. 

Diagnosis. — Rickets  should  be  separated  from  scurvy,  with  which  disease 
it  is  very  nearly  related,  and  which  may  be  present  simultaneously.  In 
scurvy  the  nutrition  of  the  mucous  membranes  and  of  the  bloodvessels 
seems  to  be  chiefly  involved,  hsematoma  and  purpuric  rashes  often  develop, 
and  bleeding  gums  are  seen.  These  lesions  are  practically  never  seen  in 
rickets.  There  is  great  muscular  soreness  on  moving  the  child,  and  para- 
plegia is  more  commonly  met  with  in  scurvy,  although  in  both  states  this 
palsy  may  be  present.  Again,  the  scorbutic  child  rapidly  improves  when 
given  fresh  orange-juice  and  beef-juice.  Palsy  may  be  due  to  acute  anterior 
poliomyelitis,  but  if  a  careful  study  of  the  case  is  made  it  will  be  found  in 
rickets  that  the  muscular  weakness  is  universal,  whereas  in  poliomyelitis  it 
is  limited  to  certain  groups  of  muscles  and  the  associated  rachitic  symp- 
toms are  absent. 


RICKETS  829 

Prognosis. — The  prognosis  as  to  life  is  good  so  far  as  the  rickets  itself  is 
concerned.  That  is  to  say,  death  is  never  due  to  rickets.  On  the  other 
hand,  a  child  with  rickets  is  a  fair  mark  for  every  infection  to  w^hich  it  may 
be  exposed,  and  so  the  mortality  of  these  cases  from  intercurrent  maladies 
is  high.  If  marked  deformities  exist  they  of  course  persist  through  life, 
except  they  be  in  the  extremities,  when  they  can  be  corrected  by  surgical 
procedures. 

Treatment. — From  what  has  been  said  it  is  evident  that  the  first  thing  to 
be  done  in  a  case  of  rachitis  is  to  regulate  the  diet,  and  to  see  to  it  that  the 
patient  receives  foodstuffs  which  contain  all  the  ingredients  which  are  neces- 
sary for  the  maintenance  of  normal  nutrition.  It  not  infrequently  happens 
that  the  milk  which  is  given  to  the  child  is  lacking  in  mineral  ingredients 
or  contains  such  an  excess  of  casein  that  the  child's  digestion  is  disordered 
and  assimilation  is  disturbed.  The  mere  fact  that  the  child  does  not  sub- 
sist upon  market  milk,  but  upon  milk  which  is  obtained  by  keeping  a  cow 
for  the  special  purpose  of  providing  sustenance  for  the  infant,  is  more  indic- 
ative of  a  dietetic  cause  for  the  rickets  than  if  the  child  is  obtaining  milk 
which  is  given  by  a  number  of  cows,  for  it  not  infrequently  happens  that 
the  milk  of  a  single  cow  disagrees  with  the  child  or  does  not  contain  all  the 
materials  which  are  necessary  for  its  proper  growth.  If  the  child  has  been 
largely  fed  upon  proprietary  foods,  these  should  be  eliminated  from  the 
diet  list  and  fresh  milk  and  cereals  used  in  their  place.  In  some  instances, 
as  already  stated,  the  rickets  does  not  depend  upon  a  lack  of  normal  ingre- 
dients in  the  food,  but  upon  the  inability  of  the  child  to  utilize  these 
ingredients.  This  may  depend  upon  digestive  disorder,  or  upon  a  disturb- 
ance of  trophic  function.  Under  these  circumstances  it  is  not  only  neces- 
sary to  investigate  the  diet,  but  to  administer  tonics  which  will  improve 
digestion,  such  as  small  doses  of  quinine,  i  to  ^  grain,  twice  or  thrice  a 
day;  minute  doses  of  nux  vomica,  or  small  quantities  of  the  hypophosphites 
or  the  more  modern  elixir  of  the  glycerophosphates.  Of  the  latter  10  to  25 
minims  may  be  given  twice  or  thrice  a  day.  In  other  instances  -^w^  grain 
of  phosphorus  given  in  a  sugar-coated  pill  may  be  used  twice  or  thrice  a 
day;  or  in  its  place  we  may  administer  drachm  doses  of  cod-liver  oil,  or 
cod-liver  oil  in  the  form  of  a  well-made  emulsion. 

If  ansemia  is  present  5  drops  of  the  syrup  of  the  iodide  of  iron  may  be 
given  to  a  child  of  two  or  three  years  of  age  two  or  three  times  a  day.  As 
constipation  is  often  a  troublesome  symptom  in  rickets,  careful  attention 
must  be  paid  to  the  state  of  the  bowels.  They  may  be  moved  either  by  the 
use  of  a  little  calcined  magnesia  and  followed  by  a  few  teaspoonfuls  of 
orange-juice,  or  by  one  of  the  non-bitter  preparations  of  cascara  sagrada, 
such  as  aromatic  cascara  or  cascara  cordial. 

It  is  important  that  a  child  suffering  from  rickets  should  be  allowed  to 
have  exercise  without  bearing  weight  upon  its  long  bones.  Such  a  child 
should  not  be  encouraged  to  walk,  but  should  be  placed  upon  a  rug  on  the 
floor,  where  it  can  crawl  and  roll  about.  An  endeavor  on  the  part  of  the 
parents  to  teach  such  a  child  to  walk  when  its  bones  are  unable  to  bear  its 
weight  results  in  deformities  which  may  be  so  severe  as  to  require  operative 
measures  for  their  relief. 


830  DISEASES  OF  NUTRITION 

It  is  hardly  necessary  to  add  that  fresh  air  and  sunshine  are  essential  in 
the  care  of  such  children.  A  few  weeks  at  the  seashore  will  often  cause  a 
remarkable  change  in  nutrition;  whereas  the  most  skilful  dietetic  and  medi- 
cinal treatment,  if  carried  out  with  unfavorable  hygienic  surroundings,  may 
produce  no  results  whatever. 

In  families  in  which  rickets  is  prone  to  occur  it  is  often  wise  to  administer 
to  the  mother  during  the  later  months  of  pregnancy  the  hypophosphites 
or  the  glycerophosphates,  and  other  nerve  and  bone  tonics,  as  by  this  means 
the  antenatal  nutrition  of  the  child  can  be  materially  influenced.  In  a  well- 
known  case  in  Philadelphia  the  first  tliree  pregnancies  resulted  in  the  destruc- 
tion of  the  mother's  teeth  and  in  the  birth  of  children  which  speedily  showed 
rickets;  whereas,  the  last  three  pregnancies,  during  which  a  diet  rich  in 
mineral  ingredients  was  provided,  resulted  in  the  birth  of  children  which 
remained  perfectly  healthy. 

SCURVY. 

Definition. — Scurvy,  or  scorbutus,  is  a  disease  characterized  by  more  or 
less  profound  nutritional  changes  in  the  body  which  are  largely  dependent 
upon  the  use  of  certain  forms  of  unsuitable  food.  There  may  be  extrava- 
sations of  blood  into  the  subcutaneous  tissues,  under  the  mucous  mem- 
branes, and  about  the  joints,  and  there  is  often  great  spinal  tenderness  when 
the  disease  occurs  in  infants. 

Etiology. — There  can  be  no  doubt  that  scurvy  is  due  entirely  to  the  use 
of  food  which  fails  to  provide  all  the  substances  needed  for  the  perfect  nutri- 
tion of  the  body.  Not  only  does  it  follow  the  continued  use  of  food  which 
is  bad  in  the  sense  that  it  is  unwholesome,  but  it  arises  in  those  who  are 
subjected  to  a  very  limited  diet  of  certain  kind  for  long  periods  of  time. 
Prior  to  the  introduction  of  steamships  it  was  a  prevalent  disease  upon 
vessels  in  both  the  navy  and  in  the  mercantile  marine,  often  disabling  the 
crews  and  rendering  impossible  commercial  and  exploring  expeditions.  The 
use  of  steam  now  causes  short  voyages,  and  the  better  method  of  preserv- 
ing foodstuffs  provides  a  change  of  diet  almost  daily,  if  it  be  needed. 

In  certain  parts  of  Russia  scurvy  still  occurs  in  epidemics  and  is  thought 
to  be  infectious.  If  this  be  true  it  is  probably  only  because  lowered  vital 
resistance  permits  an  infection  to  take  place. 

Some  investigators  have  believed  that  the  disease  arises  from  a  lack  of 
vegetable  acids  found  in  fruits  and  vegetables,  others  that  the  condition  is 
due  to  an  excess  of  sodium  chloride  in  the  blood,  and  still  others  that  it  is 
due  to  the  presence  of  certain  toxic  substances  developed  in  the  food.  Alber- 
toni  has  recently  shown  that  in  scurvy  there  is  a  complete  absence  of  free 
hydrochloric  acid  in  the  gastric  juice  and  that  intestinal  putrefaction  is 
marked,  and  that  the  absorption  of  fats  and  carbohydrates  is  impaired. 

Pathology  and  Morbid  Anatomy. — Anatomically  there  is  nothing  charac- 
teristic. The  condition  of  the  blood  in  scurvy  resembles  that  of  the  blood  in 
ordinary  secondary  ansemia  with  a  decrease  in  the  color  index  which  is  quite 
marked.  If  the  case  is  studied  at  autopsy  hemorrhages  into  the  internal 
organs  and  upon  the  serous  surfaces  of  the  abdominal  and  thoracic  viscera 


SCURVY  831 

are  found  and  ulceration  of  the  small  and  large  bowel  may  be  present. 
Swelling  of  the  gums,  loosening  of  the  teeth,  enlargement  of  the  spleen,  and 
degenerative  changes  in  the  heart,  liver,  and  kidneys  are  found.  Subperi- 
osteal hemorrhages  may  detach  the  periosteum  over  the  shafts  of  the  long 
bones  and  hemorrhage  into  the  joints  may  also  occur. 

Symptoms. — The  symptoms  of  scurvy  in  adults  begin  with  a  sense  of  gen- 
eral wretchedness,  pallor,  and  feebleness.  These  are  followed  by  swelling  and 
sfonginess  of  the  gums,  which  may  bleed  if  pressed  upon  and  which  may 
partly  cover  the  teeth  by  a  process  of  granulation.  The  teeth  become  loosened, 
the  mouth  becomes  joul,  the  salivary  glands  swell,  and  petechioB  appear  over 
the  surface  of  the  body.  The  skin  is  dry  and  badly  nourished,  and  extrava- 
sations of  blood  may  take  place  into  the  sheaths  of  the  muscles  and  joints 
or  beneath  the  periosteum  of  the  long  bones.  These  lesions  at  times  cause 
patches  of  hardness  or  induration  in  the  muscles  of  the  thighs  or  calves.  I 
saw  this  well  developed  in  a  case  which  I  had  in  the  wards  of  St.  Agnes' 
Hospital  some  years  ago. 

Infantile  scurvy,  sometimes  called  "Barlow's  disease,"  is  an  interesting 
result  of  modern  life.  As  seamen  have  escaped  the  disease  by  a  better 
diet,  babies  have  fallen  victims  to  it  as  a  result  of  feeding  them  with  artificial 
foods,  and  these  babies  are  not,  as  a  rule,  the  children  of  the  poor,  but  the 
offspring  of  the  rich. 

It  is  only  within  the  last  decade  that  the  possibility  of  scurvy  occurring  in 
young  children  has  been  generally  recognized  by  the  profession.  During 
this  period,  however,  evidence  has  been  presented  which  shows  very  clearly 
that  scurvy  is  by  no  means  a  very  rare  affection  in  early  life,  and  that  it 
often  manifests  itself  in  such  a  way  as  to  lead  the  physician  to  make  a 
very  erroneous  diagnosis  when  the  patient  is  first  brought  to  him. 

Perhaps  the  most  frequent  error  in  diagnosis  under  these  circumstances 
is  that  the  child  is  suffering  from  muscular  or  articular  rheumatism;  this 
decision  being  reached  by  reason  of  the  fact  that  the  child  seems  to  suffer 
great  pain  upon  movement,  and  sometimes  has  a  moderate  degree  of  fever. 

The  characteristic  symptoms  of  scurvy  in  a  young  child,  when  they  are 
well  developed,  are  so  pathognomonic  that  it  is  difficult  to  see  how  an  error 
in  diagnosis  can  be  made  if  the  physician  is  acquainted  with  the  possibility 
of  the  occurrence  of  this  disease.  Like  all  diseases,  however,  instances  are 
met  with  in  which  many  of  the  characteristic  symptoms  are  entirely  absent, 
and  it  is  not  uncommon  for  the  painful  manifestations  spoken  of  to  be  the 
only  evidence  of  the  malady.  In  still  others,  we  find  a  peculiar  spongy  state 
of  the  gums,  which  tend  to  bleed  when  lightly  touched,  and  which  are  fre- 
quently so  swollen  that  teeth  which  have  recently  broken  through  the  gum 
are  speedily  covered  in  by  the  overgrowth  of  the  mucous  membrane,  the 
edges  of  which,  about  the  teeth,  frequently  look  as  if  they  were  composed 
of  tiny  blebs  of  blood  of  a  dark  color.  Another  symptom  of  scurvy,  which  is 
by  no  means  as  constant,  and  yet  which  is  equally  characteristic,  when  it 
occurs,  is  the  development  of  petechise  in  different  portions  of  the  body,  very 
frequently  about  the  ankles  and  feet.  In  still  other  cases  subperiosteal  hcema- 
toma  develops  with  surprising  rapidity,  and  as  pain  on  movement  and  the 
development  of  great  swelling  are  frequently  first  noticed  after  a  fall  or  a 


832  DISEASES  OF  NUTRITION 

blow,  it  not  rarely  occurs  that  the  physician  is  led  into  the  belief  that  trauma- 
tism is  the  cause  of  the  illness,  without  recognizing  the  fact  that  it  has  played 
but  a  small  part  in  causing  the  sudden  development  of  a  state  which  really 
indicates  grave  systemic  conditions.  It  is  true  that  these  subperiosteal 
hsematomata  have  been  chiefly  reported  by  French  clinicians,  and  have 
been  rarely  seen  in  this  country;  whereas,  on  the  other  hand,  considerable 
extravasations  of  bloody  serum  have  been  met  with  in  the  loose  tissues 
after  exposure  to  injuries  which  in  the  healthy  infant  would  produce  no 
symptoms  whatever.  Paraplegia  may  also  be  present. 
^  The  peculiar  characteristics  of  scurvy  in  infants  are  the  very  grave  appear- 
ance of  the  child  when  suffering  from  the  disease  in  its  severe  forms,  the 
rapidity  with  which  it  improves  under  proper  treatment,  and  the  rarity 
with  which  death  occurs  as  the  direct  result  of  the  malady,  since  a  fatality 
is  usually  produced  by  some  intercurrent  disease.  Reinert  has,  however, 
recorded  a  fatal  case  with  red  cells  at  976,000  and  haemoglobin  at  17  per 
cent. 

Scorbutus  in  infancy  is  distinctly  a  disease  of  the  children  of  the  well-to-do 
in  distinction  from  rickets  which,  on  the  other  hand,  seems  to  be  a  disease 
of  the  poor.  Clinical  experience,  I  think,  indicates  that  scorbutic  cases  are 
rarely  brought  to  hospital  dispensaries  while  rachitic  cases  are  constantly 
seen.  On  the  other  hand,  scorbutic  cases  are  not  uncommonly  met  with  in 
private  practice.  This  clinical  fact  seems  to  carry  out  certain  theories  which 
have  been  advanced  in  regard  to  rickets  in  a  way  which  is  interesting.  It  is 
not  many  years  since  everyone  believed  that  rickets  was  due  to  a  deficient 
quantity  of  bone-forming  material  in  the  food  of  a  child,  but  since  that 
time  other  clinicians  have  stated  their  beUef  that  more  commonly  it  depends 
upon  inability  of  the  child  to  assimilate  and  utilize  the  ingredients  in  its  food 
which  it  needs  for  proper  bone  growth.  Or,  in  other  words,  the  fault  lies  not 
with  the  food,  but  with  the  child.  Among  the  poor  this  inability  is  probably 
due  to  unhealthy  surroundings  and  a  general  lack  of  sanitation  which  inter- 
feres with  development.  On  the  other  hand,  such  influences  are  not  at  work 
among  the  children  of  the  well-to-do,  but  these  cliildren  often  receive,  for 
long  periods  of  time,  the  various  artificial  foods  which,  in  many  instances, 
they  are  incapable  of  digesting;  and  not  only  this,  but  no  change  is  made  in 
their  diet  for  months,  either  in  the  quantity  of  the  various  ingredients  which 
it  contains,  or  in  their  quality.  These  children,  therefore,  suffer  from  the 
nutritive  changes  which  come  on  as  a  result  of  a  limited  and  fixed  diet  with 
no  variation;  whereas,  the  children  of  the  poor,  who  often  have  too  great 
a  variation  in  their  diet,  rarely  present  scorbutic  symptoms  and  often  do 
manifest  distinct  rachitic  symptoms. 

Physicians,  in  the  presence  of  obscure  illness  occurring  in  early  childhood, 
should  remember  the  possibility  of  either  one  of  these  affections  being  the 
underlying  cause  for  the  manifestations  of  disease,  and  thoroughly  investigate 
the  question  of  diet  before  administering  remedies,  such  as  the  salicylates 
for  rheumatism,  iron  for  the  blood,  or  bromides  for  nervous  irritation. 

Treatment. — The  treatment  of  scurvy  in  adults  consists  in  providing  good 
and  varied  food, with  plenty  of  oranges  or  lemons  and  green  vegetables.  Sun- 
shine and  fresh  air  are  also  essentials.     Arsenic  and  iron  may  be  given  as 


OBESITY  833 

hsematics.  If  digestion  is  impaired  it  should  be  aided  by  hydrochloric  acid 
and  pepsin  or  hme- juice  and  pepsin.  For  the  lesions  in  the  mouth  a  chlorate 
of  potash  and  myrrh  mouth-wash  (see  Stomatitis)  may  be  used. 

If  the  disease  occurs  in  a  child  it  is  to  be  treated  by  changing  the  food 
and  in  using  raw  milk  instead  of  sterilized  milk.  Beef-juice  squeezed  from 
a  half-cooked  steak  and  orange-juice  are  also  very  useful. 


OBESITY. 

Definition. — The  term  obesity,  or  adiposity,  is  used  to  describe  a  state  in 
which  an  individual  suffers  from  an  excessive  deposit  of  fat  in  those  parts 
of  the  body  where  a  moderate  amount  of  fat  is  found  in  health.  In  its 
advanced  forms  fat  is  also  deposited  in  parts  where  it  is  never  found  in  the 
normal  state. 

Etiology. — It  must  be  clearly  understood  that  the  mere  presence  of  an 
unusual  amount  of  fat  does  not  in  any  way  indicate  ill-health  or  that  the 
functions  of  the  body  are  perverted.  In  many  instances  a  considerable 
degree  of  obesity  exists,  because  it  is  the  natural  state  of  the  individual.  In 
others,  however,  the  deposition  of  fat  in  excess  is  a  manifestation  of  disease 
or  at  least  of  perverted  function. 

In  the  first  class,  of  what  may  be  called  normally  obese  persons,  the  con- 
dition arises  from  inherited  tendency.  It  is  in  this  class  that  we  find  indi- 
viduals who  have  never  been  heavy  eaters  and  who  for  years  have  deprived 
themselves  of  foods  of  which  they  are  fond,  but  still  gain  weight.  In  another 
class  it  develops  from  overeating  and  lack  of  exercise,  and  in  the  third  class 
it  is  due  to  disorders  of  metabolism,  whereby  foodstuffs  are  not  properly 
dealt  with  by  the  economy  after  they  are  ingested. 

These  three  types  are  worth  recalling,  because  when  a  patient  seeks  relief 
from  obesity  much  depends  upon  the  type  to  which  he  or  she  belongs,  as  to 
advice,  prognosis,  and  treatment. 

Symptoms. — It  is  not  necessary  to  describe  all  the  symptoms  of  obesity, 
for  the  manifest  increase  in  the  size  of  the  patient  determines  the  diagnosis 
of  an  excess  of  fat.  There  are,  however,  certain  other  symptoms  which  are 
of  importance,  not  only  because  they  are  part  of  the  symptom-complex  of 
obesity,  but  also  because  their  presence  determines  the  degree  to  which 
the  excess  of  fat  is  really  annoying  or  harmful.  A  symptom  usually  com- 
plained of  by  the  patient  is  dyspnoea  on  exertion,  which  arises  from  the  fact 
that  the  heart  and  lungs  are  put  under  stress  because  great  muscular  activity 
is  needed  to  move  the  heavy  body.  This  dyspnoea  is  also  due  to  the  fact 
that  the  vascular  network  is  greater  in  the  obese  than  in  those  who  are  lean, 
and  therefore  the  heart  has  to  drive  the  blood  through  a  greater  number  of 
bloodvessels.  Thirdly,  the  heavy  deposits  of  fat  on  the  chest  walls,  in  the 
omentum,  in  the  mesentery,  about  the  diaphragm,  and  around  the  heart 
interfere,  mechanically,  with  the  free  action  of  the  respiratory  and  cardiac 
muscles.  In  many  cases  of  severe  obesity  the  layers  of  fat  are  projected 
between  the  cardiac  muscular  fibres,  and  thus  seriously  impede  its  move- 
ments, forming  the  so-called  "fatty  heart  of  the  obese,"  which  is,  of  course, 
53 


834  DISEASES  OF  NUTRITION 

a  very  different  state  from  the  true  fatty  heart  of  myocardial  degeneration. 
The  pulse  is  often  small  and  rapid.  The  arterial  tension  is  also  lower  than 
normal,  as  a  rule. 

While  many  of  these  patients  are  mentally  and  physically  slow  and  some- 
what somnolent,  others  are  active  and  restless  and  even  unduly  wakeful. 

Next  to  the  dyspnoea  the  chief  complaint  is  of  constipation  or  indigestion 
and  excessive  sweating.  Some  cases  of  obesity,  however,  have  a  digestive 
system  all  too  good. 

In  some  cases,  too,  there  is  an  excess  of  urates  in  the  urine,  and  these  cause 
vesical  irritahiliiy,  chiefly  because  the  larger  surface  of  the  body  and  the  free 
perspiration  cause  a  great  loss  of  fluid,  and  this  in  time  causes  a  scarcity  of 
urinary  flow  with  consequent  concentration  of  the  urinary  solids. 

Treatment. — The  first  point  in  treatment,  as  von  Noorden  has  said,  is  to 
determine  whether  we  shall  diminish  the  fat  abeady  present  or  content  our- 
selves with  the  prevention,  if  possible,  of  an  increase  in  the  obesity.  As  a 
rule,  the  patient  is  not  content  with  a  plan  of  treatment  which  does  not 
actually  diminish  the  fat,  partly  because  he  has  delayed  consulting  a  physi- 
cian until  the  condition  is  far  beyond  what  she  desires.  This  is  particularly 
the  case  with  women  who  have  arrived  at  middle  life  and  who  begin  accu- 
mulating weight  at  the  time  of  late  childbearing,  or  in  other  cases  immediately 
after  marriage.  These  patients  are  often  normally  fat — that  is  to  say,  their 
condition  is  physiological — and  they  should  be  content  in  the  majority  of 
cases  to  try  to  prevent  further  obesity,  rather  than  to  remove  fat  already  in 
existence.  Such  patients  are  often  not  unduly  fat,  and  in  their  desire  to  main- 
tain a  "girlish  figure"  are  willing  to  resort  to  almost  any  measure  to  become 
thin.  Indeed,,  women  in  the  fashionable  walks  of  life,  with  little  to  think 
about,  often  make  their  lives  miserable  and  destroy  good  health  of  mind 
and  body  by  endeavoring,  on  the  one  hand,  to  get  thin,  or,  on  the  other 
hand,  to  get  stout. 

In  such  cases  the  physician  should  advise  against  severe  measures,  point 
out  that  the  plumpness  is  natural,  and,  if  need  be,  assert  that  it  is  better  to 
be  in  good  health,  and  a  little  more  weighty  than  the  average  woman,  than 
to  be  in  bad  health  and  slender.  I  have  seen  several  splendid  specimens 
of  healthy  womanhood  made  physical  wrecks  by  ill-advised  efforts  to  get 
thin. 

The  great  difficulty  with  all  plans  of  treatment  for  the  reduction  of  fat,  in 
those  women  who  desire  to  be  slim  for  the  sake  of  vanity,  is  that  no  plan  can 
be  so  nicely  adjusted  as  not  to  remove  fat  from  where  its  presence  is  needful 
to  good  looks.  With  the  decrease  in  the  bulkiness  of  the  hips  and  waist  a 
hideous  leanness  of  the  chest  and  mammary  glands  ensues  and  leaves  these 
parts  covered  with  a  skin  thrown  in  wrinkles  by  disappearing  fat,  so  that  a 
well-preserved  woman  of  middle  age  is  soon  converted  into  a  hag.  Further 
than  this,  pads  of  fat  keep  organs  in  place,  and  those  who  wilfully  remove 
these  pads  may  subsequently  suffer  from  floating  kidney,  gastroptosis, 
uterine  disorders,  and  constipation. 

There  is  a  sad  lack  of  knowledge  on  our  part  as  to  the  metabolism  of 
obesity  and  nutrition  in  general,  and  the  patient  and  physician  must  be 
careful  how  they  attempt  to  disarrange  processes  so  intricate  and  important. 


OBESITY  835 

On  the  other  hand,  it  is  often  necessary  to  arrest  a  process  which  is  mani- 
festly excessive  and  in  need  of  control. 

In  young  persons  whose  nutritive  processes  are  still  in  a  formative  stage 
and  who  are  obese,  we  should  not  reduce  weight  already  present,  but  simply 
try  to  prevent  an  abnormal  increase.  This  holds  true  of  those  persons  in 
later  life  who  give  a  history  of  having  alwa.ys  been  fat.  It  is  very  unwise  to 
ignore  this  rule  if  advanced  years  are  already  upon  the  patient,  for  under 
these  conditions  the  effects  of  age  and  the  efforts  at  reduction  may  produce 
disastrous  nutritional  changes. 

The  most  favorable  period  of  life  for  reduction  in  weight  is  from  twenty- 
five  to  forty  years  of  age. 

Before  ordering  a  diet  and  mode  of  life  the  patient  should  be  subjected 
to  a  very  careful  physical  examination;  the  urine  should  be  repeatedly 
examined,  and  the  state  of  the  heart  and  vascular  system  carefully  noted. 
If  the  urine  contains  albumin  and  sugar  a  reduction  treatment  is  contra- 
indicated,  and  if  the  heart  is  weak  from  myocardial  degeneration  and  if  the 
vessels  are  fibroid  it  is  dangerous  to  institute  a  plan  of  this  sort. 

When  it  is  determined  that  the  patient  is  in  normal  health  as  to  his  vital 
organs  the  treatment  for  the  prevention  of  increase  is  to  be  instituted,  the 
patient  being  informed  that  a  good  result  cannot  be  reached  by  a  sudden 
and  rapid  process,  and  that  patience  and  persistence  are  necessary  for  really 
valuable  results. 

The  first  factor  is  exercise  taken  to  the  degree  of  moderate  fatigue.  Many 
patients  take  it  to  excess,  and  then  not  only  eat  and  drink  heavily,  but  lie 
down  and  rest  while  the  nervous  system  lazily  permits  vital  oxidizing 
processes  to  go  on  too  slowly,  and  so  more  weight  is  gained  than  lost. 

In  many  cases  no  material  reduction  in  fat  can  be  attained  unless  the 
patient  can  be  treated  in  a  sanatorium,  or  at  least  in  some  place  where  an 
absolute  diet  can  be  maintained  for  a  long  period  of  time.  It  is  not  sufficient 
to  order  a  reduced  diet  and  but  little  to  drink  and  much  exercise.  Such 
aids  to  reduction  in  weight  will  not  in  the  ordinary  case  produce  much 
improvement,  because  the  patient  is  not  willing  to  persist  in  the  annoyance 
of  such  a  strict  diet  for  a  sufficient  length  of  time  to  establish  a  new  nutri- 
tional abscissa.  Unless  the  state  of  reduced  weight  is  maintained  for  a  long 
period  the  patient  often  gains  more  flesh  on  returning  to  the  ordinary  diet 
than  if  no  attempt  at  reduction  had  been  made. 

The  order  for  actual  reduction  of  weight  consists  in  cutting  from  the  diet 
list  all  sugars  and  sweet  articles,  all  fats  and  richly  prepared  foods,  and  in 
the  prescribing  of  lean  meat,  and  of  vegetables  which  are  bulky  but  contain 
little  starch.  Celery,  lettuce,  string-beans,  spinach,  cabbage,  cauliflower, 
and  limited  amounts  of  tomatoes  may  be  permitted ;  whereas  potatoes,  bread, 
peas,  and  beans  are  to  be  forbidden.  All  alcoholic  drinks  are  to  be  avoided, 
because  the  alcohol  has  to  be  oxidized  in  the  body  and  so  prevents  an  active 
oxidation  of  the  foodstuffs  and  tissues.  Alcohol  is  also  contraindicated, 
because  it  stimulates  the  digestive  organs  and  so  increases  the  desire  for 
food. 

If  the  avoidance  of  the  fattening  foods  named  above  does  not  prevent 
an  increase  in  weight,  then  a  more  rigid  diet  must  be  arranged.    The  patient 


836  DISEASES  OF  NUTRITION 

is  not  to  be  given  all  the  food  he  desires,  but  must  suffer  from  privation 
and  hunger.  Instead  of  ordering  an  amount  of  food  which  will  give  the 
2500  to  3000  calories  necessary  for  comfortable  existence,  an  amount  cal- 
culated to  allow  about  2000  calories  or  less  must  suffice. 

For  breakfast  the  patient  is  allowed  3  ounces  of  lean  meat,  1  ounce  of 
bread  with  no  butter,  and  a  cup  of  tea  or  coffee  with  no  milk  and  no  sugar, 
the  sweetening  being  done  by  the  use  of  saccharin.  At  an  early  luncheon  a 
single  soft-boiled  egg  may  be  given  with  an  ounce  of  bread.  At  dinner  a  cup 
of  clear  soup,  such  as  consommd  or  Julienne  (but  no  thickened  soup  or 
pur^e),  may  be  allowed,  followed  by  2  ounces  of  fresh  or  salt  fish,  and  this  by 
2  or  3  ounces  of  lean  meat.  At  this  meal  small  quantities  of  the  various 
green  vegetables  already  named  may  be  taken.  The  dessert  should  consist 
of  some  fresh  fruit,  such  as  an  apple,  an  orange,  a  grape  fruit,  or  a  pear.  In 
the  middle  of  the  afternoon  a  glass  of  milk  or  a  cup  of  tea  with  a  thick  water 
cracker  may  be  given,  and  at  supper-time  3  ounces  of  lean  meat,  some 
lettuce  with  oil  and  vinegar,  celery,  2  ounces  of  toasted  bread  or  Zwei- 
bach  or  crackers  may  be  given.  At  bedtime  a  biscuit  and  a  glass  of  milk 
may  be  allowed.  While  excessive  drinking  of  water  is  unwise,  the  patient 
should  not  be  deprived  of  water  to  such  extent  that  he  suffers  from  thirst 
or  has  not  sufficient  liquid  in  his  body  to  carry  out  to  the  full  every  physio- 
logical function.  Although  overfilling  the  tissues  with  water  will  make  the 
patient  appear  fat,  a  certain  amount  of  fluid  is  necessary  to  healthy  life. 

In  the  way  of  drugs  there  is  but  one  remedy  which  exercises  a  great  influ- 
ence in  reducing  flesh,  and  that  is  the  thyroid  gland.  This  substance  does 
not  reduce  the  weight  of  all  cases  of  obesity,  and  often  fails  unless  it  is 
given  in  doses  which  are  so  large  as  to  cause  distinct  cardiac  feebleness. 
The  doses  usually  given  vary  from  2  to  6  grains  of  the  extract  of  the  gland 
once,  twice,  or  thrice  a  day.  It  is  important  to  give  a  large  amount  of  nitro- 
genous food  at  the  same  time,  for  the  thyroid  causes  a  loss  of  nitrogenous 
tissue  in  the  body  as  well  as  a  loss  of  fat.  Small  doses  of  strychnine  and 
of  digitalis  are  also  useful  to  protect  the  heart  from  depression.  The  patient 
should  be  warned  against  severe  exercise  while  using  this  drug,  and  often 
will  do  best  if  confined  to  bed  and  given  massage  and  electricity. 


ADIPOSIS  DOLOROSA. 

Under  the  name  of  adiposis  dolorosa  my  colleague,  F.  X.  Dercum,  first 
described  in  1889  a  condition  in  which  masses  of  fat  are  deposited  in  differ- 
ent parts  of  the  body,  chiefly  on  the  chest,  arms,  buttocks,  and  legs.  These 
formations  are  usually  symmetrical,  and,  as  the  name  implies,  are  accom- 
panied by  neuralgic  pains  which  vary  from  slight  dartings  to  severe  suffering. 
The  disease  is  of  unknown  origin,  and  affects  women  in  or  past  middle  life, 
as  a  rule.  The  deposits  on  the  extremities  are  usually  firm  and  even  brawny, 
but  they  may  be  so  soft  as  to  be  pultaceous  in  character.  So  far  the  best 
results  in  its  treatment  have  been  obtained  by  the  use  of  thyroid  gland  to 
the  point  of  tolerance.  The  condition  is  quite  uncommon,  but  a  consider- 
able number  of  cases  have  been  reported. 


ACROMEGALY  837 


ACROMEGALY. 

Definition. — Acromegaly  is  a  slowly  developing  chronic  disease  of  nutri- 
tion characterized  by  an  overgrowth  of  the  extremities  and  head,  and,  to  a 
less  degree,  of  the  trunk,  with  associated  curvature  of  the  dorsal  and  cervical 
spine.  It  is  sometimes  called  "Marie's  disease,"  because  Marie  first  de- 
scribed it  in  1886. 

Etiology. — Many  theories  have  been  advanced  by  various  clinicians  with 
the  object  of  determining  the  causation  of  this  extraordinary  malady,  but 
none  of  them  are  adequate.  The  one  which  seems  most  probable  from  our 
present  knowledge  is  that  the  condition  arises  from  disease  of  the  pituitary 
body  and  that  the  enlargement  of  the  thyroid  gland,  which  is  often  present, 
is  an  effort  of  this  gland  to  supplant  its  function.  Acromegaly  rarely  appears 
before  the  thirtieth  year. 

Symptoms. — The  appearance  of  a  patient  suffering  from  this  disease  is 
so  peculiar  and  striking  that  there  is  no  difficulty  in  diagnosis,  if  the  malady 
is  well  developed.  The  massive  and  gigantic  appearance  of  the  head,  of 
the  features  of  the  face,  and,  on  closer  inspection,  the  enlargement  of  the 
hands,  and  the  increase  in  the  length  of  the  long  bones,  combined  with  the 
kyphosis  of  the  spine,  make  the  clinical  picture  complete.  The  upper  part 
of  the  forehead  appears  low  because  of  the  abnormally  prominent  super- 
ciliary ridges,  and  this  effect  is  exaggerated  by  the  projection  of  the  lower  jaw. 
As  a  consequence,  the  shape  of  the  face  is  elliptical.  The  skin  of  the  face 
is  thick  and  sallow  and  greasy  in  appearance,  and  lies  upon  the  forehead 
in  heavy  transverse  creases.  The  cheeks  appear  sunken,  chiefly  because  of 
the  great  overgrowth  of  the  malar  bones.  The  nose  is  not  only  greatly 
enlarged,  but  often  increases  in  size  more  rapidly  than  the  other  features, 
so  that  it  seems  out  of  proportion  with  the  rest  of  the  head.  The  nostrils 
are  heavy,  thick,  and  immovable.  Not  rarely  the  superior  maxillary  bone 
fails  to  develop  as  rapidly  as  nearby  tissues,  and  as  a  consequence  the  upper 
jaw  may  seem  sunken,  an  effect  increased  by  the  enormous  nose  above  and 
the  overgrown  lower  jaw  below  it.  This  effect  is  also  increased  by  the  great 
enlargement  and  thickening  of  the  lower  lip.  An  examination  of  the  mouth 
will  reveal  the  fact  that  the  tongue  and  uvula  are  broader  and  thicker  than 
normal.  The  thorax  on  inspection  will  be  seen  to  be  greatly  increased  in  its 
anteroposterior  diameter,  which  is  in  excess,  as  compared  to  its  lateral  diameter. 
The  ribs  are  enlarged  and  the  clavicles  thickened,  but  the  abdomen  often 
appears  sunken  because  of  the  projection  forward  of  the  lower  part  of  the 
thorax.  The  muscles  may,  in  the  early  stages,  seem  increased  in  size  and 
in  power,  but  the  dominant  tendency  is  to  muscular  atrophy.  No  changes 
of  importance  take  place  in  the  internal  viscera.  Blindness,  partial  or  com- 
plete, may  develop,  due  to  optic  neuritis.  Rarely  nystagmus  and  squint 
have  appeared.    (See  Figs.  108  and  109.) 

The  subjective  symptoms — that  is,  those  complained  of  by  the  patient — 
consist  in  headache,  dimness  of  vision,  and  pains  in  the  joints.  There  is 
usually  slowness  of  thought  and  perhaps  actual  drowsiness. 


838 


DISEASES  OF  NUTRITION 

Fig.  108 


Acromegaly,  showing  the  large  hands,  nose,  and  superciliary  ridges. 


OSTEITIS  DEFORMANS  839 

Diagnosis. — Acromegaly  must  be  differentiated  from  gigantism,  leon- 
tiasis  ossea,  myxoedema,  arthritis  deformans,  osteitis  deformans,  and  pul- 
monary hypertrophic  osteoarthropathy.  Perhaps  the  most  frequent  error 
in  diagnosis  is  that  of  confusing  myxoedema  with  acromegaly,  but  in  myx- 
oedema there  is  never  any  actual  increase  in  the  size  of  the  bones.  The  face 
in  myxoedema  is  round  and  full  instead  of  elliptical,  and  the  ends  of  the 
fingers  are  swollen  and  thickened  instead  of  the  whole  hand  being  manifestly 
enlarged,  as  in  the  disease  under  consideration.  Again,  in  myxoedema 
the  skin  is  pale,  puffy,  and  waxen  in  appearance,  devoid  of  hair  and  also  of 
wrinkles,  whereas  in  acromegaly  the  skin  upon  the  face  is  wrinkled  and 
there  is  no  marked  falling  of  the  hair. 

Gigantism  is  separated  from  acromegaly  by  the  fact  that  there  is  a  sym- 
metrical overgrowth  all  over  the  body,  whereas,  as  has  already  been  pointed 
out,  the  enlargements  in  acromegaly  affects  chiefly  the  extremities  and  the 
tissues  of  the  face.  Further  than  this,  in  gigantism  the  ends  of  the  bones 
are  not  enlarged  to  such  an  extent  as  to  be  out  of  proportion  to  the  shaft, 
and  in  acromegaly  this  disproportion  is  quite  constant. 

Leontiasis  ossea  is  characterized  by  the  development  of  bony  tumors  or 
osteophytes  on  the  face  and  cranium  which  produce  great  deformity,  but 
there  is  no  marked  enlargement  of  any  one  feature  nor  of  the  extremities. 

Osteitis  deformans  is  differentiated  from  acromegaly  by  the  facts  that 
the  long  bones  are  chiefly  affected,  are  apt  to  be  curved,  and  so  produce 
great  deformity.  But  there  is  no  marked  enlargement  and  the  deformity 
is  very  apt  to  be  asymmetrical.  In  osteitis  deformans  the  facial  bones  are 
rarely  affected,  but  the  cranial  bones  are  involved  in  the  pathological  process; 
whereas,  in  acromegaly  it  is  the  facial  bones  which  are  affected,  the  other 
cranial  bones  being  but  slightly  diseased.  Finally,  and  perhaps  most  impor- 
tant, the  face  of  a  case  of  osteitis  deformans  is  broadened  in  its  upper  portion 
and  narrowed  in  its  lower  portion,  giving  it  a  triangular  appearance;  whereas, 
in  acromegaly  the  lower  part  of  the  face  is  broad,  and  therefore  the  general 
effect  is  elliptical. 

In  pulmonary  hypertrophic  osteoarthropathy  there  is  enlargement  of 
the  hands  and  feet,  but  no  enlargement  of  the  face,  and  there  is  always  found 
marked  chronic  pulmonary  lesions,  such  as  bronchiectasis,  empyema,  or 
other  serious  thoracic  disease.  A  close  examination  of  the  hands  and  feet 
will  show  that  the  enlargement  is  confined  chiefly  to  the  joints,  and  that  the 
whole  hand  is  not  thickened  and  increased  in  size  as  in  acromegaly. 

Treatment. — No  plan  of  treatment  is  of  any  value. 


OSTEITIS  DEFORMANS. 

Osteitis  deformans  is  sometimes  called  "Paget's  disease."  It  is  charac- 
terized by  enlargement  and  softening  of  the  shafts  of  the  long  bones,  by  pain 
and  deformity.  The  bones  of  the  face  are  not  affected,  but  the  bones  of  the 
rest  of  the  head  are  often  involved.  A  careful  examination  of  the  long  bones 
in  a  case  of  this  kind  reveals  the  presence  of  a  rarefying  osteitis  associated 
with  the  development  of  new  but  imperfect  lamellae  in  the  bones.    The  face 


340  DISEASES  OF  NUTRITION 

has  a  curious  triangular  appearance  because  of  the  broadening  of  the 
upper  portion  and  the  narrowness  of  the  chin.  By  the  yielding  of  the 
bones  under  pressure,  not  only  the  tibise  but  the  femurs  also  undergo  great 
deformity,  so  that  an  extreme  degree  of  bow-legs  develops.  Occasionally, 
the  bending  of  these  bones  is  forward  or  backward.  There  is  also  some 
spinal  curvature.  Osteitis  deformans  rarely  develops  before  the  fiftieth 
year.     No  treatment  which  has  yet  been  discovered  is  of  any  value. 


HYPERTROPHIC  PULMONARY  OSTEO-ARTHROPATHY. 

This  is  a  condition  first  recognized  by  Bamberger,  but  the  name  was 
given  by  Marie.  It  does  not  affect  the  bones  of  the  head  or  of  the  face,  nor 
the  long  bones  of  the  arms  or  leg.  In  every  instance  it  develops  in  associa- 
tion with  chronic  pulmonary  disease,  such  as  chronic  bronchitis,  bronchi- 
ectasis, fibroid  lung,  and  chronic  empyema. 

The  symptoms  consist  in  the  enlargement  of  the  hands  and  feet,  particu- 
larly about  the  small  joints.  The  growth  of  the  nails  is  often  influenced  so 
that  they  are  thickened  and  incur vated. 


LEONTIASIS  OSSEA. 

Leontiasis  ossea  is  a  disease  in  which  there  is  a  development  of  multiple 
osteophytes  or  symmetrical  enlargement  in  the  bones  of  the  cranium,  and 
sometimes  in  those  of  the  face.     It  is  a  very  rare  affection. 


SCLERODERMA. 

Scleroderma  is  a  chronic  disease  characterized  by  locahzed  or  general 
stiffening  or  rigidity  of  the  skin,  which  is  usually  pigmented,  and  which 
seems  to  be  bound  over  the  tissues  beneath  it  in  much  the  same  manner 
that  a  leather  binding  is  sometimes  placed  over  a  wooden  or  metal  object. 
In  some  instances  the  sclerodermatous  process  is  sharply  circumscribed. 
In  other  cases  it  shades  off  into  the  surrounding  tissues,  and  may  have  a 
slightly  reddened  edge. 

The  first  symptom  usually  noticed  by  the  patient  is  stiffness  of  the  part 
affected,  which  gradually  increases  until  movement  may  become  almost 
impossible.  The  skin  undergoes  atrophic  changes,  and  becomes  silvery 
and  shiny  in  appearance,  with  a  certain  amount  of  yellowish  or  hght-brown 
discoloration.  When  the  disease  affects  the  skin  of  the  extremities,  it  may 
cause  much  interference  with  the  movement  of  the  large  joints,  and  be 
followed  by  atrophy  of  the  muscles  underlying  the  area  involved.  The 
lesions  most  commonly  take  place  in  the  skin  of  the  neck,  in  the  neighbor- 
hood of  the  shoulders,  and  over  the  back  and  chest.  It  not  infrequently 
attacks  the  skin  of  the  face.  The  general  health  is  not  seriously  impaired. 
There  may  be  some  local  discomfort,  with  a  sense  of  formication,  or  ting- 
ling.   The  skin  is  exceedingly  dry,  and  rarely  sweats. 


AINHUM  841 

Treatment. — In  the  way  of  treatment  thyroid  extract  has  been  highly 
recommended  by  certain  cHnicians.  Locally  the  parts  should  be  treated 
by  massage  and  the  local  application  of  oils,  which  should  be  of  a  sedative 
character.  Occasionally,  however,  if  the  process  is  exceedingly  chronic,  it 
may  be  advisable  to  apply  turpentine  diluted  with  six  times  its  amount  of 
sweet  oil.  Even  with  the  best  of  treatment  the  prognosis  is  anything  but 
favorable  as  to  cure,  although  the  spread  of  the  malady  may  be  delayed. 


AINHUM. 

Ainhum  is  a  peculiar  trophoneurotic  disease,  commonly  affecting  the 
feet  of  negroes  and  other  dark-skinned  races.  It  is  widely  distributed  in 
Africa,  particularly  along  the  west  coast,  and  it  occurs  in  India,  and  Brazil. 
It  is  a  rare  affection  among  negroes  in  the  United  States.  The  disease 
usually  begins  in  the  little  toe  of  one  foot  or  both  feet,  as  a  narrow  fissure 
or  groove,  on  the  plantar  surface  at  the  junction  of  the  toe  and  foot.  The 
groove  gradually  surrounds  the  toe  and  slowly  deepens  until  eventually  it 
is  amputated.  Microscopic  examination  shows  that  the  constricting  band 
consists  of  dense  fibrous  tissue.  As  it  tightens,  the  toe  becomes  very  much 
enlarged,  and  disorganized  before  it  finally  separates.  As  a  rule,  the  dis- 
ease is  confined  to  the  one  toe,  although  other  toes  may  be  successively 
attacked  and  the  disease  may  even  appear  in  the  leg. 

The  cause  of  this  condition  has  not  been  determined.  It  has  been 
ascribed  to  traumatism,  such  as  frequent  cuts  from  blades  of  grass.  By 
some  writers  it  has  even  been  regarded  as  an  expression  of  a  very  much 
attenuated  form  of  leprosy.     It  is  evidently  a  trophic  disturbance. 

Treatment. — The  treatment  is  surgical,  and  consists  in  free  division  of  the 
constricting  bands  in  recent  cases  and  amputation  in  advanced  cases. 


INTOXICATIONS. 


ALCOHOLISM. 

Definition. — By  alcoholism  is  meant  a  condition  in  which  the  patient  suffers 
from  the  effects  of  alcohol  when  taken  in  sufficient  quantities  to  act  as  a 
poison. 

Etiology. — An  idea  exists  among  the  laity  that  chronic  alcoholism  is  a 
manifestation  of  an  inherited  tendency  in  many  instances,  and  this  is  some- 
times offered  as  an  excuse  by  a  patient  for  his  unlimited  libations.  There  is 
no  such  disease  as  alcoholism,  nor  does  an  alcoholic  have  any  justification 
in  this  excuse.  The  tendency  to  consume  alcohol  is  not  an  inheritance. 
The  inheritance  is  a  lack  of  self-control,  a  cowardly  inability  to  meet  the 
hard  sides  of  life,  and  a  willingness  to  escape,  if  only  for  a  time,  by  drown- 
ing sensation  in  the  stupor  of  a  narcotic.  In  many  cases,  therefore,  we  may 
not  only  have  to  combat  a  habit,  but  a  state  of  degeneracy  which  permits 
a  habit  to  exist. 

Symptoms. — Alcoholism  may  be  divided  for  readiness  of  consideration 
into  the  acute  and  chronic  forni. 

Acute  Alcoholism.— The  symptoms  of  the  acute  form  are  familiar  to 
everyone  who  sees  life  in  the  town  or  city,  and  consist  in  disorderly 
conduct  due  to  removal  of  the  inhibitory  functions  of  the  brain,  so  that 
every  silly  thought  or  foolish  idea  is  carried  out  in  action.  Later,  as  the 
drug  affects  the  muscle  sense,  and  consequently  disorders  co-ordination, 
the  individual  staggers  and  perhaps  falls,  and  finally,  if  the  quantity  of  the 
drug  is  adequate,  passes  into  a  deep  sleep,  or  coma,  from  which  he  wakes 
more  or  less  confused,  with  depression  of  the  nervous  system  and  a  disordered 
digestive  tract.  In  cases  where  the  dose  has  been  very  large,  death  may  be 
caused  by  depression  of  all  the  vital  functions,  of  which  the  one  most  involved 
is  probably  that  of  bodily  heat,  the  death  being  in  part  due  to  cold.  In  the 
majority  of  cases,  however,  in  which  death  follows  acute  alcoholism,  it  is 
due  not  directly  to  the  depressing  effects  of  the  alcohol,  but  to  the  fact  that 
the  lowering  of  temperature  and  the  disorder  of  vital  function  in  the  various 
organs  permits  infection  by  the  pneumococcus  to  take  place  so  that  pneu- 
monia causes  death,  or  some  complication  such  as  acute  nephritis  is 
developed. 

The  symptoms  of  profound  acute  alcoholism  are  pallor  of  the  face,  duhiess 
of  the  eyes,  widely  dilated  pupils,  profound  uncojisciousness ,  stertorous 
breathing,  and  a  temperature  several  degrees  below  normal.  Occasionally 
convidsive  attacks  may  develop. 

(843) 


844  INTOXICATIONS 

Although  the  symptoms  of  acute  alcohoHsm  are  so  famlhar,  there  is  no 
state  so  often  confused  with  conditions  of  disease  or  with  the  results  of 
injury.  This  is  due  to  the  fact  that  the  symptoms  of  acute  alcoholism  are 
much  like  those  of  cerebral  congestion,  apoplexy,  ursemia,  or  hemorrhage 
from  a  meningeal  artery,  or  fracture  of  the  skull.  It  is  also  due  to  the  fact 
that  alcohol  often  causes  all  these  states  directly  or  indirectly,  and  as  there 
is  a  history  of  alcoholism  or  an  odor  of  alcohol  on  the  breath,  it  is  natural 
to  make  a  diagnosis  of  alcoholism  without  recognizing  that  another  condi- 
tion is  present.  x4gain,  it  not  rarely  happens  that  an  alcoholic  takes  a 
poisonous  dose  of  opium,  and  so  suffers  and  dies  from  the  effect  of  this 
drug.  The  raised  temperature  in  apoplexy  is  in  contrast  to  the  lowered 
temperature  of  alcoholism,  as  is  also  the  full-bounding  pulse  as  compared 
to  the  rapid-running  pulse  of  alcoholic  poisoning.  Again,  apoplexy  is  char- 
acterized by  hemiplegia  and  facial  palsy.  Opium  poisoning  is  characterized 
by  pinpoint  pupils,  slow  breathing,  and  a  warm  skin,  as  opposed  to  the 
normal  or  relaxed  pupils,  the  cool,  moist  skin,  and  the  normal  or  rapid 
breathing  of  alcoholism. 

Treatment. — -Thetreatment  of  acute  alcoholism  consists  in  the  administration 
of  an  emetic  to  empty  the  stomach  of  any  alcohol  still  unabsorbed.  Apomor- 
phine  is  probably  the  best  drug  for  this  purpose,  as  it  can  be  given  hypoder- 
mically,  acts  promptly,  is  sedative  in  its  influence,  and  is  safe  in  a  moderate 
emetic  dose  of  f  grain.  In  other  cases,  or  after  the  emetic  has  acted,  an  active 
cathartic,  such  as  30  grains  of  compound  jalap  powder  or  15  grains  of  com- 
pound extract  of  colocynth,  may  be  used  to  unload  the  bowels  and  the  portal 
system,  and  decrease  cerebral  congestion.  If  circulatory  feebleness  is  present, 
the  aromatic  spirit  of  ammonia  in  drachm  doses,  diluted  with  water,  may  be 
given.  In  other  cases  the  physician  must  give  full  doses  (2^  grain)  of  strych- 
nine by  the  mouth,  or  by  the  hypodermic  needle  if  depression  is  marked, 
and  hot  bottles  must  be  applied  to  maintain  body  heat.  Strong  black  coffee 
by  the  mouth  or  by  the  rectum  may  be  given  if  active  stimulation  seems 
needful.  The  effects  manifested  on  the  next  day  are  to  be  removed  by  the 
use  of  calomel,  followed  by  a  saline  purge  and  the  administration  of  elixir 
of  celery  and  guarana,  or,  if  the  patient  is  very  nervous,  by  the  use  of 
guarana  and  bromide  of  sodium,  5  grains  of  the  extract  of  the  former  and 
30  grains  of  the  latter  at  a  dose. 

Subacute  and  Chronic  Alcoholism. — Chronic  alcoholism  is  divisible  into 
three  classes.  In  one  the  patient  suffers  from  a  prolonged  alcoholic  debauch 
lasting  over  days,  or  even  weeks,  during  which  time  he  is  never  com- 
pletely sober.  In  the  other  type  he  is  never  drunk,  but  always  under  the 
influence  of  the  drug  to  an  extent  which  eventually  produces  a  train  of 
symptoms  even  more  grave  than  those  which  follow  a  debauch.  Those 
who  have  made  a  special  study  of  alcoholism  also  recognize  that  there  is  a 
certain  class  of  persons,  of  the  first  division  just  named,  who  take  no  alcohol 
for  a  comparatively  long  period,  varying  from  wrecks  to  months,  and  then  go 
on  a  terrific  debauch,  the  so-called  "  periodical  drunkard."  It  isthe  individual 
who  takes  alcohol  up  to  the  stage  of  intoxication  for  several  days  consecu- 
tively, and  who  has  often  used  alcohol  in  large  quantities  for  weeks  before 
the  acute  exacerbation,  who  most  commonly  develops  delirium  tremens; 


ALCOHOLISM  845 

while  the  constant,  moderate  "soaker"  is  more  prone  to  hepatic  cirrhosis 
and  affections  of  the  peripheral  nerves.  Delirium  tremens  is  very  prone  to 
develop  in  persons  who  are  the  subjects  of  subacute  or  chronic  alcoholism 
if,  perchance,  they  suffer  from  a  severe  injury,  surgical  operation,  or  great 
shock.     Xot  rarely  the  onset  of  an  acute  illness  may  precipitate  an  attack. 

Morbid  Anatomy. — The  morbid  changes  produced  by  the  continuous  use 
of  alcohol  in  excess  are  chiefly  found  in  the  organs  by  which  the  drug  gains 
access  to  and  egress  from  the  body;  that  is,  the  stomach,  the  liver,  and  the 
kidneys.  Next  to  the  effect  of  the  drug  upon  these  organs  it  expends  its 
deleterious  influences  upon  the  circulatory  system.  The  passage  of  alcohol 
directly  to  the  liver  from  the  stomach  through  the  portal  vessels  causes  con- 
gestion, irritation,  and  finally  atrophic  cirrhosis  of  this  organ.  (See  Hepatic 
Cirrhosis.)  By  reason  of  the  direct  effect  of  the  drug  upon  the  stomach,  and 
the  indirect  effect  produced  by  the  impairment  of  its  blood  supply,  which 
arises  from  the  hepatic  changes,  chronic  gastric  catarrh  develops.  The 
changes  found  in  the  kidneys  in  very  chronic  alcoholism  consist  in  a  con- 
dition practically  identical  with  that  found  in  contracted  kidney,  and 
with  this  state  an  arteriocapillary  fibrosis  develops,  just  as  it  does  in  cases 
of  cardiovascular  change  arising  from  other  causes.  The  most  common 
change  in  the  kidneys,  however,  consists  in  a  hypostatic  congestion,  or 
stasis,  which  causes  them  to  be  swollen,  cyanotic,  and  to  be  functionally 
inactive.  Not  rarely  these  patients  develop  acute  tuberculosis,  because  of 
their  lowered  vital  resistance.  An  alcoholic  multiple  neuritis  may  develop, 
and  atrophy  of  the  optic  nerve  may  occur. 

Symptoms.— The  symptoms  of  delirium  tremens  are  great  nervous  rest- 
lessness and  apprehension  with  anxiety,  and  finally  delusions  of  persecution 
and  terror.  The  delusions  are  largely  those  connected  with  vision,  and  all 
sorts  of  hideous  objects  are  described  as  crawling  about  the  patient.  Because 
of  these  delusions  the  patient  is  often  violent  and  difficult  to  control,  but  is 
rarely  offensive  unless  he  believes  that  the  attendant  is  in  league  with  the 
"objects  of  evil"  about  him.  The  pulse  is  usually  rapid  and  feeble,  the  skin 
relaxed,  and  the  tongue  exceedingly  foul.  The  bowels  are  constipated  and 
the  urine  scanty.  Hypostatic  congestion  of  the  lungs  and  congestion  of  the 
kidneys  are  very  commonly  developed,  and  these  states  often  contribute  to 
the  death  of  the  patient. 

It  is  not  to  be  forgotten  that  acute  croupous  pneumonia  at  the  apex  not 
rarely  is  associated  with  an  acute  delirium  not  unlike  that  of  delirium  tremens. 

In  that  form  of  chronic  alcoholism  in  which  the  patient  is  never  drunk, 
but  always  has  alcohol  in  his  body,  the  chief  symptoms  are  irritability  of 
temper,  gradual  mental  deterioration,  localized  sensory  and  motor  palsies, 
and  finally  dementia. 

Treatment. — The  treatment  of  this  state  consists  in  the  use  of  an  active 
cathartic,  as  already  advised  for  acute  alcoholism,  and  the  use  of  full  doses 
of  morphine  hypodermically,  if  the  kidneys  are  not  diseased,  to  produce 
nervous  rest  if  the  patient  is  becoming  exhausted  by  his  lack  of  sleep  or 
struggling.  Care  must  be  taken  that  more  than  a  few  doses  are  not 
given,  for  such  a  patient  may  become  a  morphine  habitu^  very  quickly. 
Strychnine   and  atropine  are   to  be  used  hypodermically  if   any  signs  of 


846  INTOXICATIONS 

pulmonary  congestion  arise,  and  they  must  be  given  boldly.  Dry  cups 
should  be  applied  to  the  back  of  the  chest,  and  Hoffmann's  anodyne  is 
useful  as  a  rapidly  acting  diffusible  stimulant.  Every  measure  must  be 
taken  to  disperse  and  prevent  the  congestion,  v^hich,  if  it  develops  in  full 
degree,  means  the  death  of  the  patient. 

The  question  as  to  the  medicinal  use  of  alcohol  in  these  cases  is  debatable. 
In  those  who  are  not  accustomed  to  its  constant  use,  and  who  may  have  been 
intoxicated  for  but  a  few  days,  it  is  not  necessary  to  give  the  drug;  but  if 
the  patient  has  been  in  the  habit  of  taking  alcohol  in  considerable  amounts 
prior  to  his  acute  alcoholic  outbreak,  whiskey  must  be  used  freely  in  many 
cases  if  signs  of  great  nervousness  develop.  Aside  from  pulmonary  and 
renal  complications  the  most  frequent  one,  and  a  most  fatal  one,  is  a  state 
of  nervous  tension  in  which  the  symptoms  are  those  of  meningeal  irritation 
with  stiffness  of  the  limbs  and  neck.  This  stage  of  tonicity  in  the  muscles 
is  preceded  by  muttering  delirium,  with  periods  of  wakefulness  in  which 
hallucinations  may  make  the  patient  difficult  of  control.  The  pupils  are 
contracted  and  the  pulse  rapid  and  feeble.  The  temperature  is  often  as 
high  as  103°  or  even  104°,  and  not  rarely  hypostatic  congestion  of  the  lungs 
can  be  found  if  the  bases  are  examined.  Marked  hypersesthesia  of  the 
skin  usually  exists.  Patients  with  these  manifestations  usually  die,  but 
they  may  recover  after  a  prolonged  illness  lasting  several  weeks.  My 
experience  is  in  accord  with  that  of  Dana,  that  if  there  is  stiffness  of  the 
cervical  muscles  the  patient  usually  dies.  This  condition  is  not  due  to  a 
true  meningitis,  but  to  a  toxcemia  with  serous  effusion  into  the  meninges. 
Dana  and  others  have  given  the  name  "wet  brain"  to  this  condition. 

The  diet,  if  food  can  be  given  to  the  patient,  should  consist  of  hot  and 
stimulating  liquid  nourishment,  such  as  highly  seasoned  beef-tea  or  pep- 
tonized milk,  to  which  capsicum  and  salt  have  been  added  to  stimulate  the 
digestion  to  activity.    The  various  highly  seasoned  broths  are  useful. 

The  treatment  of  the  alcoholic  who  continually  takes  the  drug  day  in  and 
day  out  presents  grave  difficulties.  Those  who  have  been  wont  to  take  this 
drug  every  day  for  many  years  are  rarely  willing  to  put  up  with  the  discom- 
fort which  follows  abstinence,  and  after  a  few  days  almost  invariably  return 
to  the  use  of  alcohol.  The  only  treatment  which  is  of  any  value  in  such 
cases  is  to  send  the  patient  to  some  isolated  region  where  he  is  too  far 
removed  from  the  grog-shop  to  be  able  to  obtain  alcohol  when  his  desire 
for  it  arises,  and  to  take  care  that  he  does  not  provide  himself  beforehand 
with  alcohol  to  be  used  during  the  trip.  Usually,  if  the  man  is  well-to-do, 
several  weeks  or  months  of  hunting  in  isolated  regions,  and  in  the  company 
of  someone  who  does  not  drink  alcohol  and  has  considerable  mental  force, 
will  be  the  best  means  of  cure. 

For  those  who  take  alcohol  more  or  less  constantly  to  the  point  of 
intoxication,  either  this  measure  can  be  employed  or  the  patient  may  be 
placed  in  a  private  room  in  a  hospital,  where  he  is  under  absolute  control 
of  the  nurses  and  physicians  attached  to  the  institution,  and  the  alcohol 
can  then  be  immediately  stricken  off  the  list  of  permissible  articles,  or,  if 
his  condition  is  one  of  feebleness,  it  can  be  gradually  diminished  so  that  at 
the  end  of  a  week  he  is  getting  none  of  it.    In  the  great  majority  of  instances 


ALCOHOLISM  847 

it  is  utterly  futile  to  attempt  home  treatment  of  these  cases.  Even  if  the 
family  can  prevent  the  man  from  getting  alcohol,  home  life  lacks  the  disci- 
pline which  is  necessary  for  the  control  of  the  patient,  not  only  in  the  sense 
of  preventing  him  from  procuring  alcohol,  but  in  the  sense  of  making  a 
powerful  mental  impression. 

In  those  cases  in  which  removal  of  alcohol  causes  nervous  excitation  and 
evidences  of  threatened  delirium  tremens,  it  is  occasionally  permissible  to 
administer  full  doses  of  chloral  and  the  bromides  to  produce  nervous 
quiet  at  night.  Small  doses  of  these  drugs  practically  have  no  influence 
whatever,  and  if  the  heart  is  at  all  feeble  full  doses  of  chloral  are  danger- 
ous. Morphine  possesses  the  disadvantage  that  the  alcoholic  is  very  prone 
to  develop  the  morphine  habit  in  addition  to  his  alcoholism.  This  drug  is, 
however,  exceedingly  valuable  if  used  on  those  occasions  when  the  violence 
of  the  patient's  nervous  symptoms  demand  sedation.  It  should  not  be  given 
day  after  day,  but  only  occasionally,  when  insomnia  is  so  pressing  that  the 
consequent  exhaustion  demands  relief. 

Within  the  last  few  years  very  strong  claims  have  been  made  for  the 
use  of  hyoscine  for  the  purpose  of  relieving  the  nervous  irritation  and  craving 
for  alcohol.  The  drug  must  be  given  in  suflSciently  large  doses,  hypoder- 
mically,  to  place  the  patient  deeply  under  its  influence.  If  necessary  as  much 
as  Yw^  o^  ^  grain  every  two  hours  may  be  given  hypodermically  until  the 
patient  sleeps  or  is  resting  quietly.  These  doses,  of  course,  produce  the  full 
physiological  action  of  hyoscine  and  often  cause  great  dryness  of  the  mouth 
and  talkative  delirium.  They  may  be  continued  for  several  days  and  then 
gradually  remitted  until  the  patient  is  no  longer  taking  either  alcohol  or 
hyoscine. 

If  the  circulation  fails  in  these  cases  strychnine  and  digitalis  may 
be  administered.  For  the  purpose  of  combating  signs  of  acute  collapse 
Hoffmann's  anodyne  and  strychnine  are  valuable,  as  is  also  the  aromatic 
spirit  of  ammonia.  Another  drug  which  has  been  highly  praised  in  this 
condition  is  apomorphine  given  in  the  dose  of  ^  of  a  grain  hypodermically 
as  a  nervous  sedative,  the  emetic  effect  of  the  drug  not  being  desired.  In 
some  instances  larger  doses  have  to  be  given  and  may  be  used  without  pro- 
ducing emesis. 

It  must  be  constantly  borne  in  mind  that  the  most  important  portion 
of  the  treatment  consists  in  the  isolation  of  the  patient,  and  in  a  com- 
plete control  of  his  methods  of  life  for  the  period  covering  several  weeks. 
Drugs  are  of  little  value  except  to  support  him  through  the  period  when  his 
system  lacks  his  customary  doses  of  alcohol.  If  the  patient  is  unwilling  or 
unable  to  resort  to  this  form  of  treatment,  the  employment  of  drugs  is  usually 
worse  than  useless. 

Careful  attention  to  the  digestive  system  is  needful  in  all  these  cases.  The 
liver  should  be  unloaded  by  blue  mass,  followed  by  a  saline  purge,  every 
few  days,  and  bitter  tonics,  such  as  gentian  with  bicarbonate  of  sodium,  are 
advantageous. 


848  INTOXICATIONS 


MORPHINISM. 

Chronic  morphinism,  or  the  morphine  habit,  is  usually  acquired  as  the 
result  of  the  employment  of  this  drug  for  the  purpose  of  relieving  insomnia. 
Sometimes  the  insomnia  is  due  to  neurasthenia,  but  more  frequently  the  patient 
is  one  who  primarily  suffers  from  sleeplessness  due  to  pain.  If  the  condition 
producing  the  pain  is  continued  over  any  considerable  period  of  time,  the 
patient  finally  becomes  so  dependent  upon  the  use  of  morphine,  as  a  nervous 
sedative,  that  he  cannot  sleep  without  it,  and  so  even  although  the  pain  no 
longer  continues  he  resorts  to  the  drug  for  the  nervous  quiet  which  can  be 
obtained  only  under  its  influence.  Not  infrequently  these  patients  continue 
the  use  of  the  morphine  long  after  the  physician  intends  that  it  should  be 
stopped,  and  so  develop  the  habit  of  taking  the  drug  without  the  knowledge 
of  the  physician  who  has  first  prescribed  it.  Because  of  the  possibility  of 
this  occurrence  he  should  only  prescribe  that  quantity  of  morphine  which 
is  absolutely  essential  for  the  relief  of  pain  upon  a  particular  occasion, 
and  if  he  writes  a  formal  prescription  ordering  the  drug  from  a  pharmacist, 
this  prescription  should  contain  the  words  "Do  not  renew,"  so  that  the 
patient  will  not  be  able  to  continue  taking  the  drug  after  the  physician 
believes  that  he  has  stopped  it. 

In  a  certain  number  of  cases  of  morphine  habit,  the  employment  of  the  drug 
rests  upon  the  fact  that  the  patient  is  a  degenerate  without  the  necessary 
mental  and  nervous  vigor  to  meet  the  vicissitudes  of  life.  In  other  words, 
he  is  one  who,  in  the  presence  of  any  condition  which  produces  mental  per- 
turbation or  distress,  at  once  resorts  to  some  sedative  to  quiet  his  nervous 
system,  instead  of  dominating  it  by  his  will  power  and  conquering  the  depres- 
sion with  a  knowledge  that  any  yielding  either  to  that  depression  or  to  the 
desire  for  a  drug  is  certain  in  the  end  to  wreck  his  moral  and  physical 
condition.  This  is  an  important  factor  to  be  taken  into  consideration  when- 
ever a  morphine  habitue  is  to  be  treated.  This  condition  may  be  hereditary, 
or  it  may  be  acquired.  Not  rarely,  when  it  is  acquired,  the  mental  and 
physical  condition  of  the  patient  has  been  impaired  by  grief,  excessive 
business  worry,  illness,  or  other  cause.  When  the  morphine  has  been  used 
for  any  length  of  time  this  very  fact  tends  to  increase  the  lack  of  moral 
stamina  on  the  part  of  the  patient. 

Symptoms. — One  of  the  most  noteworthy  symptoms  of  morphinism  is 
great  irritability  of  the  nervous  system  so  that  slight  causes  may  produce 
outbreaks  of  rage,  or,  on  the  other  hand,  a  lacrymose  state  may  develop.  In 
some  instances,  where  the  drug  has  been  used  for  a  long  time,  there  is  not 
only  a  loss  in  mental  power,  but  the  patient  develops  melancholia  or  delu- 
sions closely  resembling  those  seen  in  an  ordinary  case  of  insanity.  Before 
the  mental  degradation  is  so  complete  that  intellectual  processes  are  greatly 
impaired,  the  patient  develops  a  slyness  quite  different  from  his  ordinary 
frank  methods  of  life  when  in  health.  In  association  with  this  slyness  there 
is  always  developed  a  skill  at  prevarication  or  lying  which  is  quite  remark- 
able. Persons  who  previously  have  been  regarded  as  eminently  truthful  tell 
the  most  skilful  falsehoods,  and  in  such  a  way  that  the  hearer  is  convinced 


MORPHINISM  849 

of  their  truth.  As  a  rule,  these  falsehoods  are  never  so  clever  as  when  they 
are  intended  to  result  in  the  obtaining  of  the  drug  which  is  desired,  the 
patient  resorting  to  every  possible  means,  honest  and  dishonest,  in  order 
that  he  may  obtain  the  nervous  quiet  which  his  system  craves. 

Treatment. — It  may  be  asserted  with  truth  that  it  is  useless  to  attempt  to 
treat  a  patient  who  is  suffering  from  the  morphine  habit,  with  the  idea  of 
curing  him  of  his  taste  for  the  drug,  unless  he  or  she  is  willing  to  enter  a 
private  room  at  a  hospital  and  be  placed  under  the  constant  supervision 
of  a  night  and  day  nurse.  This  isolation  is  necessary  not  only  because  it  is 
a  form  of  discipline  which  is  advantageous  for  the  mental  condition  of  the 
patient,  but  it  is  the  only  way  in  which  the  physician  can  be  assured  that 
the  patient  is  not  surreptitiously  continuing  his  daily  dose  of  the  narcotic. 
It  must  be  remembered  that  the  most  pious  individuals,  when  they  become 
addicted  to  this  drug,  develop  an  extraordinary  ability  to  tell  lies  which  are 
so  like  the  truth  that  they  can  deceive  the  most  cautious.  In  one  breath, 
the  patient,  with  tears  running  down  his  face,  will  beseech  the  physician  to 
cure  him  of  the  habit  which  is  destroying  his  happiness,  and,  at  the  next 
moment,  he  will  iise  every  form  of  deceit  and  cleverness  to  obtain  the  drug 
which  he  craves.  Even  when  the  patient  is  under  the  observation  of  trained 
nurses  night  and  day,  any  sudden  improvement  in  his  condition  after  with- 
drawal of  the  morphine,  or  failure  to  develop  symptoms  produced  by  its 
withdrawal,  should  make  the  physician  believe  that  in  some  unknown  way 
the  drug  has  been  obtained.  In  some  instances  the  patient  enters  the  hos- 
pital with  the  morphine  carefully  sewed  in  the  hem  of  the  night-dress ;  in 
others,  a  friend  or  servant  is  bribed  to  bring  the  drug  each  day  in  some 
article  of  food.  Nothing  but  ceaseless  watchfulness  can  possibly  prevent 
these  patients  from  obtaining  morphine.  This  being  so,  it  can  readily  be 
understood  that  home  treatment  can  rarely  succeed. 

Having  obtained  special  control  of  the  patient,  the  method  of  treating 
him  should  consist  in  one  of  two  plans  which  have  found  general  accept- 
ance. The  first  of  these  is  the  gradual  diminution  of  the  morphine  so  that 
at  the  end  of  three  or  four  days,  or  a  week,  none  of  the  drug  is  permitted. 
If  this  method  is  carried  out  the  patient  usually  develops  after  a  few  days, 
or  sooner,  great  restlessness  and  irritability,  not  infrequently  active  purging, 
and  profound  mental  and  physical  depression.  Cramps  in  the  extremi- 
ties also  add  to  the  suffering.  Under  these  circumstances  it  is  necessary  to 
support  the  patient  by  the  use  of  hot,  stimulating  foods,  such  as  broths  highly 
seasoned  with  pepper  and  salt,  the  use  of  digitalis  and  strychnine  if  the  cir- 
culation fails,  and  the  employment  of  hyoscyamus  or  hyoscine  to  diminish 
irritability  of  the  nervous  system.  The  employment  of  alcohol,  coca  wine, 
or  similar  stimulants  for  the  purpose  of  aiding  the  patient  at  this  time  is 
unwise,  because  he  is  prone  to  develop  the  alcohol  or  coca  habit.  If  the 
diarrhoea  is  so  violent  as  to  require  control,  aromatic  sulphuric  acid  with 
a  vegetable  astringent,  like  the  fluid  extract  of  ha^matoxylon,  may  be  used. 
Hot  compresses  may  be  applied  about  the  painful  limbs.  Great  mental  excite- 
ment may  be  relieved  by  chloral,  but  the  danger  of  producing  the  chloral 
habit  is  not  to  be  forgotten.  In  place  of  chloral,  sulphonal  or  trional  may 
be  used.  Occasionally  nerve  quiet  can  be  produced  by  wrapping  the  patient 
54 


850  INTOXICATIONS 

in  a  hot,  wet  blanket,  care  being  taken  that  the  hot  pack  is  not  continued 
so  long  as  to  produce  cardiac  depression. 

A  second  method  of  treatment  is  one  which  has  been  largely  employed 
in  the  last  few  years,  and  for  which  we  are  chiefly  indebted  to  a  Texas 
physician,  Dr.  Lott.  This  consists  in  putting  the  patient  where  we  can 
have  him  under  absolute  control,  and  in  the  administration  of  full  doses  of 
hyoscine  hypodermically,  giving  him  as  much  as  3-^  of  a  grain  every  two 
hours,  if  need  be,  until  a  condition  of  nervous  quiet  is  produced.  In  the 
writer's  experience  these  large  doses  fail  to  produce  sleep,  and  instead  cause 
a  condition  in  which  the  patient  lies  awake  but  stupefied,  and  often  mum- 
bles continuously.  Curiously  enough  the  mouth  does  not  become  as  dry 
as  one  would  expect  from  the  administration  of  such  a  powerful  drug  in 
these  large  doses.  Should  the  circulation  seem  at  all  feeble,  strychnine  may 
also  be  given.  The  idea  in  employing  hyoscine  is  to  use  that  quantity 
which  is  necessary  to  keep  the  patient  under  control,  and  to  prevent  suffer- 
ing. These  doses  may  be  continued  for  a  number  of  days,  at  the  end  of 
which  time  they  are  gradually  diminished  and  the  patient  is  permitted  to 
return  to  his  normal  condition  as  the  effects  of  the  hyoscine  pass  away. 
By  this  means  the  acute  mental  and  physical  suffering  caused  by  the  sudden 
withdrawal  of  morphine  is  avoided,  and  in  some  instances  the  patient 
actually  seems  to  be  cured  of  his  malady,  although,  of  course,  there  is  great 
danger  in  every  case  of  his  speedily  returning  to  its  use,  particularly  if  any 
nervousness  or  mental  stress  is  experienced.  So  common  is  it  for  the  habitu6 
to  go  back  to  the  employment  of  this  drug  habit  that  many  men  of  experi- 
ence have  gone  so  far  as  to  assert  that  no  case  of  the  morphine  habit  is  ever 
permanently  cured.  This  view  is,  however,  undoubtedly  incorrect.  The 
writer  has  seen  a  number  of  cases  in  which  permanent  cure  certainly  took 
place. 

ARSENICAL  POISONING. 

Arsenical  poisoning  occurs  in  two  forms,  the  acute  and  chronic.  Usually 
after  the  first  stage  of  acute  poisoning,  if  the  patient  survives,  there  develops 
a  second  subacute  stage  due  to  the  effects  of  the  retained  arsenic.  Acute 
poisoning  usually  follows  the  ingestion  of  "Rough  on  Rats,"  Paris  green, 
or  Scheele's  green.  The  symptoms  are  those  of  severe  gastroenteritis, 
with  vomiting  and  purging,  followed  by  death  in  collapse.  The  antidote 
is  the  hydrated  sesquioxide  of  iron  with  magnesia.  When  the  patient  sur- 
vives the  acute  stage  he  suffers  from  secondary  lesions  in  the  stomach  and 
intestines,  kidneys  and  fiver.  Widespread  fatty  degeneration  also  occurs 
and  peripheral  neuritis  may  be  present.^ 

The  causes  of  chronic  arsenical  poisoning  are  almost  as  numerous  as 
are  those  of  lead  poisoning.  It  may  find  its  way  into  the  body  through 
the  lungs  from  the  air  of  a  room  the  walls  of  which  are  covered  by  a  paper 
heavily  laden  with  arsenical  dyes;  it  may  enter  in  beer  made  from  glucose 
prepared  by  the  use  of  iron  pyrites  contaminated  with  arsenic,  as  in  the 

1  For  this  train  of  symptoms  see  the  author's  Text-book  of  Therapeutics,  10th  edition. 


LEAD  POISONING  851 

recent  celebrated  epidemic  in  England;  or  it  may  be  given  in  moderate 
poisonous  dose  for  a  long  time  with  homicidal  intent,  as  in  a  case  recently 
tried  in  the  Philadelphia  courts. 

Not  very  rarely  a  mild  form  of  chronic  arsenical  poisoning  is  met  with 
in  cases  to  which  a  physician  has  found  it  necessary  to  give  large  doses  of 
arsenic  for  long  periods,  as  in  chorea,  in  leukaemia,  and  Hodgkin's  disease. 

Symptoms. — Chronic  arsenical  poisoning  manifests  itself  chiefly  in  the 
form  of  a  widespread  peripheral  neuritis,  with  the  development  of  a  secondary 
degeneration  of  the  epithelium  of  the  kidneys.  The  chief  symptoms  are 
tingling  and  pains  in  the  limbs,  followed,  after  a  time,  by  paralysis  which 
affects  the  distal  portions  of  the  body  much  more  than  it  does  the  nerves  and 
muscles  of  the  thighs  or  arms.  Atrophy  of  the  muscles  supplied  by  the 
paralyzed  nerves  soon  takes  place.  Other  trophic  changes  also  develop, 
such  as  herpetic  eruptions  resembling  those  of  herpes  zoster  or  pemphigus, 
and  glossiness  of  the  skin  sometimes  supervenes.  At  times  curious  deposits 
of  pigment  take  place  in  the  skin.  As  in  lead  poisoning,  the  nerve  supply  to 
the  extensor  muscles  suffers  chiefly,  but  in  addition  the  small  flexor  muscles 
are  also  affected  much  more  commonly  than  they  are  in  neuritis  due  to  alco- 
hol or  lead.  The  lower  limbs  are  affected  as  much  as  the  upper  limbs, 
whereas  in  lead  poisoning  it  is  the  upper  extremities  which  suffer  most. 
Again,  arsenical  neuritis  affects  the  sensory  and  motor  fibres,  and  for  this 
reason  pain  as  well  as  anaesthesia  is  often  met  with.  The  pulse  is  quickened 
and  the  mind  confused  in  some  cases.  Because  of  the  involvement  of  the 
sensory  and  motor  fibres  of  the  peripheral  nerves  the  patient  may  present 
symptoms  of  tabes  dorsalis  (arsenical  pseudotabes).  The  Argyll-Robertson 
pupil  is  a  useful  differential  factor,  for  if  it  is  present  the  cause  of  the 
disordered  gait  is  probably  due  to  true  locomotor  ataxia. 

Prognosis. — ^The  prognosis  in  such  cases  depends  upon  the  severity  of 
paralysis  and  the  state  of  the  kidneys.  If  the  latter  organs  are  affected  the 
outlook  is  more  grave  than  if  they  are  intact.  Even  when  the  symptoms  of 
neuritis  are  severe,  remarkable  recovery  may  ensue  if  the  patient  is  removed 
from  the  exposure  to  the  drug. 

Treatment. — ^The  treatment  consists  in  the  removal  from  exposure,  the 
use  of  the  iodide  of  potassium  to  aid  in  the  elimination  of  the  poison,  the 
administration  of  strychnine  in  full  doses  if  the  nerves  are  not  irritable,  and 
in  the  application  of  massage  and  electricity  to  improve  the  nutrition  of 
the  affected  parts.    Iron  may  be  used  to  combat  the  anaemia. 


LEAD  POISONING  OR  PLUMBISM. 

Acute  lead  poisoning  is  not  of  frequent  occurrence.  Its  consideration  is 
distinctly  toxicological  in  character,  and  for  this  reason  it  is  not  discussed 
in  these  pages. 

Chronic  lead  poisoning,  on  the  other  hand,  is  of  exceedingly  common 
occurrence,  not  only  in  those  who  are  exposed  to  the  poison  by  reason  of 
their  occupation,  but  in  persons  who  have  suffered  no  such  exposure  but 
have  absorbed  the  lead  from  sources  in  which  its  presence  would  not  be 


852  INTOXICATIONS 

suspected.  Further  than  this,  lead  poisoning  in  its  chronic  form  may  pro- 
duce the  most  varied  symptoms,  which  are  oftentimes  so  unusual  that  no 
thought  of  lead  as  a  cause  is  entertained.  In  speaking  of  the  nervous  mani- 
festations which  are  often  present,  a  well-known  teacher  was  wont  to  say: 
"When  you  cannot  explain  a  curious  train  of  nervous  symptoms,  always 
suspect  syphilis,  hysteria,  or  lead  as  the  cause." 

Etiology. — It  is  the  insoluble  rather  than  the  soluble  salts  of  lead  which 
usually  cause  chronic  lead  poisoning.  The  most  frequent  sufferers  are 
workers  in  manufactories  where  paint  is  made,  and  house  painters  who 
are  continually  engaged  in  the  handling  of  lead  paint.  In  rarer  instances 
the  patient  is  poisoned  by  the  use  of  water  which  in  passing  through  new 
lead  pipes  dissolves  some  of  the  lead;  or  lead  is  present  in  a  hair-dye  or 
cosmetics  and  is  absorbed  by  the  skin;  or,  again,  it  has  occurred  that  a  miller 
has  filled  holes  in  his  grindstones  with  lead,  which  has  then  been  ground 
with  the  flour  and  eaten  in  bread.  In  one  instance,  in  Pennsylvania,  a 
peddler  sold  a  large  number  of  crocks  to  farmers'  wives.  In  these  was 
placed  apple  butter,  and  as  the  acid  in  the  fruit  eroded  the  lead  glazing 
which  lined  the  jars,  a  widespread  epidemic  of  chronic  lead  poisoning  de- 
veloped. Perhaps  the  most  notorious  illustration  of  how  lead  may  cause 
poisoning  in  unsuspecting  persons  is  the  celebrated  "chrome-yellow  cases" 
in  Philadelphia,  in  which  a  wholesale  druggist  sold  chrome  yellow  to  a 
number  of  confectioners,  who  saved  the  cost  of  eggs  by  coloring  their 
cakes  with  this  substance.  As  a  result  a  large  number  of  men,  women,  and 
children  died,  and  a  much  larger  number  suffered  from  chronic  poisoning 
for  months  before  the  source  of  the  trouble  was  discovered.  An  extraor- 
dinary cause,  however,  is  the  habit  of  chewing  silk  thread  weighted  with 
lead.  At  least  two  cases  of  chronic  poisoning  from  this  cause  have  been  met 
with  in  seamstresses. 

The  fact,  therefore,  that  no  history  of  exposure  to  lead  is  to  be  found  in  a 
given  case  does  not  negative  the  diagnosis  of  lead  poisoning. 

Prevention. — Chronic  lead  poisoning  is  to  be  prevented  in  workers  in  lead 
by  the  exercise  of  the  greatest  possible  cleanliness  as  to  their  hands,  which 
should  be  thoroughly  washed  before  food  is  touched,  as  otherwise  lead  may 
be  taken  in  small  amounts  and  finally  cause  poisoning.  If  the  workman 
is  employed  in  grinding  lead,  he  must  wear  a  mask  to  prevent  the  poison 
from  being  inhaled  in  dust.  The  use  of  vessels,  the  glazing  of  which 
contains  lead,  for  holding  food  should  be  avoided.  Small  amounts  of 
dilute  sulphuric  acid  to  form  insoluble  sulphates  in  the  mouth  and  stomach 
may  be  resorted  to,  and  purgation  every  few  days  by  sulphate  of  mag- 
nesium is  advantageous. 

Pathology  and  Morbid  Anatomy. — There  is  no  other  poison  from  the  mineral 
kingdom  which  taken  into  the  body  produces  such  widespread  changes  in 
different  organs  as  does  lead  in  the  chronic  form  of  poisoning.  Even  alcohol, 
that  most  ubiquitous  poison,  does  not  cause  such  a  multitude  of  changes. 
The  nervous  system  is  the  portion  of  the  body  which  bears  the  brunt 
of  the  attack,  and  it  is  the  peripheral  nerves  that  suffer  most.  In  them 
the  lead  produces  a  toxic  neuritis.  In  advanced  cases  there  is  segmentation 
of  the  myelin  and  breaking  up  of  the  axis  cylinder,  with  a  proliferation  of 


LEAD  POISONING  853 

the  nuclei  in  the  sheath  of  Schwann.  The  early  changes  in  the  nerves 
affect  chiefly  the  medullary  sheath,  which  is  affected  in  patches  at  irregular 
intervals — the  so-called  periaxial  neuritis  of  Gombault.  Although  the 
lesions  are  more  severe  as  the  distal  end  of  the  nerves  is  approached, 
D^jerine  has  found  them  even  in  the  anterior  roots.  Conspicuous  changes 
in  the  spinal  cord  are  almost  never  seen,  but  Oppenheim  states  that  he  has 
found  alterations  in  the  anterior  cornua,  and  Gowers  asserts  that  in  some 
cases  the  cells  in  these  cornua  are  degenerated.  No  constant  lesions  are 
found  in  the  brain,  even  in  those  cases  in  which  severe  cerebral  symptoms 
are  present,  except  those  dependent  upon  vascular  lesions  which  are  part 
of  the  general  vascular  disease  produced  by  the  poison. 

It  is  to  be  especially  noted  that  the  sensory  fibres  of  the  nerves  are  not 
affected,  and  that  the  musculospiral  is  the  nerve  chiefly  involved  in  those 
cases  which  have  peripheral  neuritis.  As  a  result  of  the  neuritis,  produced 
by  the  lead,  atrophy  of  a  severe  character  may  develop  in  the  muscles 
supplied  by  the  affected  nerves.  Fatty  degeneration  of  the  muscles  does 
not  ensue.  The  second  portion  of  the  body  to  feel  the  effect  of  the  lead  is 
the  kidneys,  which  are  not  rarely  the  seat  of  chronic  interstitial  nephritis, 
and  with  this  renal  lesion  a  process  of  arteriofibrosis  develops,  which  asso- 
ciated conditions  often  cause  the  death  of  the  patient. 

Sailer  has  recently  shown  that,  in  some  cases  at  least,  there  is  an  absence 
of  hydrochloric  acid  in  the  gastric  juice. 

Symptoms. — From  what  has  been  said  of  the  changes  in  various  organs 
caused  by  lead,  it  is  evident  that  the  symptoms  may  be  very  varied.  Paraly- 
sis of  the  extensor  muscles  of  the  forearm,  causing  wrist-drop,  is  the  most  con- 
stant symptom.  This  paralysis  is  nearly  always  bilateral,  but  occasionally 
but  one  arm  is  affected.  The  supinator  longus  muscle  and  the  short  extensor 
of  the  thumb,  however,  usually  escape,  which  is  curious  in  view  of  the  fact 
that  the  supinator  longus  muscle  receives  its  nerve  supply  from  the  musculo- 
spiral nerve.  In  atypical  cases  Oppenheim  states  that  the  supinator  longus, 
the  biceps,  and  even  the  deltoid  are  involved. 

In  the  legs  palsy  is  far  less  frequent  than  in  the  forearms,  and  the  muscles 
involved  are  the  peroneal  group,  but  the  tibialis  anticus  is  not  affected. 

Although  motor  paralysis  is  present  sensory  disturbances  are  rare. 

Palsy  of  the  ocular  muscles  producing  squint  may  be  due  to  lead,  as  may 
also  optic  neuritis.  In  very  rare  cases  of  severe  plumbism  cerebral  symp- 
toms develop,  consisting  in  epileptiform  convulsions,  or  coma.  This  state 
is  called  "  encephalopathia  saturnina." 

Tremor  of  the  forearms  is  sometimes  present  in  lead  poisoning. 

Chronic  lead  poisoning  greatly  aids  in  producing  gouty  lesions,  probably 
by  forming  a  urate  of  lead  in  the  tissues  about  the  joints.  Others  believe 
that  the  lead  decreases  the  alkalinity  of  the  blood  and  so  permits  the  pre- 
cipitation of  urates  to  occur. 

There  still  remain  to  be  considered  several  symptoms  of  chronic  lead 
poisoning  which  are  so  constant  in  their  appearance  and  so  characteristic 
that  they  are  most  valuable  aids  in  diagnosis.  The  first  of  these  is  the  blue 
line  in  the  edges  of  the  gums  next  the  teeth,  formed  by  the  deposit  of  sul- 
phide of  lead  in  the  capillaries  of  the  part.    This  sign  is  often  absent  in  those 


354  INTOXICATIONS 

who  are  cleanly  in  the  care  of  the  mouth.  The  second  is  the  characteristic 
pain  in  the  belly,  which  is  exceedingly  severe  in  the  region  of  the  umbiHcus, 
and  is  described  as  a  pain  due  to  twisting  the  bowels  around  a  stick.  This 
is  called  "painters'  colic,"  or  "cohca  pictonum."  The  latter  term  is  given 
to  this  state  because  it  was  frequently  met  with  in  Picton  at  one  time.  A 
third  symptom  of  chronic  lead  poisoning  is  anosmia,  which  is  in  part  due  to 
the  direct  effect  of  the  lead  and  in  part  to  the  renal  changes  induced  by 
this  agent.  Microscopic  examination  of  the  blood  will  often  reveal  a  granu- 
lar degeneration  of  the  erythrocytes. 

Diagnosis. — In  a  case  in  which  the  blue  line  on  the  gum  is  present  the 
diao-nosis  is  easy.  ^Vhen  wrist-drop  is  present  it  must  be  separated  from 
that  due  to  pressure,  as  by  resting  the  head  on  the  arm  when  sleeping  or 
by  the  pressure  of  a  crutch.  As  a  rule,  pressure  palsy  is  unilateral  and  lead 
palsy  bilateral,  but  this  is  not  so  invariably,  and  the  history  of  the  patient 
may  be  necessary  to  decide  the  diagnosis.  When  the  palsy  is  distributed 
in  various  parts,  particularly  if  it  affects  the  legs,  it  must  be  separated  from 
acute  poHomyehtis  Lead  poisoning  is  rare  in  children  and  acute  polio- 
myelitis is  common.  In  adults  chronic  lead  poisoning  is  more  frequent  than 
is  acute  poUomyelitis,  PoHomyelitis  in  its  acute  form  has  a  history  of  sudden 
onset  with  fever,  and  the  onset  of  lead  palsy  is  rarely  so  abrupt  and  is  usually 
not  febrile.  The  history  of  exposure  to  lead  will  aid  in  deciding  the  diag- 
nosis. In  chronic  pohomyelitis  the  only  way  to  determine  the  question  is 
by  the  history  and  the  frequent  examination  of  the  patient's  urine  for  lead. 
Often  lead  will  not  be  found  in  the  urine  unless  iodide  of  potassium  is  given 
to  set  it  free  from  the  tissues  where  it  has  been  deposited. 

Saturnine  epilepsy  must  be  separated  from  true  epilepsy  by  the  history 
of  the  patient  and  by  the  association  of  other  signs  of  plumbism.  It  must 
also  be  separated  from  ursemic  convulsions,  if  possible,  by  the  urinary 
examinations,  but  this  may  be  impossible  because  the  lead  may  at  once 
cause  encephalopathia  saturnina  and  uraemia  through  its  effects  on  the 
cerebral  vessels  and  the  kidneys. 

Prognosis. — The  prognosis  as  to  the  duration  of  life  in  chronic  lead  poison- 
ing is  good  unless  cerebral  symptoms  are  present,  or  renal  changes  are  well 
marked.  The  prognosis  as  to  the  paralysis  depends  largely  upon  the  general 
nutrition  of  the  patient  and  the  stage  to  which  the  neuritis  has  advanced. 
If  the  muscles  involved  have  lost  all  reaction  to  electrical  stimulation,  the 
prognosis  must  be  bad  as  compared  with  that  in  a  case  in  which  the  palsy 
has  lasted  for  but  a  short  time.  Even  when  the  reactions  of  degeneration  are 
present  the  outlook  is  not  hopeless,  because  if  the  patient  is  no  longer  exposed 
to  the  poison  recovery  sometimes  ensues,  particularly  in  young  persons. 

Treatment. — The  treatment  of  chronic  lead  poisoning  consists  in  remov- 
ing the  patient  from  continued  exposure  to  the  poison.  If  he  is  an  artisan 
he  must  cease  working  in  lead.  If  he  has  been  poisoned  by  the  metal  tlirough 
some  accident,  the  source  must  be  discovered  and  he  must  no  longer  be 
exposed  to  it. 

The  second  duty  of  the  physician  is  to  eliminate  the  lead  already  in 
the  body  as  rapidly  as  possiple.  For  this  purpose  the  iodide  of  potas- 
sium should  be  given  in  full  doses,  with  the  object  of  forming  double 


FOOD  POISONING  855 

soluble  iodides  with  the  lead.  Not  only  have  we  every  reason  to  believe, 
from  a  chemical  standpoint,  that  this  medicinal  treatment  is  advantageous, 
but  it  is  a  well-known  clinical  fact  that  chemical  examination  of  the  urine 
in  a  case  of  lead  poisoning  will  fail  repeatedly  to  show  lead,  and  will  at  once 
indicate  its  presence  after  iodide  of  potassium  is  administered,  proving  that 
by  this  means  lead  is  carried  to  the  kidneys  and  speedily  passed  out  of  the 
body.  It  must  also  be  remembered  that  the  liver  eliminates  lead  freely  in 
the  bile. 

The  third  indication  is  to  improve  the  patient's  general  health  not 
only  by  the  use  of  such  tonics  as  iron  and  strychnine,  but  also  by  ordering 
an  out-door  existence,  with  as  much  sunshine  as  it  is  possible  for  the  patient 
to  find  in  the  twenty-four  hours. 

The  paralysis  of  chronic  lead  poisoning  is  to  be  treated  by  the  adminis- 
tration of  full  doses  of  strychnine  and  the  simultaneous  use  of  large  doses 
of  iodide  of  potassium.  The  paralysis  of  the  extensor  muscles  of  the  arms 
and  legs  is  to  be  treated  not  only  by  the  use  of  strychnine,  but  by  the  employ- 
ment of  the  slowly  and  rapidly  interrupted  faradic  current.  In  those  cases 
in  which  cerebral  symptoms  develop,  the  patient  should  receive  full  doses 
of  iodide  of  potassium,  with  the  object  of  getting  rid  of  the  lead  as  rapidly 
as  possible.  If  the  symptoms  are  acute,  and  if  a  convulsion  is  already  present, 
the  patient  should  receive  a  hot  pack  in  order  that  the  sedative  effect  of  this 
therapeutic  measure  may  be  exercised  upon  the  nervous  system,  in  order 
that  the  blood  may  be  drawn  away  from  the  congested  brain,  and  with  the 
hope  that  by  increasing  the  action  of  the  skin  the  convulsions  may  be  re- 
lieved of  some  of  the  work  which  they  would  otherwise  be  forced  to  perform. 
In  other  respects  the  convulsions  should  be  treated,  as  are  all  other  con- 
vulsions, by  the  use  of  nitrite  of  amyl  inhalations,  and  by  the  employment  of 
full  doses  of  chloral  and  the  bromides  to  quiet  the  brain  and  spinal  cord. 

Painters'  colic  with  its  attendant  constipation  is  not  to  be  treated  by  the 
use  of  purgatives,  but  by  the  use  of  morphine  given  hypodermically.  This 
drug,  which  so  often  causes  constipation  in  the  ordinary  patient,  often  pro- 
duces active  purgation  in  these  cases,  by  quieting  the  intestinal  irritation 
and  spasm  and  simultaneously  relieving  the  pain. 


FOOD  POISONING. 

Bromatotoxismus. — Symptoms  of  poisoning  produced  by  the  ingestion  of 
food  which  is  impure  by  reason  of  faulty  preparation,  or  the  changes  due  to 
decomposition,  are  occasionally  met  with.  It  is  rather  remarkable,  consider- 
ing the  long  period  of  time  during  which  many  foods  are  kept  after  they  are 
prepared  for  the  table,  that  more  cases  of  poisoning  do  not  ensue.  Much  of 
the  information  given  in  this  article  is  obtained  from  the  excellent  summary 
of  this  subject  which  can  be  found  in  Vaughan  and  Novy's  Cellular  Toxins. 

Poisoning  may  be  produced  by  the  use  of  grains  which  have  become  infected 
by  poisonous  fungi.  Animals  may  eat  substances  which  may  render  their 
milk  or  flesh  or  both  poisonous.  The  flesh  of  certain  animals"  also  becomes 
poisonous  at  certain  stages  of  their  life  history.     Foods  may  also  become 


856  INTOXICATIONS 

infected  by  the  discharges  of  human  beings;  the  flesh  of  animals  may  suffer 
from  some  specific  disease  which  may  be  transmitted  to  man,  and  milk  may 
carry  the  disease  of  an  animal  to  man  or  may  be  infected  by  the  discharges 
of  man,  and  so  convey  specific  germs  to  other  individuals.  Food  may  also 
contain  micro-organisms  which  in  their  process  of  development  produce 
poisonous  symptoms  in  man. 

The  term  sitotoxismus  is  applied  to  poisoning  by  vegetable  foods  which 
are  infected  by  moulds  or  bacteria. 

The  most  familiar  form  of  poisoning  by  grains,  or  vegetable  food,  is 
Ergotism  due  to  the  eating  of  rye  flour  made  from  rye  which  has  been  infected 
by  the  fungus  Claviceps  purpurea.  This  ergot  is,  of  course,  largely  employed 
in  medicine.  Several  poisons  are  found  in  ergot,  such  as  ergotinic  acid, 
sphacelinic  acid,  and  cornutin.  The  first  of  these,  however,  seems  to  be 
poisonous  only  when  it  is  injected  hypodermically.  Sphacelinic  acid,  on  the 
other  hand,  is  supposed  to  be  responsible  for  the  gangrene  and  cachexia 
which  sometimes  develop  in  persons  who  have  eaten  infected  rye.  On  the 
other  hand,  cornutin  seems  to  be  the  poison  which  affects  the  nervous  system 
and  produces  spasms  and  convulsions. 

Mytilotoxismus. — Under  the  name  of  mytilotoxismus  is  described  the 
symptoms  of  poisoning  which  are  produced  by  eating  poisonous  mussels. 
These  symptoms  consist  in  some  cases  in  violent  gastrointestinal  irritation 
with  purging,  but  in  the  majority  of  instances  the  manifestations  of  the 
poisoning  are  nervous  in  character.  A  rash  resembling  urticaria  and  finally 
becoming  vesicular  may  develop  over  the  body,  and  the  eyelids  may  be  so 
swollen  as  to  prevent  vision  by  extravasation  of  the  serum  into  their  tissues. 
There  is  often  difficulty  in  breathing,  apparently  due  to  intense  hypereemia 
of  the  bronchial  mucous  membrane.  Convulsions  and  coma  may  develop 
and  death  may  be  due  to  this  cause. 

Treatment. — The  treatment  of  mytilotoxismus  consists  in  the  use  of  an 
active  saline  cathartic  to  sweep  the  poisonous  material  from  the  alimentary 
canal,  and  in  the  use  of  ether  as  a  diffusible  stimulant. 

Ichthyotoxismus. — When  fish  produces  poisonous  symptoms  the  term 
ichthyotoxismus  is  used  to  describe  the  condition.  As  is  well  known,  cer- 
tain fish  are  unfit  to  eat,  and  other  fish  become  poisonous  during  the  season 
at  which  they  are  spawning.  In  still  other  instances  fish  suffer  from  bacte- 
rial infections  which  render  their  flesh  unsuitable  as  food.  The  ingestion 
of  poisonous  fish  so  seldom  occurs,  at  least  in  this  country,  that  the  symp- 
toms produced  need  not  be  described. 

Poisoning  from  the  flesh  of  fish  which  has  undergone  decomposition  is 
often  very  violent  in  its  manifestations.  The  most  common  symptoms  are 
dilatation  of  the  pupils,  nausea,  vomiting,  and  severe  abdominal  pain,  fol- 
lowed by  the  development  of  a  scarlatinal  rash  all  over  the  body.  In  such 
cases  a  purge  to  sweep  out  the  offending  materials  and  also  stimulants  are 
needed. 

Elreotoxismus. — The  word  kreotoxismus  is  applied  to  poisoning  result- 
ing from  the  ingestion  of  meat  unfit  for  food,  because  of  the  presence  of 
bacterial  or  animal  poisons.  Perhaps  the  most  frequent  instance  of  this 
is  in  so-called  sausage  poisoning.     Sausages   are   often  made  from  what 


PELLAGRA  857 

may  be  called  the  refuse  following  the  butchering  of  animals  ordinarily 
employed  as  food,  and  the  treatment  of  this  material  is  such  that  early 
decomposition  changes  may  readily  set  in.  In  most  instances  the  process 
of  cooking  destroys  the  poisons,  but  when  cooking  is  not  resorted  to  the 
symptoms  which  are  induced  are  exceedingly  severe,  and  death  may  ensue. 
There  is,  in  many  cases  of  sausage  poisoning,  difficulty  in  breathing  and 
swallowing,  violent  vomiting,  severe  abdominal  pain,  hoarseness,  dimness^ 
of  vision,  and  delirium.  In  other  cases  the  mind  remains  clear.  From  some ' 
of  these  forms  of  food  ptomaines  have  been  isolated.  In  other  instances 
certain  bacteria  have  been  found  which  have  been  considered  responsible, 
either  directly  or  indirectly,  for  the  symptoms.  Meat-pie  poisoning  and 
poisoning  by  mince-meat  are  essentially  similar  to  sausage  poisoning. 

Tyrotoxismus  and  Galactotoxismus. — Under  the  name  galactotoxismus 
is  described  the  poisoning  which  results  from  the  ingestion  of  impure  milk. 
When  poisoning  follows  the  use  of  bad  cheese  it  is  called  tyrotoxismus.  This 
term  is  also  applied  to  the  poisoning  produced  by  impure  ice-cream.  The 
symptoms  are  sometimes  exceedingly  severe,  and  consist  in  evidences  of 
gastroenteritis  followed  by  collapse.  To  a  substance  which  Vaughan 
states  he  is  able  to  isolate  from  cheese  and  ice-cream  he  gave  the  name 
of  "  tyrotoxicon." 

PELLAGRA  (MAIDISMUS). 

Definition. — Pellagra  is  a  chronic  intoxication  due  to  eating  fermented 
maize.  It  is  characterized  by  gastric  and  intestinal  symptoms,  by  marked 
motor,  sensory,  and  psychical  disturbances,  and  by  a  constant  skin  eruption. 

History. — Pellagra  has  been  known  for  about  two  hundred  years.  From 
that  time  until  now  it  has  been  seen  in  various  countries  of  Europe,  particu- 
larly in  Spain,  Portugal,  and  Central  Italy.  In  the  Province  of  Venice  343 
cases  occurred  in  the  year  1901,  and  in  the  marshes  of  Umbria  and  Tuscany 
the  cases  are  very  numerous.  In  1881  the  number  of  cases  in  Italy  was 
officially  estimated  at  104,607,  or  0.36  per  cent,  of  the  entire  population. 
The  disease  occurs  in  Hungary,  in  certain  departments  of  Southern  France, 
in  Egypt  and  in  Algiers.  On  this  continent  it  is  found  in  Mexico  (Yucatan 
and  Campeachy). 

Etiology. — Pellagra  is  primarily  due  to  eating  unsound  maize  or  its  products. 
Thus,  whiskey  prepared  from  such  maize  may  give  rise  to  pellagra  just  as 
corn-mush,  corn-pap  (polenta),  or  corn-bread  may  convey  it.  The  cause 
of  the  fermentation  of  the  maize  is  harvesting  in  unfavorable  years,  before 
the  grain  has  thoroughly  ripened,  and  storing  in  damp  cellars  or  granaries. 
With  respect  to  the  specific  changes  in  the  grain,  there  is  some  conflict  of 
opinion  as  to  their  exact  nature.  Lombroso  isolated  a  watery  extract,  an 
alcoholic  extract,  and  an  oil  with  which  he  could  produce  the  symptoms  of 
pellagra  in  man  and  animals.  Ceni  and  Besta  have  recently  extracted,  with 
ether,  from  the  spores  of  Aspergillus  fumigatus  and  Aspergillus  flavescens 
a  body  which  produced  all  the  symptoms  of  pellagra.  They  have  further 
shown  that  these  organisms  are  constantly  present  in  smutted  maize. 

Both  sexes  are  equally  attacked.     All  ages  are  subject  to  the  disease 


858  INTOXICATIONS 

although  the  majority  of  cases  occur  in  later  adult  life.  Bad  food,  priva- 
tion, and  malaria  predispose  to  the  development  of  pellagra.  Alcoholism 
is  a  very  prominent  factor  in  the  etiology  of  the  disease.  Some  writers, 
indeed,  consider  it  to  be  the  principal  cause. 

Pathology. — The  post-mortem  changes  observed  in  pellagra  are  extreme 
emaciation,  with  loss  of  the  subcutaneous  fat  and  extensive  wasting  of  the 
muscles.  The  heart,  liver,  spleen,  and  kidneys  are  atrophied.  Marked 
pigmentation  is  seen  in  the  liver,  spleen,  heart,  and  spinal  ganglia.  In  the 
central  nervous  system  various  changes  are  met  with,  principally  chronic 
inflammation  of  the  meninges  with  exudation,  and  occasionally  hemorrhages. 
The  spinal  cord  shows  marked  sclerosis  of  the  posterior  and  posterolateral 
columns.    The  peripheral  nerves  are  degenerated. 

Symptoms. — In  pellagra  there  is  first  of  all  an  ill-defined  prodromal  stage. 
The  patient  feels  out-of-sorts  and  shows  marked  disinclination  to  work.  He 
has  dyspeptic  symptoms  and  complains  of  constant  pain  in  the  head  and 
spine.  At  this  early  stage  insomnia  is  common  and  there  may  even  be  some 
degree  of  mental  disturbance.  These  symptoms  continue  tliroughout  the 
winter,  until,  with  the  advent  of  spring,  the  first  marked  symptoms  of  pellagra 
present  themselves  in  an  erythematous  rash  and  marked  gastrointestinal  dis- 
turbances. The  rash  appears  on  the  exposed  surfaces  of  the  body,  particu- 
larly on  the  backs  of  the  hands,  the  extensor  surfaces  of  the  forearms,  and 
on  the  face  and  neck.  It  persists  several  weeks,  when  desquamation  occurs, 
leaving  a  thickened  patch  of  scurfy  skin.  The  gastrointestinal  symptoms 
consist  in  severe  dyspepsia;  there  are  flatulence,  eructations,  and  anorexia. 
Diarrhoea  is  commonly  present,  sometimes  approaching  dysentery  in  severity. 
These  symptoms  persist  throughout  the  spring.  With  the  advent  of  summer 
the  patient  becomes  very  much  better  and  continues  in  a  fair  state  of  health 
until,  with  the  next  succeeding  spring,  a  recrudescence  takes  place.  Thus, 
from  year  to  year  a  cachectic  state  is  developed,  with  marked  nervous  phe- 
nomena. 

The  motor  symptoms  are  spastic  paralysis  of  the  legs,  wasting,  and  con- 
tracture. The  superficial  reflexes  are  normal,  the  deep  reflexes  increase.  The 
sensory  symptoms  are  severe  pain  in  the  head  and  spine,  with  intolerable 
burning  and  itching,  referred  to  various  skin  areas.  Girdle  pains  are  com- 
mon. Disorders  of  vision  and  taste  occur.  Psychical  symptoms  are  extremely 
common,  and  a  large  percentage  of  cases  end  in  permanent  insanity.  In  all 
Italy,  out  of  every  100  insane  patients,  10  are  sufferers  from  pellagra.  In 
Venice  the  proportion  is  35  out  of  every  100.  The  common  type  of 
insanity  is  melancholia,  with  delusions  of  persecution  and  impulses  to 
self-destruction,  particularly  by  drowning.  Mania  occurs  in  a  small  pro- 
portion of  cases  and  dementia  is  a  common  ending  of  all  of  them. 

In  long-standing  cases  pronounced  cachexia  develops,  with  profound 
anoemia  and  marked  emaciation.  Alpago-Novello  calls  attention  to  the 
evidences  of  premature  senility  in  these  patients.  They  become  prema- 
turely bald,  prematurely  gray,  a  marked  arcus  senilis  may  be  present,  and 
early  atheroma  is  frequently  observed.  The  disease  is  very  chronic  and  may 
last  from  ten  to  fifteen  years.  Cases  that  have  had  more  than  three  or  four  . 
attacks,  in  succeeding  springs,  are  regarded  as  hopeless. 


LATHYRISM  859 

Treatment. — Treatment  consists,  first  of  all,  in  the  interdiction  of  unsound 
maize  as  an  article  of  food,  and  the  prohibition  of  alcohol  as  a  beverage. 
With  respect  to  medicinal  treatment,  Lombroso  recommends  large  doses 
of  arsenic.  Wurzel  confirms  the  value  of  arsenic  and  also  advises  the  use 
of  quinine  and  strychnine  in  large  doses.  For  the  nervous  symptoms  massage, 
electricity,  and  salt-water  baths  are  of  service.  The  patches  of  erythema 
should  be  kept  moist  and  supple  with  oily  ointments  to  which  cocaine, 
carbohc  acid,  salicylic  acid,  or  chloral  may  be  added  to  control  the  itching. 

The  frojjhylaxis  of  the  disease  includes  education  of  the  people  in  the 
infected  area  of  the  danger  of  fermented  maize  as  an  article  of  food.  Maize 
should  only  be  harvested  when  ripe  and  should  only  be  stored  in  dry,  well- 
ventilated  granaries.  When  maize  is  a  staple  article  of  import  it  should  be 
rigorously  inspected  at  the  first  port  of  entry  and  all  spoiled  grain  rejected. 


LATHYRISM   (CHICKPEA   DISEASE;  LUPINOSIS). 

Definition. — Lathyrism  is  a  chronic  intoxication  characterized  by  spastic 
paralysis  of  the  lower  limbs  without  disturbance  of  sensation.  It  is  caused 
by  the  use  of  various  species  of  lathyrus  as  food.  That  the  vetches,  or  chick- 
peas, were  capable  of  producing  a  disease  of  this  type  was  known  in  the  time 
of  Hippocrates. 

History. — The  disease  was  exceedingly  common  in  Italy  and  France  dur- 
ing the  seventeenth  and  eighteenth  centuries.  It  was  first  accurately  studied 
by  Irvin  in  1859.  The  present  geographical  distribution  is  France,  Italy, 
Algiers,  and  British  India. 

Etiology. — Lath}Tism  is  due  to  the  use  of  different  varieties  of  lathyrus 
as  foods;  chiefly  Lathyrus  sativus,  Lathyrus  cicer a,  and  Lathyrus  clyTnenuvi 
(the  common  vetch,  or  chickpea) .  In  time  of  famine  and  want  the  seeds  of 
these  legumes  are  ground  and  mixed  with  flour  and  other  meal  and  used  in 
bread-making.  Observation  has  shown  that  they  must  be  eaten  for  some 
length  of  time,  several  weeks  or  a  month,  before  symptoms  begin.  The 
poison  lies  in  the  peas  themselves,  and  mustiness  or  fermentation  is  not  a 
factor  as  in  pellagra.  It  is  stated  that  "Teora"  {Lathyrus  sativus)  in  India 
only  causes  the  disease  when  baked;  when  boiled  it  is  said  to  be  innocuous. 
As  immediate  exciting  causes  for  the  outbreak  of  the  disease,  exposure  to 
cold,  rain,  and  damp  weather  are  recognized.  Consequently  men,  being 
much  more  exposed  to  climatic  changes  in  their  daily  avocations,  are  more 
frequently  attacked  than  women.  Cattle  eating  the  peas  also  develop  the 
disease. 

Symptoms. — ^There  may  be  prodromal  symptoms,  such  as  jever,  dyspepsia, 
and  diarrhoea.  Usually  the  disease  begins  suddenly,  after  exposure  or  a 
wetting.  There  is  pain  in  the  loins,  legs,  and  knees,  with  weakness  and 
tremors.  From  this  point  on  there  is  a  gradual  and  continuous  development 
of  a  spastic  paralysis  of  both  legs  with  marked  spasms,  particuarly  of  the 
adductor  muscles  of  the  thighs.  The  reflexes  are  exaggerated.  Sensation 
is  not  impaired.  The  bladder  and  rectum  are  not  involved,  as  a  rule,  except- 
ing in  severe  cases,  when  the  paralysis  may  include  the  sphincters.     The 


860  INTOXICATIONS 

upper  limbs  are  not  involved.  The  course  of  the  disease  is  exceedingly 
chronic  and  the  paralysis  is  usually  permanent. 

Death  from  lathyrism  itself  is  very  rare.  In  one  patient  who  died  of  an 
intercurrent  malarial  infection  Grandjean  found  a  softened  area  in  the  cord 
extending  6  cm.  above  the  lumbar  enlargement.  The  clinical  symptoms 
point  to  a  degeneration  of  the  lateral  columns. 

Treatment. — Treatment  consists  in  the  withdrawal  of  lathyrus  from  the 
patient's  food,  and  the  education  of  the  masses  to  the  danger  that  lies  in  the 
use  of  these  products.  Scheube  reports  good  results  from  sharp  counter- 
irritation  over  the  lumbar  vertebra. 


ATRIPLICISM. 

Atriplicism  ("intoxication  par  I'arroche")  is  an  intoxication  due  to  eating 
the  coast  orach,  and  is  characterized  by  marked  local  disturbances  of  sensi- 
bility, by  local  oedema  and  trophic  disorders.  This  disease  was  first 
reported  by  Matignon  in  1898,  from  North  China.  He  ascribes  it  to  eating 
Atriplex  augustissima  and  Atriplex  serrata  of  the  order  ChenopodiacecB,  both 
common  weeds  in  China.  They  are  eaten  baked  or  fried  in  dough,  or  raw 
as  a  salad. 

Within  ten  to  twenty  hours  after  eating  the  orach  there  is  tingling  and 
cold  in  the  thumbs,  fingers,  and  hack  of  the  hand,  followed  by  itching  and 
oedema,  which  spreads  over  the  back  of  the  hand  and  forearm  and  ends 
sharply  at  the  elbow.  Later,  swelling  and  itching  of  the  face  occur.  The 
parts  are  cold,  the  nose  and  finger-tips  cyanotic.  The  oedema  persists  from 
two  to  ten  days.  After  it  subsides  the  skin  is  exfoliated.  In  severe  cases 
large  blebs  may  form  which  subsequently  ulcerate.  Matignon  reports  one 
case  in  which  gangrene  of  the  fingers  occurred.  The  disease  superficially 
resembles  erythromelalgia. 

Treatment. — Treatment  consists  in  free  purgation  at  the  beginning  of  the 
disease  and  the  application  of  sedative  lotions  locally. 


LACQUER  POISONING. 

This  is  a  troublesome  poisoning  of  the  skin  observed  in  China  and  Japan 
among  workers  in  lacquer.  Lacquer  is  derived  from  the  balsamic  exudate 
from  the  lacquer  tree  (Rhus  vernicifera).  The  poisoning  is  limited  to  the 
skin  and  is  entirely  analogous  to  that  produced  by  the  varieties  of  rhus,  so  com- 
mon in  America,  excepting  that  it  is  much  more  severe.  The  infection  takes 
place  not  only  through  contact  with  the  raw  lacquer,  but  Scheube  states  that 
it  may  be  conveyed  from  the  vapors  arising  during  the  evaporation  of 
lacquer,  and  that  susceptible  individuals  may  even  acquire  it  by  visiting 
lacquer  warehouses  where  there  are  newly  lacquered  articles.  The  attack 
begins  a  few  hours  after  exposure,  with  intense  itching  of  the  skin  of  the 
face  and  limbs.  The  skin  becomes  oedematous;  numerous  papules  appear, 
which  later  become  vesicular  and  are  filled  with  a  yellow  seropus.     The 


LACQUER  POISONING  861 

vesicles  may  coalesce  and  form  large  blebs.  The  disease  is  limited  to  the 
arms,  legs,  face,  and  genitals.  When  the  face  is  severely  affected,  the  adjacent 
mucous  membrane  shares  in  the  disturbance,  and  there  may  be  a  sharp 
febrile  reaction. 

Treatment. — Treatment  consists  in  soothing  local  applications.  Lead- 
water  with  or  without  opium  and  lime-water  are  principally  used. 

The  gingko  tree  (Gingko  hiloba)  causes  a  dermatitis  exactly  like  lacquer 
poisoning  excepting  that  it  is  not  so  severe.  The  question  of  gingko 
poisoning  is  of  some  little  interest  in  the  United  States  at  present.  The 
tree  is  a  native  of  China,  but  has  recently  been  introduced  in  America  as 
an  ornamental  foliage  plant. 


DISEASES  DUE  TO  ANIMAL  PAEASITES. 


MALARIAL  INFECTION. 


Definition. — By  malarial  infection  we  refer  to  a  condition  produced  by  the 
entrance  into,  and  development  in,  the  blood  of  specific  micro-organisms 
known  as  the  Plasmodium  malarioB,  the  hsematozoon  of  malarial  fever,  or, 
more  correctly  speaking,  the  Hoemamceba  malarioB. 

The  infection  is  manifested  by  four  different  types:  First,  the  so-called 
intermittent  type,  in  which  the  patient  has  recurring  attacks  which  are 
characterized  by  a  chill,  a  fever,  and  a  sweat.  These  recurrences  com- 
monly take  place  daily,  on  alternate  days,  or  on  every  third  day,  and  are 
called  quotidian,  tertian,  or  quartan.  Second,  a  type  in  which  there  is 
present  continued  fever  with  remissions  in  its  course,  the  so-called  remit- 
tent malarial  fever.  Third,  a  type  in  which  the  infection  is  of  a  mahg- 
nant  or  pernicious  form  with  profound  toxaemia.  Fourth,  that  form  in 
which  more  or  less  subacute,  or  chronic,  and  profound  cachexia  is  present, 
associated  with  marked  anaemia  and  enlargement  of  the  spleen,  and  often 
of  the  liver.  The  first  is  due  to  the  tertian  or  quartan  parasite,  the  second 
and  third  to  the  aestivo-autumnal  parasite,  while  the  fourth  form  may  be  due 
to  any  one  of  the  three  parasites. 

History. — Malarial  fever  was  recognized  as  a  distinct  disease  as  long 
ago  as  five  hundred  years  before  Christ,  and  Hippocrates  divided  it  into  the 
quotidian,  tertian,  and  quartan  types  we  recognize  to-day.  Empedocles 
(500  B.C.)  recognized  the  relationship  of  the  disease  to  stagnant  water  and 
stopped  an  epidemic  by  draining  stagnant  pools;  but  it  was  not  until  1880 
that  Laveran,  a  French  army  surgeon,  first  recognized  the  specific  organism, 
and  in  1886  Marchiafava  and  Celli  described  it  more  fully.  In  the  same 
year  Golgi  showed  that  the  malarial  attack  occurred  simultaneously  with 
the  sporulation  of  the  parasite,  but  not  until  1898  did  Manson  and  Ross, 
of  England,  and  Grassi  and  Bignami,  of  Italy,  prove  that  the  infection  is 
spread  from  man  to  man  by  a  certain  species  of  mosquito  known  as  the 
Anopheles.  In  the  United  States  excellent  work  has  been  done  by  a 
number  of  investigators,  of  whom  the  most  noteworthy  are  Osier,  Thayer, 
and  Hewetson  in  Baltimore,  James  in  New  York,  Craig  of  the  U.  S.  Army, 
and  Dock  in  Texas. 

Distribution. — Malarial  infection  is  more  widely  diffused  throughout 
the  tropical  and  temperate  zones  than  any  other  disease.  It  is,  as  a 
rule,  prevalent  and  severe  in  direct  proportion  to  the  proximity  to  the 
equator  and  is  rare  in  far  northern  latitudes.    Certain  parts  of  the  world, 

(863) 


864  DISEASES  DUE   TO  ANIMAL  PARASITES 

which  at  one  time  suffered  severely  from  the  disease,  are  now  free  from  it. 
Forty  or  fifty  years  ago,  for  example,  the  valleys  of  the  Delaware  and 
Schuylkill  Rivers  near  Philadelphia  suffered  greatly,  whereas  at  present 
cases  of  the  disease  are  rarely  met  with  in  these  localities.  On  the  other 
hand,  it  is  very  prevalent  on  the  shores  of  the  Chesapeake  Bay,  which  is 
not  more  than  one  hundred  miles  away.  At  present  the  disease  appears 
in  its  mild  forms  in  France,  Germany,  and  England,  and  in  the  Middle 
Atlantic  and  Central  United  States,  and  in  its  severe  forms  in  the  Southern 
States,  particularly  in  certain  lower  portions  of  the  Mississippi  Valley.  The 
virulent  forms  are  chiefly  met  with  in  Africa,  in  certain  parts  of  India,  and 
in  the  tropics,  as  in  the  West  Indies  and  in  the  Philippines,  and  in  the 
tropical  parts  of  South  America.  On  the  Pacific  coast  of  the  United  States 
the  disease  is  rare.  So  far  as  season  is  concerned,  it  may  be  said  that  the 
greater  proportion  of  cases  occur  in  July,  August,  September,  October,  and 
November  in  semi-tropical  or  temperate  regions. 

The  frequency  of  malarial  fever  varies  greatly  and  depends  entirely  upon 
the  prevalence  of  the  Anopheles,  the  sources  for  its  infection,  and  the  climate 
which  permits  of  the  growth  of  the  mosquito.  In  the  United  States  the 
greatest  prevalence  of  this  disease  is  in  the  States  bordering  the  Gulf  of 
Mexico  and  that  tier  lying  immediately  north  of  them.  The  death  rate 
from  malaria  in  this  area  is  about  30  per  1000  deaths  from  known  causes. 

Etiology.  The  Mosquito. — There  is  but  one  direct  etiological  factor  in 
the  dissemination  of  malarial  fever  in  man,  namely,  that  form  of  mosquito 
known  as  Anopheles.  Many  species  of  the  genus  Anopheles  have  been 
described,  but  only  three  have  so  far  been  found  to  be  present  as  malaria- 
bearing  hosts  in  the  United  States,  namely,  the  Anopheles  quadrimaculatus, 
which  is  the  most  common,  the  Anopheles  punctipennis,  and  the  Anopheles 
crucians.  In  Europe  the  infection  is  always  borne  by  the  Anopheles 
claviger,  sometimes  called  Anopheles  maculipennis.  Fortunately,  the  ano- 
pheles is  not  universally  distributed,  the  culex  being  the  genus  which  is 
most  commonly  met  with,  at  least  in  the  temperate  zones,  and  this  mos- 
quito seems  to  be  incapable  of  carrying  the  infection.  The  anopheles  can 
be  readily  differentiated  from  the  culex  by  the  fact  that  when  it  rests 
upon  a  plane  surface  its  body  is  held  at  right  angles,  or  at  an  angle  of 
forty-five  degrees,  whereas  the  body  of  the  culex  lies  parallel  to  the  plane. 
Again,  the  wings  of  the  anopheles  show  very  distinct  mottling,  as  its  names 
punctipennis  or  quadrimaculatus  indicate.  Most  of  the  culex  species  lay 
their  eggs  in  rafts  or  bottle-shaped  masses,  which  remain  intact  until  the 
larvae  are  discharged.  The  eggs  of  the  anopheles  are  laid  in  groups  that 
are  readily  broken  up  and  scattered.  Any  stagnant  or  semi-stagnant  accu- 
mulation of  water  is  a  suitable  breeding-ground. 

The  indirect  factors  in  the  causation  of  malarial  infection  are,  therefore, 
stagnant  or  semi-stagnant  water  in  which  this  mosquito  can  breed,  and 
the  presence  of  a  source  from  which  it  can  obtain  the  parasite  so  that  it 
can  transmit  it  to  a  healthy  individual;  for  even  if  the  Anopheles  be 
present,  it  cannot  inoculate  a  human  being  with  malarial  fever  unless 
it  has  first  bitten  a  person  whose  blood  contains  the  hsemamoeba.  No 
more  interesting   experiments  proving  these  facts  can  be  adduced  than 


MALARIAL  INFECTION  865 

those  made  by  Patrick  Manson  on  his  son,  who  had  never  had  malarial 
infection.  Bignami  and  Bastianelli  sent  Manson  in  England  relays  of 
mosquitoes  which  in  Italy  had  been  fed  upon  the  blood  of  patients 
suffering  from  pure  benign  tertian  malaria.  These  mosquitoes  were 
allowed  to  bite  the  younger  Manson,  and  as  a  result  he  developed  the 
same  form  of  malarial  fever  as  that  suffered  by  the  Italian  patients,  and 
the  same  parasite  was  found  in  his  blood. 

The  HtEmamceba  Malaria  in  Man. — The  parasite  itself  passes  through 
two  cycles  of  existence,  namely,  one  which  is  carried  out  in  the  body 
of  man,  and  another  in  the  body  of  the  mosquito.  It  appears  in  three 
distinct  forms,  namely,  as  the  tertian  parasite,  the  quartan  parasite,  and 
the  sestivo-autumnal  parasite.  Each  of  these  live  in  the  red  cells  of  the 
blood  and  to  some  extent  exist  in  the  plasma  as  well. 

Marchiafava,  Celli,  Bignami,  and"  Grassi,  of  Italy,  have  endeavored  to 
show  that  several  species  of  the  sestivo-autumnal  parasite  exist,  but  their 
views  have  not  been  generally  accepted,  and  recently  they  have  admitted 
that  there  are  not  sufficient  grounds  for  advocating  this  proposition. 

In  certain  cases  the  patient  suffers  from  a  mixed  infection  in  which  the 
tertian  and  sestivo-autumnal  parasite  are  both  present  at  the  same  time. 

The  young  tertian  'parasite  is  a  small  colorless  and  hyaline  body  which 
occupies  a  small  space  in  the  corpuscle.  When  in  a  state  of  quiescence  it  is 
round,  but  if  the  specimen  under  the  microscope  is  fresh  and  the  temperature 
suitable  it  manifests  active  amoeboid  movements.  As  the  parasite  grows, 
reddish-brown  granules  develop  in  its  interior.  These  pigment  granules 
move  rapidly,  and  are  often  seen  in  the  amoeboid  projections  of  the  para- 
site, so  that  it  may  appear  that  several  parasites  are  in  one  corpuscle.  As 
the  growth  continues  the  infected  red  cell  becomes  more  and  more  pallid 
and  swells  up  or  expands,  the  amoeboid  movements  of  the  contained  para- 
site diminish  in  activity,  and  the  pigment  granules  arrange  themselves 
about  the  periphery  of  the  parasite.  At  this  time  the  corpuscle  is  nothing 
more  than  a  shell  of  its  former  self.  Later  the  pigment  granules  accu- 
mulate near  the  centre  of  the  body,  and  as  they  do  so  the  process  of  seg- 
mentation begins;  radial  lines  divide  the  parasite  into  twelve  to  twenty 
segments  arranged  around  the  central  mass  of  pigment.  Each  segment 
has  a  nucleus,  and  as  soon  as  the  process  of  segmentation  is  completed 
these  segments  break  out  of  the  corpuscular  shell  and  float  freely  in  the 
blood  plasma,  where  they  speedily  attack  and  enter  fresh  red  cells.  The 
evolution  and  segmentation  require  about  forty-eight  hours,  and  the  chill 
and  other  acute  manifestations  of  illness  in  the  patient  develop  at  the  time 
of  segmentation.  In  some  instances  the  parasite  becomes  unusually  large, 
the  pigment  bodies  become  stationary  without  aggregation  in  the  centre, 
vacuoles  develop  in  it,  and  the  parasite  seems  to  die.     (See  Plate  V.) 

The  tertian  parasite  is  the  one  which  produces  that  form  of  intermittent 
fever  in  which  the  paroxysm  occurs  every  second  day.  If  the  attack  occurs 
daily,  it  is  due  to  a  double  infection,  in  which  one  set  of  parasites  sporulates 
on  one  day  and  the  other  set  on  the  next  day. 

The  following  distinctions  serve  to  separate  the  tertian  from  the  sestivo- 
autumnal  parasite:  The  nuclear  body  and  chromatin  mass  of  the  young 
55 


866  DISEASES  DUE   TO  ANIMAL  PARASITES 

tertian  parasite  are  achromatic  to  methylene  blue,  whereas  the  nucleus  of 
the  sestivo-autumnal  parasite  is  densely  stained  by  this  agent  (Ewing). 
The  tertian  ring  is  coarse  and  granular,  whereas  the  sestivo-autumnal  ring 
is  a  perfect  circle  and  more  delicate.  The  tertian  ring  is  usually  pigmented 
before  the  chromatin  becomes  subdivided,  while  in  the  sestivo-autumnal 
parasite  the  chromatin  is  subdivided  before  pigmentation  appears.  There 
are,  however,  exceptions  to  this  rule.  Lastly,  the  infected  red  blood  cor- 
puscle is  usually  distended  or  swollen  as  soon  as  it  is  attacked  by  the  tertian 
parasite,  whereas  it  is  shrunken  in  appearance  when  the  sestivo-autumnal 
parasite  enters  it. 

The  quartan  parasite — that  is,  the  organism  that  causes  an  attack  every 
third  day — resembles  the  tertian  organism  just  described,  but  differs  from 
it  in  the  following  respects :  In  the  early  stages  it  occurs  as  a  hyaline  body 
which  is  smaller  than  the  tertian  parasite.  It  speedily  develops  a  sharper 
outline,  it  is  more  refractive,  and  the  amoeboid  movements  are  slower.  The 
pigment  granules  are  larger  and  darker,  less  active,  and  lie  near  the  edge  of 
the  parasite.  Again,  it  is  noteworthy  that  the  red  cell  does  not  swell  as  do 
those  containing  the  tertian  parasite,  but  grows  smaller,  darker,  more 
refractive  and  metallic  looking.  The  quartan  parasite  reaches  its  growth 
in  from  sixty-four  to  seventy-two  hours,  and  then  appears  as  occupying 
nearly  the  entire  red  blood  cell,  or  it  seems  to  float  free  in  the  blood  serum. 
As  the  time  for  the  paroxysm  approaches  the  pigment  granules  at  the 
periphery  flow  toward  the  centre  in  radial  lines,  so  that  it  becomes  arranged 
in  stellate  form  and  the  protoplasm  divides  into  from  six  to  twelve  pear- 
shaped  segments,  each  of  which  has  a  refractive  centre.  These  segments 
escape  and  infect  new  cells.  Some  of  the  parasites  do  not,  however,  go 
on  to  this  development,  but  fail  to  sporulate  and  become  sexual  bodies 
or  gametocytes. 

The  third  form  of  parasite,  the  cEstivo-autumnal  form,  is  smaller  than 
the  tertian  and  quartan  organism,  and  presents  a  ringed  appearance.  It 
contains  much  less  pigment  and,  moreover,  it  soon  causes  the  corpuscle 
into  which  it  enters  to  become  shrivelled  and  brassy  looking.  After  a  time, 
possibly  a  week,  the  parasite  increases  in  size,  becomes  refractive,  crescentic, 
or  round,  or  ovoid  in  form,  and,  in  the  centre,  masses  of  dark  pigment  accu- 
mulate. It  is  these  latter  bodies  which  are  indicative  of  infection  by  the 
sestivo-autumnal  type,  and  it  is  to  be  remembered  that,  as  a  rule,  they 
are  not  constantly  present  in  the  peripheral  circulation  but  only  in  the 
blood  of  such  internal  organs  as  the  liver,  spleen,  and  in  the  bone-marrow. 
Because  of  their  small  size,  slow  development,  and  the  difficulty  of  obtain- 
ing blood  from  deeply  situated  organs,  they  are  less  readily  discovered  than 
the  other  two  types.  It  appears  established  that  the  crescentic  and  ovoid 
bodies  do  not  undergo  segmentation  or  sporulation,  but  correspond  to  the 
sexual  bodies  described  above,  the  gametocytes.  These  crescentic  and  ovoid 
bodies  do  not  continue  their  development  in  the  human  being,  sporulation 
being  the  human  cycle.  The  fertilization  of  the  female  by  the  male  body 
occurs  in  the  extracorporeal  or  intermediate  cycle.     (See  Plate  VI.) 

The  three  forms  of  malarial  parasite  as  they  appear  in  man  have  now 
been  described.     The  mosquito  cycle  of  its  existence  is  as  follows: 


DESCRIPTION  OF  PLATES  Y.  AND  VI.^ 

The  drawings  were  made  with  great  care  and  skill  by  Mr.  Max  Broedel,  Vvuth  the 
assistance  of  the  camera  lucida,  from  specimens  of  fresh  blood.  A  AVinkel  microscope, 
objective,   1-14  (oil-immersion),  ocular,  4,  was  used. 

Figs.  4,  13,  23,  24,  and  42  of  Plate  V.  were  drawn  from  fresh  blood,  without  the 
camera  lucida. 

PLATE  V. 
The  Parasite  of  Tertian  Fever. 

1. — Normal  red  corpuscle. 

2,  3,  4. — Young  hyaline  forms.    In  4  a  corpuscle  contains  three  distinct  parasites. 

5,  21. — Beginning  of  pigmentation.  The  parasite  was  observed  to  form  a  true  ring 
by  the  confluence  of  two  pseudopodia.  During  observation  the  body  burst  from  the  cor- 
puscle, which  became  decolorized  and  disappeared  from  view.  The  parasite  became, 
almost  immediately,  deformed  and  motionless,  as  shown  in  Fig.  21. 

6,  7,  8. — Partlj^  developed  pigmented  forms. 
9. — Full-grown  bod}'. 

10-14. — Segmenting  bodies. 

15. — Degenerative  form  simulating  a  segmenting  body. 

16,   17. — Precocious  segmentation. 

18,  19,  20. — Large  swollen  and  fragmenting  extracellular  bodies. 

22.— Flagellate  body. 

23,   24. — Degenerative  forms  showing  vacuolation. 

The  Parasite  of  Quartan  Fever.' 

25. — Normal  red  corpuscle. 
26. — Young  hyaline  form. 

27-34. — Gradual  development  of  the  intracorpuscular  bodies. 

35. — Full-grown  body.  The  substance  of  the  red  Corpuscle  is  not  visible  in  the 
fresh  specimen. 

36-39. — Segmenting  bodies. 

40. — Large  swollen  extracellular  form. 

41. — Flagellate  body. 

42. — Degenerative  form  showing  vacuolation. 

PLATE  VL 

The   Parasite   op  ^F^stivo-axjtumnal   Fever   (Hccmatozodn  falciparum). 

1,  2. — Small  refractive  ring-like  bodies. 

3-6, — Larger  disk-like  and  amoeboid  forms. 

7. — Ring-like  body  with  a  few  pigment  granules  in  a  brassy,  shrunken  corpuscle. 

8,  9,  10,   12. — Similar  pigmented  bodies. 

11. — Amceboicl  body  with  pigment. 

13. — Body  with  a  central  clump  of  pigment  in  a  corpuscle  showing  a  retraction  of 
the  haemoglobin-containing  substance  about  the  parasite. 

14-20. — Bodies  with  central  pigment  clumps  or  blocks.     Presegmenting  forms. 

21-24. — Larger  bodies  with  central  pigment  blocks.  Presegmenting  bodies.  Seen 
in  the  peripheral  circvilation  during  a  severe  paroxysm. 

25-28. — Segmenting  bodies  from  the  spleen.  Figs.  25-27  represent  one  body  where 
the  entire  process  of  segmentation  was  observed.  The  segments,  eighteen  in  number,  were 
accurately  counted  before  separation,  as  in  Fig.  27.  The  sudden  separation  of  the  seg- 
ments, occurring  as  though  some  retaining  membrane  were  ruptured,  w'as  observed. 

29-37. — Crescents  and  ovoid  bodies.  Figs.  34  and  35  represent  one  body  which  was 
seen  to  extrude  slowly,  and  later  to  withdraw,  two  rounded  protrusions. 

38,  39.— Round  bodies. 

40. — Pseudogemmation,   fragmentation. 

41. — Vacuolation  of  a  crescent. 

42-44. — Flagellation.  The  figures  represent  one  organism.  The  blood  was  taken 
from  the  ear  at  4.15  p.m.;  at  4.17  the  bodv  was  as  represented  in  Fig.  42.  At  4.27  the 
flagella  appeared;  at  4.33  two  of  the  flagella  had  already  broken  awa}^  from  the  mother 
body. 

45-49. — Phagocytosis.     Traced  with  the  camera  lucida. 

^  These  platef,  are'taken  by  permission  fron\  Thayer  and  Hewetson's  classical  report  in  the  ./oAns 
Hopkins  Hospital  Reports,  vol.  v.,  1895.  Four  figures — viz.,  Figs.  21,  22,  23,  and  24 — have  been  added  to 
PlateVI.,and  .ire  also  from  the  drawings  of  Mr.  Max  Broedel. 

^  The  color  of  the  pigment  in  these  figures  of  the  quartan  parasite  has  too  much  of  a  reddish  tint. 


PLATE    V, 
The  Parasite  of  Tt 


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The  Parasite  of  Quartan  Fever 


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PLATE  VI. 
The  Parasite  of  Aestivo-Autumnal  l~ev^:i 


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'■'.1-- 


MALARIAL  INFECTION  867 

The  H^mamceba  Malaria  in  the  Mosquito. — A  mosquito  of  the  genus 
Anopheles,  when  it  sucks  blood  from  an  individual  in  whom  the  parasite  has 
developed  sexual  forms,  receives  into  its  stomach  bodies  ready  for  the  sexual 
process;  in  other  words,  gametocytes.  The  male  bodies,  or  microgameto- 
cytes,  develop  long,  actively  moving  flagella,  called  microgametes,  which 
break  loose  from  the  organism  and  penetrate  and  fertilize  the  larger  female 
bodies  or  macrogametes,  these  bodies  being  simply  macrogametocytes 
which  have  extruded  from  their  nuclear  substances.  The  impregnated 
female  now  penetrates  the  wall  of  the  mosquito's  stomach,  within  which 
further  development  occurs.  Within  forty-eight  hours  there  may 
be  seen  encapsulated  in  the  muscular  wall  of  the  mosquito's 
stomach  small,  round,  refractive,  and  granular  bodies  which  have 
in  them  pigment  granules  much  like  those  present  in  the  parasite 
existing  in  the  red  blood  corpuscles.  At  the  end  of  a  week  the  parasite 
has  grown  considerably,  and  it  is  found  to  be  marked  by  radial  striations 
forming  sporoblasts.  When  this  stage  is  completed  the  mother  body, 
sometimes  called  the  oocyst,  bursts,  and  so  sets  free  in  the  coelomic  cavity 
of  the  mosquito  a  multitude  of  sporozoids.  These  sporozoids  gain  access 
to  the  veneno-salivary  glands  of  the  mosquito,  and  thence  to  the  veneno- 
salivary  ducts,  from  which  they  are  ejected  into  the  human  being  bitten 
by  that  mosquito.  No  sooner  are  the  sporozoids  deposited  in  the  blood  of 
man  than  they  speedily  become  parasites  which  attack  blood  cells.  Blood 
cells  are  therefore  attacked  in  two  ways:  by  parasites  formed  during  the 
asexual  or  human  cycle,  and  by  parasites  produced  in  the  sexual  or 
mosquito  cycle. 

Prevention. — ^The  prevention  of  malarial  fever  consists  in  (a)  protection 
from  the  bites  of  the  anopheles  by  the  use  of  mosquito  bars,  particularly 
at  night;  (b)  in  the  removal  of  all  marshes  by  filling  them  in  or  draining 
them  so  that  the  breeding-place  of  the  mosquito  is  destroyed;  (c)  in  the 
destruction  of  the  larvae  of  the  mosquito  by  diffusing  coal-oil  over  the  surface 
of  pools  or  ponds,  and  (d)  by  not  permitting  a  patient  who  has  the  parasite 
in  his  blood  to  mingle  with  his  fellows  when  the  anopheles  are  present,  for 
from  him  they  derive  their  supply  of  infection.  The  latter  measure  can 
often  only  be  carried  out  in  private  honses  and  barracks.  Such  patients 
should  always  sleep  under  a  mosquito-proof  canopy.  Finally,  it  is  a  well- 
recognized  fact  that  by  the  use  of  small  doses  of  quinine  taken  daily  (5 
grains)  it  is  often  possible  to  prevent  infection. 

Pathology  and  Morbid  Anatomy. — The  changes  produced  in  the  body  by 
the  presence  of  the  malarial  parasite  are  much  less  pronounced  if  the  tertian 
and  quartan  parasite  is  present  than  if  the  sestivo-autumnal  is  the  offend- 
ing body.  Indeed,  in  many  cases  the  morbid  changes  are  so  slight  that 
they  are  speedily  overcome  by  the  natural  processes  of  repair,  and  hence 
rarely  cause  death.  For  this  reason  our  knowledge  of  the  acute  changes 
produced  in  internal  organs  is  very  limited.  These  changes  may,  however, 
for  the  sake  of  study,  be  divided  into  two  forms,  the  acute  and  chronic.  In 
the  acute  type  the  parts  of  the  body  which  suffer  chiefly  are  the  blood,  the 
liver,  the  spleen,  the  kidneys,  and  the  alimentary  canal. 

The  changes  in  the  blood  consist  in  a  distinct  decrease  in  the  number  of 


868  DISEASES  DUE  TO  ANIMAL  PARASITES 

red  cells  which  are  destroyed  primarily  by  the  growth  of  the  parasites,  and 
possibly  secondarily  by  poisons  produced  by  them.  That  some  such  agent 
is  active  seems  to  be  proved  by  the  granular  degeneration  of  the  red  cells 
which  is  present  in  severe  cases,  and  in  the  polychromatophiha  which  is 
met  with  in  cells  into  which  the  parasite  has  not  entered.  There  is  also  a 
diminution  in  the  color-index,  that  is,  of  the  individual  richness  of  the  cells 
in  hsemoglobin.  The  white  blood  cells  are  usually  increased  in  the  pro- 
portion of  mononuclear  leukocytes.  Pigmented  leukocytes  are  also  found, 
and,  if  the  infection  has  been  severe,  large  white  cells  (macrophages)  are 
to  be  seen  heavily  loaded  with  pigment.  In  some  instances  particles  of 
pigment  are  seen  floating  in  the  blood  serum,  having  been  set  free  from  red 
blood  cells  destroyed  by  the  parasite. 

The  liver,  besides  showing  great  congestion,  may  present  areas  of  necrosis 
and  the  capillaries  may  be  found  filled  with  a  multitude  of  the  parasites  in 
all  degrees  of  growth.  The  capillaries  of  the  liver  may  also  contain  many 
pigment  particles. 

The  kidneys  are  enlarged  and  congested.  They  may  contain  dotlets  of 
deposited  pigment,  and  their  capillaries  may  be  filled  by  leukocytes  laden  with 
pigment.  The  number  of  parasites  found  in  the  renal  vessels,  however,  as 
compared  to  those  found  in  the  hepatic  masses,  is  small.  Rarely  an  acute 
diffuse  nephritis  may  be  manifest. 

The  spleen  is  swollen,  soft,  and  its  pulp  is  very  dark.  Many  of  the  red 
blood  cells  which  it  contains  are  inhabited  by  the  parasites,  and  these  are 
often  in  the  stage  of  sporulation.  So  intense  may  be  the  swelHng  and  con- 
gestion of  the  spleen  that  it  may  be  ruptured  by  sudden  stress. 

The  mucous  membrane  of  the  stomach  and  bowels  is  engorged  and  its 
capillaries  often  contain  the  plasmodium. 

If  the  bone-marrow  is  examined  it  is  found  to  be  filled  with  segmenting 
parasites  and  with  pigment.  The  crescentic  parasites  are  also  apt  to  be 
numerous  in  these  areas. 

The  chronic  changes  consist  in  profound  anaemia,  manifested  by  a 
diminution  in  red  cells  and  in  haemoglobin  and  by  the  presence  of  nucleated 
red  cells.  The  liver  is  deeply  pigmented,  often  slaty  in  color,  the  granules 
being  deposited  in  the  endothehal  fining  of  the  capillaries  and  the  so-called 
'  cells  of  Kiipffer,  that  is,  the  perivascular  cells.  The  hepatic  epithelium  is 
commonly  granular  and  a  certain  degree  of  hepatic  cirrhosis  may  also  be 
present. 

The  spleen  also  becomes  markedly  increased  in  size,  slate  colored 
from  the  contained  pigment  and  later,  due  to  increase  in  fibrous  tissues 
it  becomes  very  firm,  the  "ague  cake." 

The  kidneys  are  also  markedly  pigmented,  and  may  suffer  from 
chronic  diffuse  nephritis.  In  certain  cases  of  the  cerebral  type  the  para- 
sites may  be  found  in  the  vessels  of  the  brain  and  a  malarial  neuritis  has 
been  described.  As  in  the  acute  form,  the  bone-marrow  is  deeply  pig- 
mented and  the  normal  marrow  may  be  replaced  by  red  marrow  in  which 
normoblasts  and  megaloblasts  are  present  in  the  majority  of  cases.  All 
these  changes  are  the  result  of  sestivo-autumnal  infection. 

The  blood  is  to  be  examined  for  the  malarial  organism  during  life  by  the 


MALARIAL  INFECTION  869 

microscope  with  an  oil-immersion  lens  and  by  the  use  of  the  following 
methods  •/ 

"There  are  two  methods  of  examining  the  blood  for  plasmodia,  in  fresh 
preparations  and  in  stained  smears.  Both  require  considerable  training,  as 
the  artefacts  produced  by  imperfect  technique  have  often  been  mistaken  for 
organisms. 

"The  Examination  of  Fresh  Blood. — To  examine  the  fresh  blood,  a 
puncture  is  made  in  the  pulp  of  the  finger  and  a  perfectly  clean  cover-glass  just 
touched  to  the  top  of  the  drop  of  blood  which  exudes  from  the  puncture. 
The  cover  is  then  dropped  without  pressure  on  a  clean  slide.  The  diameter 
of  the  drop  on  the  cover-glass  should  never  exceed  2  mm.,  because  if  more  be 
taken  the  corpuscles  cannot  spread  out  in  a  perfectly  thin  layer,  but  will 
overlap  each  other,  and  the  preparation  will  be  useless.  The  search  for  the 
organism  should  be  made  with  a  yy  oil-immersion  lens  and  a  moderate 
illumination.  The  organisms  are  best  recognized  by  the  actively  motile 
pigment  in  the  clear,  highly  refractile  cell  body. 

"The  Examination  of  Blood  after  Fixation. — If  the  examination 
cannot  be  made  at  once,  stained  preparations  may  be  made.  The  smear  should 
be  made  on  a  slide  or  large  cover-glass.  It  is  best  fixed  in  a  mixture  of 
formalin  and  strong  alcohol  for  one  minute.  The  proportions  are  2  c.c.  of  a 
10  per  cent,  solution  of  formalin  to  100  c.c.  of  strong  ethyl  alcohol.  The 
organisms  are  most  easily  found  and  studied  in  preparations  colored  with 
thionin.  The  formula  for  the  stain  is  20  c.c.  of  a  saturated  solution  of 
thionin  in  50  per  cent,  alcohol,  added  to  100  c.c.  of  2  per  cent,  aqueous  solu- 
tion of  carbolic  acid.  The  stain  requires  several  days  to  ripen,  and  then 
keeps  indefinitely.  Its  action  is  rapid,  requiring  only  about  fifteen  seconds 
to  color  the  malarial  organisms  deeply. 

"In  order  to  demonstrate  the  nuclear  chromatin  of  the  malarial  parasites, 
it  is  necessary  to  use  special  stains,  the  most  useful  being  a  modification  of 
that  originally  devised  by  Romanowski  for  this  purpose  and  improved  by 
Giemsa.  Two  substances  are  necessary:  First,  an  aqueous  solution  of 
'methylene  azure  II,  Griibler,'  8  dgm.  to  the  litre;  and  second,  an  aqueous 
solution  of  eosin, '  extra  water-soluble,  Hochst.'  These  two  stock  solutions  are 
permanent  if  kept  in  dark-colored  bottles.  The  smears  to  be  stained  are 
fixed  in  methyl  alcohol  for  about  ten  minutes.  The  staining  mixture  is  pre- 
pared by  adding  1  c.c.  of  the  methylene  azure  II  to  10  c.c.  of  the  eosin  solu- 
tion. The  staining  mixture  is  poured  into  a  Petri  dish  and  the  slide  immersed 
in  the  fluid  with  the  blood  side  down.  The  process  is  complete  in  from 
fifteen  to  thirty  minutes.  The  slide  is  washed  off  for  about  ten  seconds 
with  a  strong  stream  of  distilled  water,  dried  in  the  air  without  heat,  and 
embedded  in  dammar  dissolved  in  xylol.  A  simpler  method  has  recenlty 
been  published,  which  is  better  adapted  for  clinical  work.  The  smear  is 
fixed  for  two  minutes  or  more  in  methyl  alcohol,  then  stained  for  ten  seconds 
with  a  1 :  1000  aqueous  eosin  solution,  the  latter  allowed  to  run  off  the  slide, 
and  the  smear  again  covered  with  a  few  drops  of  a  i  per  cent,  solution  of 

1  These  directions  are  taken  from  the  last  edition  of  Pathology  and  Morbid  Anatomy,  by  Delafield 
and  Frudden. 


870  DISEASES  DUE  TO  ANIMAL  PARASITES 

methylene  azure  II.  In  about  from  fifteen  to  thirty  seconds  the  staining  is 
complete.  The  slide  should  be  washed  in  distilled  water,  dried,  and  exam- 
ined directly  with  an  oil-immersion  lens,  no  cover-glass  being  necessary." 

Symptoms. — The  symptoms  of  malarial  infection  may  be  divided  into 
two  classes:  those  due  to  the  tertian  or  quartan  parasites,  which  are  much 
alike,  and  those  due  to  the  sestivo-autumnal  parasites,  which  are  very  different 
from  those  produced  by  the  more  benign  forms. 

The  Symptoms  of  Tertian  and  Quartan  Infection. — ^The  pre- 
dominant symptoms  of  infection  by  these  parasites  are  the  development  at 
regular  intervals  of  a  chill  followed  by  a  fever,  and  this  in  turn  by  a  sweat. 

The  stage  of  onset  begins  with  a  feeling  of  malaise,  in  which  headache  and 
a  general  sensation  of  wretchedness  are  present.  Patients  who  have  had 
previous  attacks  are  often  able  to  recognize  the  fact  that  they  will  have  a 
paroxysm  in  a  few  hours. 

After  the  lapse  of  from  one  to  five  hours  the  chill  develops  and  is 
often  in  the  form  of  a  severe  rigor,  in  which  the  teeth  actually  chattel 
and  the  patient  is  entirely  unable  to  control  his  muscular  quivering. 
At  this  time  the  skin  is  cold,  the  face  is  pinched  and  often  anxious  in 
expression;  but  while  the  patient  complains  of  being  cold  and  presents 
all  the  external  signs  of  a  lowering  of  body  temperature,  his  actual 
internal  temperature  is  raised  so  that  fever  is  really  well  developed  while 
the  so-called  cold  stage  is  still  manifest.  Thus,  it  is  not  uncommon  for  the 
rectal  temperature  to  be  as  high  as  105°  while  the  patient  is  shivering  and 
trying  to  "get  warm."  Associated  with  this  part  of  the  paroxysm  the 
patient  is  usually  nauseated  and  may  actually  vomit,  so  that  to  the  depression 
of  the  chill  is  added  the  relaxation  and  semi-collapse  of  excessive  nausea. 
Headache  of  the  congestive  type  is  also  severe.  The  urine  is  copious  in 
quantity  and  light  in  color,  and  the  pulse  small,  rapid,  and  of  high  tension. 

This  stage  of  chill  lasts  from  a  few  minutes  to  an  hour  or  more,  and  is 
followed  by  the  true  febrile  stage,  in  which  the  surface  of  the  body  becomes 
flushed  and  hot.  In  place  of  the  cold,  pinched  expression  the  face  now 
appears  hot  and  flushed,  the  eyes  may  be  brightened  by  the  fever,  and  the 
pulse,  which  has  hitherto  been  small  and  tense,  becomes  full  and  bounding. 
Headache,  however,  still  persists,  and  active  delirium  may  develop,  but  the 
actual  temperature  of  the  patient  is  rarely  higher  than  during  the  stage  of 
chill;  indeed,  it  may  be  a  little  lower.  The  so-called  febrile  stage  is  not 
therefore  any  more  febrile  than  the  stage  of  apparent  codlness,  but  the  intense 
sensation  of  heat  in  the  skin  at  this  time  when  the  physician  touches  the 
patient  is  noteworthy.  This  stage  lasts  from  thirty  minutes  to  several 
hours  and  comes  to  an  abrupt  ending  by  the  development  of  the  stage 
of  sweat,  in  which  the  temperature  drops  to  normal;  the  surface  of  the 
patient  becomes  bedewed  with  sweat,  which  may  be  so  profuse  that  it  is 
truly  a  "dripping  sweat."  The  headache  and  general  wretchedness  now 
disappear  and  the  patient  drops  to  sleep  exhausted  bv  the  violence  of  his 
attack,  but  otherwise  not  ill. 

The  accompanying  charts  (Figs.  110  and  111)  show  the  typical  temp- 
erature changes: 

As  in  all  diseases,  so  in  this  one,  it  must  be  recalled  that  all  cases  do  not 


MALARIAL  INFECTION 


871 


go  through  these  stages  in  exactly  the  same  manner.  Some  individuals  suffer 
from  a  very  moderate  chill  and  an  equally  moderate  fever  and  sweat.  Some 
suffer  the  paroxysm  for  twelve  hours  and  some  for  a  much  shorter  space  of  time. 
There  are  three  important  physical  signs  which  may  be  demonstrable  in 
many  if  not  all  these  cases.  The  spleen  is  found  on  palpation  and  percus- 
sion to  be  distinctly  enlarged,  extending  below  the  level  of  the  ribs;  some 
bronchial  rales  are  usually  to  be  heard  in  the  chest,  and  the  lips  are  apt  to 
be  affected  by  herpes  at  the  close  or  after  an  attack. 


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Chart  showing  paroxysms  of  tertian  fever,  the  segmentation  of  the  organism  occurring  at 
about  12  o'clock  every  other  day. 

The  severity  of  all  the  signs  depends,  of  course,  upon  the  resistance  of 
the  patient  and  the  virulence  of  the  malarial  infection. 

There  yet  remains  to  be  considered  the  periodicity  of  these  attacks. 
They  may  occur  daily,  in  which  case  they  are  called  quotidian;  or  every 
other  day,  when  they  are  called  tertian;  or  every  third  day,  when  they  are 
called  quartan.  The  tertian  type  is  due  to  the  tertian  parasite,  which  sporu- 
lates  every  forty-eight  hours,  so  that  the  next  paroxysm  develops  at  the 
beginning  of  the  third  day;  hence  the  term  tertian,  or  third.  tMien  the 
attack  occurs  daily  it  is  due  to  the  fact  that  a  double  infection  of  the  tertian 


872  DISEASES  DUE  TO  ANIMAL  PARASITES 

parasite  has  taken  place,  so  that  a  different  set  of  organisms  mature  each 
day;  in  other  words,  it  is  a  "double  tertian  infection."  This  form  is  more 
frequently  seen  in  the  United  States  than  any  other  type.  \^Tien  the  attack 
occurs  at  the  end  of  every  third  day — that  is,  after  the  lapse  of  seventy-two 
hours,  which  is  really  therefore  on  the  beginning  of  the  fourth  day  of  actual 
time — it  is  due  to  the  quartan  parasite.  Sometimes,  however,  the  infection 
with  this  parasite  is  a  double  one,  the  sporulation  in  each  infection  taking 
place  separately,  in  which  case  the  attacks  occur  on  two  successive  days 
with  a  free  day  following.  In  still  other  cases  a  triple  quartan  infection  may 
cause  a  daily  or  quotidian  manifestation  of  the  disease.  A  daily  malarial 
attack  may  therefore  be  due  to  a  double  tertian  or  a  triple  quartan  infection. 

On  the  days  free  from  paroxysm  the  patient  is  entirely  free  from  chills, 
fever,  or  sweats,  and  except  for  some  impairment  of  strength  may  be  almost  as 
well  as  ever.  It  is  for  this  reason  that  the  disease  is  called  "  intermittent  fever." 

Diagnosis  of  Intermittent  Fever. — The  diagnosis  of  this  type  of  malarial 
fever  is  easy  in  the  majority  of  cases,  but  the  physician  should  not  hurry  to 
this  conclusion  until  he  has  carefully  excluded  several  other  states  that 
cause  a  similar  temperature  curve.  These  states  are  tuberculosis  of  the 
lungs  with  chills,  fever,  and  sweats;  septicsemia  and  ulcerative  endocarditis 
with  the  same  train  of  symptoms,  and  typhoid  fever  with  chills  of  a  sharp, 
distinct  character.  The  number  of  poor  human  beings  who  are  dosed  ad 
nauseam  with  quinine  for  malaria  when  they  have  tuberculosis  is  appalling. 
The  history  of  the  case,  the  physical  signs  in  the  lungs,  and  the  fact  that  the 
attq,cks  of  chills  and  fever  do  not  cease  if  quinine  is  given,  prove  that  malaria 
is  not  the  cause  of  the  illness.  Careful  examination  of  the  patient  ought  to 
discover  sepsis  by  the  finding  of  a  definite  focus  of  pus,  and  in  many  cases 
ulcerative  endocarditis  can  be  discovered  by  the  changes  in  the  heart  sounds. 
Typhoid  fever  can  be  discovered  by  the  state  of  the  tongue,  that  of  the 
bowels,  the  rose  rash,  and  the  Widal  test  of  the  blood.  Better  than  all  for 
an  absolute  diagnosis  is  the  discovery  of  the  malarial  parasite  in  the  blood 
by  the  use  of  the  microscope.  Unfortunately,  this  is  only  possible  to  the 
expert.    (For  examination  of  the  blood  for  the  parasite  see  Pathology.) 

Prognosis  of  Intermittent  Fever. — Intermittent  malarial  fever  cannot  be 
considered  a  self-limited  disease.  It  is  true  that  individuals  affected  by 
it  recover  without  medication  if  they  are  otherwise  healthy  and  have  favor- 
able surroundings,  but  it  is  notorious  that  they  are  very  hable  to  subsequent 
outbreaks  of  the  disease  when  for  various  reasons  their  vital  resistance  is 
impaired  or  the  system  is  affected  by  change  of  climate.  Thus  it  is  by  no 
means  unusual  for  patients  seemingly  well  of  the  infection  to  be  attacked  by 
paroxysms  on  going  to  a  higher  altitude.  If  quinine  is  used  with  skill,  and 
further  infection  is  avoided,  complete  recovery  usually  is  reached  if  no 
complication  arises. 

Treatment  of  Intermittent  Fever. — In  the  treatment  of  intermittent  malarial 
fever  the  fact  is  always  to  be  borne  in  mind  that  in  quinine  we  have  a  true 
specific  for  the  disease  in  that  this  drug,  even  in  exceedingly  weak  solu- 
tion, is  capable  of  causing  the  death  of  the  malarial  parasite.  So  complete 
is  the  cure  produced  by  the  proper  administration  of  this  drug  that  no  other 
form  of  remedial  measure  can  be  considered  until  after  it  has  been  given 


MALARIAL  INFECTION  873 

full  opportunity  to  do  its  work.  But,  on  the  other  hand,  it  must  not  be  for- 
gotten that  quinine  cannot  destroy  the  malarial  parasite  until  it  (the  quinine) 
has  entered  the  blood,  that  it  cannot  enter  the  blood  until  it  is  absorbed, 
and  that  it  is  impossible  for  it  to  be  absorbed  if  the  gastroduodenal  and 
hepatic  circulation  is  so  disturbed  that  catarrh  of  the  stomach  and  bowels 
is  present,  making  it  impossible  for  the  quinine  to  be  taken  up  by  the  circu- 
lation. It  is  therefore  essential,  in  almost  every  case  of  intermittent  fever, 
that  the  bowels  shall  be  thoroughly  unloaded,  preferably  by  full  doses  of 
calomel  of  which  not  less  than  5  nor  usually  more  than  20  grains  are  required, 
this  in  turn  being  followed  by  a  saline  purge.  If,  in  addition  to  these  meas- 
ures, it  is  insisted  upon  by  the  physician  that  the  patient  shall  rest  in  bed 
during  the  time  that  the  quinine  is  bei,ng  given,  it  is  surprising  how  little 
quinine  is  needed  to  destroy  the  parasites;  whereas,  if  these  precautions  are 
not  taken,  enormous  doses  may  be  given  with  no  curative  effect. 

Quinine  may  be  administered  at  two  periods  in  connection  with  the 
paroxysm  of  intermittent  malarial  fever.  One  method  is  to  administer  the 
drug  several  hours  before  an  expected  paroxysm,  with  the  hope  that  it  may 
prevent  sporulation,  or  at  least  destroy  the  spores  as  soon  as  they  escape. 
This  plan  is  always  to  be  resorted  to  when  the  physician  is  confident  that 
an  attack  is  threatened  and  that  a  sufficient  time  will  elapse  to  make  it 
possible  for  the  quinine  to  be  absorbed.  The  other  method  consists  in 
administering  the  drug  in  the  sweating  stage  of  a  paroxysm,  for  the  purpose 
of  destroying  the  young  parasites  which  have  just  escaped  from  the  red 
blood  corpuscles,  in  the  hope  that  they  may  be  destroyed  before  they  can 
attack  new  cells.  It  is  evident,  therefore,  that  neither  of  these  plans  is 
contradictory,  but  are  to  be  resorted  to  according  to  the  period  at  which 
the  physician  sees  the  patient.  It  should  always  be  the  endeavor  of  the 
physician  to  have  the  quinine  in  the  blood  an  hour  or  two  before  an  expected 
paroxysm,  and  this  means  that  it  should  be  given  several  hours  before 
when  taken  by  the  stomach. 

When  the  attack  is  quotidian  quinine  must  be  given  daily,  when  it  is 
tertian  it  must  be  given  every  other  day,  and  when  it  is  quartan  a  full  dose 
of  quinine  should  be  given  on  the  day  of  the  expected  attack  and  smaller 
doses  on  the  off  days.  If  it  is  a  double  quartan  infection  the  quinine  should 
be  given  on  the  two  consecutive  days  and  only  a  small  dose  on  the  third  day. 

The  quantity  of  quinine  which  is  required  varies  of  course  with  the  severity 
of  the  infection  and  the  rapidity  of  the  absorption.  Ten  to  15  grains  are 
usually  sufficient  in  the  milder  types,  but  in  the  more  severe  types  30  to  60 
grains  are  often  required,  although  a  larger  quantity  is  usually  needless  if 
attention  is  given  to  the  processes  of  absorption.  The  quinine  should  be 
given  in  powder  in  soft  capsules  easily  dissolved. 

So  far  as  the  attack  itself  is  concerned,  aside  from  the  use  of  quinine,  the 
physician  may  modify  to  some  extent  the  effects  of  the  paroxysm  by  the  use 
of  stimulants  to  support  the  circulation,  and  prevent  congestion  by  using 
hot  compresses  or  hot  foot-baths.  If  the  alimentary  canal  is  overloaded 
with  food  or  fecal  matter,  the  stomach  should  be  emptied  by  an  emetic 
and  the  intestine  by  a  purge  or  a  large  enema.  Alcoholic  stimulants,  as  a 
rule,  are  not  advantageous.     If  the  attack  is  exceedingly  severe,  a  dose  of 


874  DISEASES  DUE  TO  ANIMAL  PARASITES 

morphine  may  be  given  hypodermically,  or  deodorized  tincture  of  opium 
may  be  used.  During  the  fever  the  patient  may  be  reheved  by  a  tepid 
sponging,  but  usually  antipyretic  measures  are  entirely  unnecessary,  and 
coal-tar  products  ought  never  to  be  employed.  The  vomiting,  if  excessive, 
may  be  controlled  by  hourly  doses  of  a  grain  of  oxalate  of  cerium  with  5 
grains  of  bismuth,  and  by  counterirritation  over  the  epigastrium.  There  is 
some  evidence  to  prove  that  methylene  blue  has  a  destructive  influence  upon 
the  malarial  parasite.    It  may  be  given  in  the  dose  of  1  to  4  grains  in  capsules. 

The  Symptoms  of  -fflstivo-autumnal  Infection  or  Remittent  Fever. — From 
the  standpoint  of  severity  and  danger  to  the  individual  attacked,  this  type 
of  malarial  infection  is  by  far  the  most  important,  although  it  is  not  as 
widely  distributed,  and  therefore  not  as  commonly  met  with  as  the  tertian 
and  quartan  forms,  except  in  certain  localities  which  are  usually  tropical 
or  semi-tropical.  The  term  "  sestivo-autumnal  fever,"  applied  to  it  first  by 
the  Italian  investigators,  Marchiafava  and  Celli,  indicates  that  it  occurs 
most  commonly  in  the  summer  and  fall  months. 

The  symptoms  of  this  type  of  infection  differ  markedly  from  the  inter- 
mittent type  of  the  disease  in  a  number  of  particulars.  Thus,  it  is  not  char- 
acterized by  an  intermittence  of  the  fever  and  of  the  other  signs  of  illness,  but 
instead  is  typically  remittent;  that  is  to  say,  the  fever  and  associated  symp- 
toms diminish  in  severity  at  times,  but  they  do  not  entirely  disappear.  On 
the  contrary,  they  persist  in  some  cases  to  such  a  degree  that  the  amount 
of  remission  is  very  slight  indeed. 

As  the  gastrointestinal  disturbance  due  to  this  infection  is  very  prone 
to  be  marked,  and  as  the  liver  is  usually  much  affected,  this  type  of  the 
disease  is  sometimes  called  "bilious  remittent  fever"  or  "bihous  fever." 
Vomiting,  which  may  be  very  persistent,  and  which  may  be  markedly 
bilious,  is  a  common  symptom. 

The  remissions  just  spoken  of  may  occur  regularly,  but  in  the  majority  of 
cases  they  are  very  irregular,  both  as  to  the  time  of  their  occurrence  and  to  the 
degree  of  their  individual  severity.  In  some  instances  the  chills  and  sweats  are 
distinct;  in  others  they  are  so  ill-defined  as  to  be  scarcely  noticeable.  Further 
than  this,  the  febrile  movement,  which  is  so  sudden  in  onset  and  which  ends 
so  sharply  by  crisis  in  the  intermittent  form,  is  usually  gradual  in  onset  and 
equally  deliberate  in  its  fall  in  the  remittent  type.  The  temperature  falls 
by  lysis,  not  by  crisis,  in  each  paroxysm.  This  lack  of  sharply  defined 
waves  of  temperature  may  deprive  the  physician  of  one  of  the  most  important 
means  of  recognizing  that  the  illness  is  really  due  to  the  sestivo-autumnal 
parasite,  and  may  mislead  him  into  the  diagnosis  of  typhoid  fever,  to  which 
conclusion  he  is  aided  by  the  heavily  coated  tongue,  the  somewhat  apathetic 
face,  the  enlarged  spleen,  the  tympanitic  belly,  and  the  state  of  the  bowels, 
which  are  lax  in  some  instances  and  constipated  in  others,  just  as  they  are 
in  typhoid  fever.  As  many  cases  of  typhoid  fever  have  chills  and  sweats, 
the  confusion  is  all  the  more  readily  made,  particularly  as  a  subacute  bron- 
chitis can  often  be  discovered  on  ausculting  the  chest,  just  as  it  can  be  found 
in  typhoid  fever. 

The  severity  of  the  symptoms  varies  over  a  wide  range.  In  some  instances 
the  patient  is  only  moderately  ill;  in  other  cases  he  is  manifestly  suffering 


MALARIAL  INFECTION  875 

from  a  severe  malady.  Delirium  may  be  marked,  and  the  mental  stupor  may  be 
very  noticeable.    The  pulse  varies  from  90  to  1 10,  as  it  does  in  typhoid  fever. 

There  still  remains  to  be  discussed  that  form  of  sestivo-autumnal  infection 
which  is  so  violent  in  its  course  that  the  term  "pernicious  malarial  fever" 
has  been  applied  to  it.  Pernicious  malarial  fever  is  very  rare  except  in  the 
tropics  and  in  a  few  isolated  places  not  far  removed  from  these  areas.  It 
manifests  itself  in  two  forms: 

(a)  The  comatose  form,  in  which  a  patient  is  seized  with  symptoms 
resembling  intense  cerebral  congestion  or  apoplexy,  or  develops  acute 
delirium  followed  by  semi-consciousness  or  coma.  The  fever  is  usually  very 
high  and  the  skin  intensely  hot.  The  patient  may  die  in  twenty-four  hours 
without  regaining  consciousness,  but  if  he  survive  so  long  a  remission  in 
the  symptoms  sometimes  appears  and  recovery  takes  place;  or,  instead,  a 
second  paroxysm  comes  on  in  which  death  is  likely  to  occur.  These 
cerebral  symptoms  are  due  in  part  to  the  profound  systemic  disturbance 
caused  by  the  infection,  but  chiefly  to  the  formation  of  thrombosis  of  the 
cerebral  vessels  by  a  host  of  the  parasites. 

(6)  The  algid  or  cold  form,  in  which  the  febrile  movement  is  absent  or 
very  mild,  and  in  its  place  signs  of  collapse  and  exhaustion  appear,  with 
great  coldness  of  the  surface  of  the  body  and  a  complaint  of  feeling  cold  on 
the  part  of  the  patient.  With  these  symptoms  of  profound  depression 
gastrointestinal  disturbances,  which  are  choleraic  in  type,  may  develop. 
There  may  be  violent  vomiting  and  active  serous  diarrhoea,  the  patient  being 
at  death's  door  by  reason  of  the  exhaustion.  Here  again  the  centraKzation  of 
the  symptoms  about  the  intestines  is  due  apparently  to  the  accumulation  of 
vast  numbers  of  the  parasites  in  the  capillaries  of  the  intestinal  mucosa. 

Complications  and  Sequelae  of  .ffistivo-autumnal  Infection. — The  most  serious 
complication  of  infection  by  the  sestivo-autumnal  parasite  is  the  develop- 
ment of  bloody  urine,  which  is  of  two  forms,  namely,  a  true  hsematuria  with 
free  blood  cells  in  the  urine,  and  a  true  hcemoglobinuria  in  which  only  the 
coloring  matter  of  the  blood  is  present.  The  former  is  obviously  the  result 
of  a  solution  of  continuity  in  the  renal  vessels,  and  the  latter  is  equally 
obviously  due  to  a  destruction  of  a  large  number  of  red  cells  in  the  blood 
itself.  This  "black-water  fever,"  as  it  is  sometimes  called,  is  practically 
unknown  except  where  the  sestivo-autumnal  parasite  is  found.  It  occurs 
chiefly  in  certain  of  the  Southern  United  States  and  in  Africa  and  in  Greece. 

The  symptoms  associated  with  the  development  of  the  bloody  urine  are 
those  which  are  often  manifested  by  ordinary  cases  of  severe  remittent 
malarial  fever.  If  the  blood  is  examined  before  the  urine  becomes  bloody, 
a  large  number  of  sestivo-autumnal  parasites  are  usually  found.  On  the 
other  hand,  after  the  bloody  urine  has  appeared,  it  is  commonly  stated  that 
an  examination  of  the  blood  does  not  reveal  the  malarial  organism. 

The  statement  that  quinine  is  capable  of  producing  malarial  hsematuria  is 
indorsed  by  so  many  practitioners  of  experience  that  it  cannot  be  ignored, 
but  we  cannot  help  feeling  that  coincidence  has  been  a  large  factor  in  the 
development  of  this  view. 

As  sequelse  of  malarial  fever  very  marked  ansemia,  with  chronic  enlarge- 
ment of  the  spleen,  sometimes  called  "  ague  cake,"  develops;  the  patient  is 


876  DISEASES  DUE  TO  ANIMAL  PARASITES 

exceedingly  pallid,  the  abdomen  may  be  distinctly  enlarged  because  of  the 
swelling  and  congestion  of  the  liver  and  spleen,  and  there  may  be  some 
swelling  about  the  ankles.  There  is  dyspnoea  on  exertion.  Hemorrhages 
in  the  retina  may  occur.  Fever  is  usually  not  marked,  unless  there  be 
attacks  of  malarial  infection  superimposed  upon  the  chronic  state. 

It  is  quite  remarkable  that  in  young  children,  who  suffer  from  severe  mala- 
rial anaemia  and  cachexia  with  associated  enlargement  of  the  spleen,  recovery 
will  take  place  under  the  administration  of  suitable  tonic  doses  of  arsenic, 
the  avoidance  of  fresh  malarial  infection,  and  resort  to  a  bracing  climate. 
Even  the  spleen,  which  seems  so  hard  and  enlarged  that  any  diminution  in 
its  size  may  appear  impossible,  undergoes  an  extraordinary  degree  of  shrink- 
age, so  that  in  adult  life  any  evidences  of  it  having  been  chronically  enlarged 
may  have  disappeared.  Similar  improvement  sometimes  takes  place  in 
adults,  but  slight  enlargement  of  the  spleen  is  often  a  persistent  evidence 
of  earlier  malarial  infection,  even  after  the  disease  has  been  apparently 
absent  for  years. 

Among  the  rarer  complications  of  malaria  may  be  mentioned  neuritis, 
pleurisy,  ascites,  intestinal  hemorrhage,  splenic  abscess,  and  inflammation 
of  the  lymphatic  glands.  Cases  of  orchitis  have  been  reported  by  French 
military  surgeons,  and  a  rapidly  developing  and  very  painful  form  has  been 
observed  in  Sumatra,  by  Martin,  who  describes  it  as  a  fulminating  inflam- 
mation of  the  testicles. 

Choux  has  collected  147  cases  of  rupture  of  the  spleen  due  to  malaria. 
He  recognizes  two  forms:  one  which  occurs  in  persons  who  have  not 
suffered  very  long  from  malaria,  and  whose  spleens  are  not  greatly  enlarged, 
and  one  which  affects  the  subjects  of  chronic  malaria  whose  spleens  are 
enlarged  and  deformed  by  splenitis.  In  the  latter  class  rupture  is  usually 
caused  by  traumatism.  Playfair,  during  a  residence  of  two  and  a  half 
years  in  the  East  Indies,  observed  twenty  deaths  from  rupture  of  the 
spleen. 

Hemiplegia,  either  with  or  without  aphasia,  is  the  most  common  of  local- 
ized cerebral  complications.  Paraplegia  is  less  common,  and  monoplegia 
is  of  still  rarer  occurrence.  Amaurosis,  deafness,  and  perversions  of  taste  and 
smell  are  occasionally  observed.  Symptoms  of  motor  irritation,  such  as 
tremor  and  choreiform  movements,  have  also  been  reported  as  rare  complica- 
tions, and  a  case  of  posthemiplegic  malarial  chorea  has  been  described  by 
Boinat  and  Salebert.  Paralysis  of  the  lower  extremities,  due  to  lesions  in  the 
cord,  occurs,  and  is  often  accompanied  by  loss  of  control  over  the  rectum 
and  bladder.  All  of  these  disturbances  may  be  transitory.  Occasionally 
some  of  the  paralyses  are  rapidly  fatal.  Multiple  sclerosis  is  a  relatively  fre- 
quent nervous  sequela,  and  tetany  and  paralysis  agitans  are  among  the 
less  frequent  complications.  Peripheral  disturbances,  such  as  hypersesthesia 
and  anaesthesia,  occur  in  a  few  cases,  and  supraorbital,  trigeminal,  and 
intercostal  neuralgia  also  complicate  a  small  number  of  cases. 

Of  functional  nervous  complications  and  sequelae,  hysteria,  neurasthenia, 
and  insomnia  may  be  mentioned.  The  various  psychoses  are  of  rare  occur- 
rence. Pasmanik  in  an  analysis  of  5412  cases  of  malaria  found  106  cases 
of  mental  derangement.     None  of  these   patients  affected  were  known  to 


MALARIAL  INFECTION  877 

have  an  hereditary  predisposition  to  insanity,  and  only  4.8  of  the  number 
were  alcohoHcs. 

Diagnosis  of  ^stivo-autumnal  Fever. — TEstivo-autumnal  fever  must  be 
carefully  differentiated  from  typhoid  fever  and  from  the  so-called  con- 
tinued thermic  fever  of  hot  climates.  Its  differentiation  from  typhoid 
fever  is  possible  and  should  always  be  achieved;  yet  during  the  recent 
Spanish-American  war  the  number  of  cases  reported  as  malarial  fever 
which  were  typhoid  fever  and  the  number  called  typhoid  fever  which  were 
malarial  was  very  large. 

The  presence  of  sestivo-autumnal  infection  is  determined  by  the  fact  that 
the  patient  is,  or  has  been,  living  in  a  region  in  which  this  disease  is  prevalent 
or  at  least  may  occur.  It  practically  never  occurs  north  of  the  State  of 
Delaware  in  the  United  States,  or  in  any  of  the  northern  parts  of  Europe. 
Again,  its  presence  is  determined  by  the  discovery  of  the  sestivo-autumnal 
parasite  in  the  blood.  This  is  not  an  easy  test  for  the  tyro,  and  the  blood 
is  not  easy  to  obtain  from  the  deeply  seated  organs  in  which  the  parasite 
is  found.  After  the  first  week  of  the  illness  the  absence  of  rose  spots  and 
the  Widal  reaction  will  determine  the  case  not  to  be  one  of  typhoid  fever. 
Finally,  good-sized  doses  of  quinine  will  modify  the  fever  of  this  type  of 
malaria,  but  will  not  affect  typhoid  fever  at  all.  The  physician  should  make 
it  a  rule  that  if  a  case  of  fever  does  not  yield  to  quinine  in  four  days  it 
is  not  malaria;  provided,  however,  that  by  the  use  of  calomel  and  other 
measures  he  has  been  able  to  put  the  alimentary  canal  in  such  a  state  that 
the  quinine  can  enter  the  blood.  If  this  cannot  be  done,  then  the  drug 
should  be  given  hypodermically. 

Treatment. — ^The  treatment  of  remittent  fever  is  much  more  difficult 
than  that  of  the  intermittent  form.  The  disease  is  more  dangerous  and 
often  more  rapid  in  its  course.  Further  than  this,  the  fever  is  so  much  more 
prolonged  that  it  is  of  itself  deleterious,  and,  as  the  patient  does  not  have 
periods  of  intermittence  in  which  he  can  make  a  partial  recovery,  strength 
is  much  more  rapidly  lost.  The  aestivo-autumnal  parasite  seems  to  be  more 
resistant  to  the  influence  of  quinine  than  either  the  tertian  or  quartan 
parasite,  and,  finally,  it  is  much  more  difficult  to  cause  the  absorption  of 
quinine  in  most  cases  of  bilious  remittent  fever,  both  because  vomiting  is 
frequently  a  persistent  symptom  and  also  because  absorption  seems  for  the 
time  being  to  be  put  aside.  It  is  evident,  therefore,  that  where  vomiting  is 
too  persistent  to  permit  of  the  administration  of  quinine  by  the  stomach,  it 
must  be  given  hypodermically.  The  best  way  to  administer  it  hypodermic- 
ally  is  in  the  form  of  the  hydrochlorate  of  quinine,  which  is  soluble  in  ten 
parts  of  water,  and  which  may  be  injected  in  the  following  manner :  Dissolve 
15  grains  of  hydrochlorate  of  quinine  in  15  minims  of  alcohol  and  2h  drachms 
of  distilled  water.  Just  before  using,  add  a  drop  or  two  of  dilute  hydro- 
chloric acid.  The  difficulty  with  the  administration  of  quinine  by  the 
rectum  in  these  cases  is  that  absorption  is  too  slow.  But,  nevertheless,  the 
drug  may  be  given  in  this  manner  dissolved  in  starch-water  whenever  it  is 
advisable  to  get  quinine  into  the  blood  by  every  possible  avenue. 

Even  when  it  is  impossible  to  administer  quinine  by  the  stomach,  it  is 
usually  advisable  to  move  the  bowels  freely,  and  this  may  be  accomplished 


878  DISEASES  DUE  TO  ANIMAL  PARASITES 

by  the  use  of  a  Seidlitz  powder  given  in  divided  doses,  or  by  the  employment 
of  citrate  of  magnesium. 

If  the  vomiting  becomes  so  excessive  as  to  be  a  dangerous  symptom  in 
itself,  it  may  be  controlled  by  hypodermic  doses  of  morphine,  or  by  5  to  20 
minims  of  spirit  of  chloroform  given  with  the  same  amount  of  compound 
spirit  of  lavender  or  of  cherry-laurel  water.  Counterirritation  may  also  be 
applied  over  the  epigastrium  in  the  shape  of  a  mustard  plaster.  Some  cases 
are  also  benefited  by  the  application  of  hot  compresses  over  the  liver.  The 
value  of  large  doses  of  calomel,  amounting  to  20  or  even  30  or  40  grains,  for 
their  effect  in  overcoming  hepatic  torpor  cannot  be  denied.  All  practi- 
tioners of  experience  in  intensely  malarial  districts  are  agreed  as  to  this  point. 

Should  hsematuria  or  hsemoglobinuria  complicate  a  case,  a  careful  con- 
sideration of  the  stage  of  the  disease  is  essential.  The  value  or  harmfulness 
of  quinine  in  malarial  hsematuria  is  still  a  "  bone  of  contention  "  with  many 
practitioners,  some  claiming  that  the  quinine  is  capable  of  actually  producing 
bloody  urine,  and  others  asserting  equally  positively  that  it  is  always  needed. 
The  writer  has  expressed  the  view  on  several  occasions  that  some  of  these 
cases  of  bloody  urine,  complicating  malarial  fever,  may  be  due  to  an 
associated  parasite  upon  which  quinine  has  little  influence.  In  a  certain 
number  of  cases  it  is  probably  true  that  the  bloody  urine  is  a  sequel  rather 
than  an  accompaniment  of  the  development  of  the  parasite  in  the  blood. 
Under  these  circumstances,  as  enormous  doses  of  quinine  can  have  little 
influence  upon  the  malarial  parasite  and  also  may  irritate  the  kidneys,  it 
is  conceivable  that  the  use  of  this  drug  at  such  a  time  is  distinctly  contra- 
indicated;  whereas,  if  an  examination  of  the  blood  reveals  the  presence  of 
the  sestivo-autumnal  parasite,  then  the  quinine  must  be  given,  since  the 
danger  of  producing  hsematuria  by  its  administration  is  more  than  counter- 
balanced by  the  desirability  of  destroying  the  cause  of  the  illness.  In  other 
words,  to  give  quinine  in  some  cases  of  malarial  hsematuria,  when  the 
specific  parasite  is  not  present,  is  like  locking  the  door  after  the  horse  is 
stolen;  while  in  others  its  administration  is  timely  and  appropriate. 

Many  physicians  of  large  experience  strongly  urge  the  use  of  hyposulphite 
of  sodium  in  doses  of  from  15  to  60  grains  every  four  hours  for  this  com- 
plication. 

Latent  Malarial  Infection. — Latent  malarial  infection  is  probably 
much  more  common  than  physicians  believe,  although  the  laity  have  an 
exaggerated  view  of  its  occurrence.  Craig  has  reported  the  results  of  exam- 
ining the  blood  of  47  men  in  one  company  of  the  United  States  Army,  all 
of  whom  had  been  exposed  to  malarial  infection  in  the  Philippines,  but  all  of 
whom  were  at  least  well  enough  to  be  on  duty.  Twenty-seven  of  them  had 
the  parasite  in  their  blood,  and  25  were  infected  by  the  sestivo-autumnal 
parasite.  This  persistence  of  infection  not  only  possesses  ordinary  interest, 
but  shows  that  by  the  distribution  of  returning  troops  to  various  parts  of 
the  country  this  parasite  may  be  disseminated  in  areas  hitherto  uninfected. 
Further,  as  Craig  points  out,  the  development  of  a  masked  malarial  infection 
may  greatly  mislead  the  surgeon,  both  before  and  after  an  operation. 


TRYPANOSOMIASIS  879 


PSOROSPERMIASIS. 

This  term  is  applied  to  an  exceedingly  rare  condition  in  which  psorosperms 
become  parasites,  growing  in  cells  and  producing  nodules.  These  nodules 
may  be  large  enough  to  be  felt  through  the  abdominal  wall.  The  patient 
presents  symptoms  which  are  like  typhoid  fever  in  character.  There  is 
diarrhoea,  stupor,  some  fever,  hepatic  and  splenic  tenderness,  and  feeble 
circulation.  Autopsy  in  such  cases  has  shown  the  presence  of  masses  closely 
resembling  tubercles,  which  are  scattered  over  the  liver,  the  spleen,  the 
peritoneum,  and  in  the  kidneys. 

Another  form  of  infection  by  sporozoa  has  been  described  as  occurring 
in  the  skin,  but  Stel wagon  states  that  the  condition  called  psorospermiasis 
by  Darier  is  now  known  not  to  be  due  to  this  cause.  On  the  other  hand, 
Rixford  and  Gilchrist,  in  Baltimore,  have  recorded  two  cases  in  which 
tuberculosis  of  the  skin  was  thought  to  be  present  for  eight  years.  During 
this  time  the  lymphatic  glands  were  enlarged,  other  parts  of  the  body  became 
affected,  and  finally  death  ensued.  Numerous  nodules,  looking  like  those 
of  tuberculosis,  were  found  scattered  very  widely  through  the  body,  and 
these  were  found  to  contain  large  numbers  of  sporozoa. 


TRYPANOSOMIASIS. 

Definition. — Two  diseases,  or  rather  two  phases  of  one  disease,  are  recog- 
nized in  man  as  due  to  infection  by  trypanosomata.  These  are,  first,  an 
ill-defined  fever  resulting  from  invasion  of  the  circulation  by  the  Trypa- 
nosoma gambiense,  and  second,  African  lethargy,  or  sleeping  sickness,  due 
to  the  presence  of  the  same  parasite  in  the  cerebrospinal  fluid. 

The  trypanosomata  are  flagellated  protozoa,  and  were  first  discovered 
by  Gruby  in  1843  in  frogs,  and  by  Doflein  in  1845  in  rats  and  hamsters. 
Since  that  time  they  have  been  found  in  practically  all  vertebrates.  These 
organisms  were  first  supposed  to  be  spirilli  before  their  animal  nature  was 
understood.  In  the  large  majority  of  instances  they  are  not  pathogenic. 
As  far  as  our  present  knowledge  goes,  the  varieties  represent  distinct  types, 
confined  to  the  particular  animal  which  they  infect.  At  least  six  trypanoso- 
mata that  are  pathogenic  occur  in  mammals.  Thus,  the  Trypanosoma  Evaxisi 
and  the  Trypanosoma  Brucei  are  the  causes  of  very  fatal  diseases,  known  as 
surra  and  nagana  among  horses,  mules,  camels,  buffaloes,  and  wild  animals. 
Trypanosoma  equiperdum  is  the  cause  of  an  exceedingly  fatal  disease  of 
horses  in  Algiers  and  the  Mediterranean  coast.  Trypanosoma  equinum  is 
also  the  cause  of  a  fatal  disease  of  horses  in  South  America.  Trypanosoma 
Theileri,  the  largest  of  the  known  trypanosomata,  is  the  cause  of  a  serious 
cattle  disease  in  South  Africa.  The  most  widely  distributed  is  Trypanosoma 
Lewisi,  the  parasite  infecting  rats.  This  particular  variety  is  very  common 
in  the  rats  of  the  United  States,  and  has  been  found  in  practically  every  city 
where  search  has  been  made  for  it.  Finally,  we  have  the  trypanosoma 
which  infects  man. 


8g0  DISEASES   DUE  TO  ANIMAL  PARASITES 

A  trypanosoma  consists  of  a  leech-shaped,  granular  body  from  13/^  to 
25//  long  and  from  2/«  to  4//  wide.  This  body  contains  a  nucleus  and  a 
rod-shaped  centre  known  as  the  centrosome,  or  micronucleus.  Along  one 
edge  of  the  parasite,  beginning  at  the  centrosome,  is  a  delicate,  fringe-Hke 
membrane  known  as  the  undulating  membrane,  upon  the  outer  edge  of 
which  is  a  single  flagellum  extending  from  7//  to  15//  beyond  the  anterior 
end  of  the  parasite.  In  freshly  drawn  peripheral  blood  these  parasites  are 
seen  to  be  in  most  active  motion,  progression  being  in  the  direction  of  the 
flagellum.  In  hanging-drop  preparation  they  live  several  days,  and  as  long 
as  fifty  days  if  the  shde  be  kept  cold  and  moist.  McNeal  and  Novy  have 
succeeded  in  cultivating  Trypanosoma  Lewisi  and  Trypanosoma  Brucei 
on  a  culture  medium  of  agar  and  defibrinated  rabbits'  blood.  This  is 
the  first  instance  in  which  animal  parasites  have  been  obtained  in  pure 
culture. 

With  respect  to  transmission  of  infection  by  trypanosomata  numerous 
carriers  have  been  found.  Experimentally,  animals  may  be  infected  by 
intraperitoneal  and  subcutaneous  injection  of  the  parasites,  or  by  inges- 
tion of  the  parasites  into  the  stomach.  Infection  may  be  carried  by 
food  and  water,  by  the  bite  of  fleas,  lice,  mosquitoes,  ticks,  and  several 
varieties  of  flies.  The  infection  of  Trypanosoma  equiperdum  is  conveyed 
during  coitus. 

The  prevailing  evidence  is  that  human  trypanosomiasis  is  disseminated 
or  conveyed  and  inoculated  by  suctorial  flies.  The  view  that  one  fly  only 
can  act  as  host  for  a  particular  trypanosome  is  generally  held,  but  is  by 
no  means  established.  The  known  transmitters  of  trypanosomiasis,  of 
which  our  knowledge  appears  accurate,  are  the  Glossina  palpalis  for  those 
of  trypanosoma  fever  and  sleeping  sickness,  and  the  Glossina  morsitans  for 
surra.    Of  other  means  of  natural  dissemination  we  know  nothing. 

Human  Tr3rpanosoniiasis  (Trypanosoma  Fever). — The  first  reported 
case  of  trypanosoma  in  man  was  made  by  Nepveu,  and  his  paper  contains  a 
fair  drawing  of  the  parasite.  Forde,  in  1901,  described  the  parasite  in  the 
case  of  a  European  from  the  Gambia  River  Colony  suffering  from  an  atypical 
fever.  Since  that  time  Manson,  Button,  Todd,  and  others  have  reported 
cases,  nearly  all  of  them  from  the  Congo  and  Gambia  River  district.  Man- 
son's  case  occurred  in  a  woman  aged  forty  years.  The  temperature  ranged 
from  97°  in  the  morning  to  100°  in  the  evening.  The  pulse  was  always 
rapid  and  feeble.  Erythema  was  a  constant  feature  in  the  case,  and  was 
first  observed  when  the  fever  began.  QEdema  was  also  present,  and  was 
most  pronounced  on  the  back  and  face.  There  was  marked  enlargement 
of  the  spleen.  Duthen  reports  a  case  of  a  European  working  along  the 
Gambia  River  who  suffered  from  an  irregularly  remittent  fever.  The 
trypanosomata  were  especially  plentiful  during  the  pyrexia.  The  symp- 
toms included  extraordinary  weakness,  oedema  of  eyelids,  enlarged  and  tender 
spleen,  and  rapid  pulse.  Malarial  organisms  were  never  found.  This 
patient  recovered  under  the  use  of  arsenic. 

The  clinical  phenomena  in  the  reported  cases  are  chiefly  these:  In  some 
cases  the  parasites  occur  in  the  blood  without  the  patient  manifesting  any 
conspicuous  symptoms.    In  other  cases  there  is  an  irregular  fever  which  may 


TRYPANOSOMIASIS  881 

be  high,  continuous,  or  remittent  in  type.  It  does  not  yield  to  quinine. 
After  persisting  from  three  days  to  two  or  three  weeks,  it  is  followed  by  an 
apyretic  intervah  During  the  course  of  the  fever  large  erythematous  patches 
occur  all  over  the  body,  associated  with  irregularly  distributed  areas  of 
cutaneous  oedema.  The  oedema  and  erythema  may  or  may  not  coincide. 
The  oedema  is  most  marked  on  the  face,  especially  on  the  lower  eyelids.  The 
pulse  is  rapid  and  running,  a  peculiarity  also  observed  in  sleeping  sickness. 
The  lymph  nodes  enlarge  and  their  expressed  or  extracted  juice  usually  con- 
tains the  parasite. 

In  many  cases  the  history  of  an  inflamed  and  painful  insect  bite  can  be 
obtained. 

The  parasites  are  found  free  in  the  peripheral  blood  and  never  in  the 
corpuscles.  They  are  not  numerous,  varying  from  one  to  twenty  in  a 
cover  preparation.  They  may  be  absent  for  days  at  a  time.  In  the  case 
reported  by  Manson  experimental  inoculation  on  animals  was  negative, 
showing  the  distinct  nature  of  the  parasite.  It  now  appears  quite  clear 
that  infection  results  from  the  bite  of  a  tsetse  fly  (Glossina  palpalis)  which 
is  the  carrier  of  the  parasite.  In  Button's  case  there  was  the  history  of 
the  patient  being  bitten  by  a  rat. 

The  blood  condition  is  interesting.  There  is  a  moderate  degree  of  anae- 
mia in  all  cases  and  a  marked  increase  in  the  large  mononuclear  leuko- 
cytes, running  as  high  as  22  per  cent.  The  increase  in  these  cells  seems 
rather  constantly  associated  with  sporozoal  infection,  just  as  metazoal 
parasitism  is  accompanied  by  eosinophilia. 

Treatment. — Some  of  the  reported  cases  have  recovered  on  large  doses  of 
arsenic  administered  in  the  form  of  sodium  cacodylate  or  arsenate  of  iron 
given  hypodermically.  Methylene  blue  and  quinine  in  large  doses  have 
also  been  tried,  but  are  not  of  any  particular  value.  The  patient  should  be 
kept  in  bed  in  a  warm  room,  and  should  be  fed  on  simple  and  nourishing 
food.  Treatment  of  the  fever  is  symptomatic.  The  most  important  pre- 
ventive measure  is  to  keep  the  individual  where  he  cannot  be  bitten  by  flies, 
and,  if  ill,  where  he  cannot  act  as  a  centre  of  infection. 

African  Lethargy  (Sleeping  Sickness). — Sleeping  sickness  is  a  chronic 
disease  characterized  by  increasing  lethargy,  and,  after  an  exceedingly 
chronic  course,  death  occurs  from  coma  or  from  inanition — "a  negro  sleeping 
himself  to  death." 

Sleeping  sickness  is  at  present  confined  to  tropical  Africa,  principally 
along  the  west  coast.  The  northern  limit  of  its  extension  is  the  Senegal 
River;  the  southern  limit  is  the  Portuguese  Colony.  It  is  common  in  Sene- 
gambia,  along  the  Gold  Coast,  and  at  Old  Calabar.  It  has  existed  for  a  long 
time  in  the  basin  of  the  Congo  River  from  Stanley  Falls,  in  the  heart  of 
equatorial  Africa,  to  the  lower  Congo.  It  has  recently  extended  from  Vic- 
toria Nyanza  to  the  head-waters  of  the  Nile.  In  the  last  two  years  the  dis- 
ease has  assumed  epidemic  proportions  in  Uganda  and  many  thousands  of 
the  natives  have  perished.  In  the  days  of  the  slave  traffic  sleeping  sickness 
was  frequently  carried  to  the  West  Indies,  Southern  United  States,  Brazil, 
and  the  Bahamas,  but  it  never  succeeded  in  establishing  a  foothold  in  any 
of  these  places. 
56 


882  DISEASES  DUE  TO  ANIMAL  PARASITES 

Etiology. — For  a  long  time  the  Filaria  perstans  was  supposed  to  be  asso- 
ciated with  sleeping  sickness,  principally  on  account  of  their  coincidence 
in  the  infected  areas.  I>ater  studies  have  shown  that  filaria  has  no  connec- 
tion with  sleeping  sickness,  and  that  many  areas  infected  by  sleeping  sickness 
do  not  show  infection  by  the  Filaria  perstans. 

The  older  views  that  sleeping  sickness  is  due  to  poisoning,  intoxication, 
and  filaria  have  been  superseded  by  the  demonstration  of  a  trypanosoma  in 
the  cerebrospinal  fluid  by  Castellani,  and  the  confirmation  of  this  obser- 
vation by  Bruce  and  other  members  of  the  English  Sleeping  Sickness 
Commission,  who  have  successfully  propagated  the  disease  in  monkeys. 
The  trypanosoma  of  sleeping  sickness  is  indistinguishable  from  that  of 
trypanosoma  fever,  and,  like  the  latter,  is  also  found  in  the  blood.  Apparently 
the  advent  of  sleeping  sickness  in  a  patient  having  trypanosoma  fever  is 
determined  by  colonization  of  the  parasites  in  the  cerebrospinal  fluid.  The 
exact  relation  of  the  hypnococcus,  described  by  Castellani  and  other  mem- 
bers of  the  Spanish  Commission,  as  the  cause  of  the  disease  is  not  as  yet 
perfectly  clear;  apparently  it  is  only  a  terminal  infection. 

Sleeping  sickness  attacks  persons  of  all  ages.  In  the  endemic  area 
negroes  are  the  most  susceptible,  mulattoes  less  so,  and  Moors  contract 
the  disease  still  less  frequently.  I  know  of  but  one  authenticated  case  of 
sleeping  sickness  in  a  white  man  on  record.  The  tsetse-fly  (Glossina  palpalis) 
is  the  intermediate  host.  It  has  been  shown  experimentally  that  this  fly,  after 
feeding  on  a  case  of  sleeping  sickness,  is  capable  of  conveying  the  dieases 
to  healthy  monkeys,  and  that  flies  from  the  endemic  area  were  found  to  be 
infected  even  without  such  feeding.  It  is  possible  that  the  disease  may 
exceptionally  be  conveyed  in  other  ways.  The  negroes  believe  that  con- 
tagion is  carried  by  water  and  also  by  the  saliva  of  the  sick. 

Pathology. — Mott  has  shown  that  the  lesion  of  sleeping  sickness  is  an 
extensive  meningoencephalomyelitis.  In  the  cord  and  brain  extensive 
round-cell  infiltration  is  found  about  the  capillary  vessels.  The  cerebro- 
spinal fluid  is  deeper  in  color  than  normal  owing  to  the  presence  of  numbers 
of  red  blood  cells.  Besides  these,  numerous  leukocytes  and  the  specific 
trypanosoma  are  found.  In  the  latter  stages  of  the  disease  there  is  some 
ground  for  believing  that  there  is  a  concomitant — in  a  terminal  sense — 

'  streptococcus  (hypnococcus)  infection. 

'  Symptoms. — The  incubation  period  is  variable,  but  always  long.  The 
natives  believe  that  the  disease  may  deyelop  as  long  as  seven  years  after 
exposure.  As  a  matter  of  fact  numerous  instances  are  on  record  where  the 
disease  has  appeared  in  negroes  several  years  after  leaving  the  endemic  area 
settling  in  other  countries.  It  would  appear,  from  the  meagre  knowledge  and 
of  the  parasite  now  available,  that  it  may  be  found  in  the  peripheral  blood 
without  producing  any  symptoms.  The  causes  that  determine  colonization 
of  the  parasites  in  the  cerebrospinal  system  are  unknown. 

The  disease  sometimes  begins  with  marked  psychical  prodromata,  includ- 
ing epileptiform  seizures,  melancholia,  and  even  transitory  mania.  In  the 
larger  number  of  cases  there  is  headache,  vertigo,  puffiness  of  the  face,  and 
slight  fever.  At  this  point  the  lethargy  begins.  The  patient  at  first  is  somno- 
lent or  stupid,  but  he  can  easily  be  roused  for  nourishment  or  to  attend 


KALA-AZAR  883 

to  the  calls  of  nature.  When  so  awakened  his  gait  is  staggering  and  the 
moment  he  is  released  he  sinks  into  a  deep  sleep.  In  the  early  stages 
there  are  no  evidences  of  paralysis,  tremor,  or  convulsion.  The  patellar 
reflexes  are  decreased,  sometimes  abolished.  Gradually  the  lethargy  deepens 
until  finally  the  patient  can  only  be  aroused  with  the  greatest  difficulty,  if 
at  all,  and  immediately  falls  again  into  a  deep  sleep.  Partly  from  the  disease 
itself,  but  largely  because  the  lethargy  prevents  regular  nourishment,  nutri- 
tion fails,  emaciation  becomes  progressively  more  marked,  and  bed-sores 
develop.  Toward  the  close  paralyses  of  various  muscle  groups  develop, 
convulsions  occur,  and  fatal  coma  supervenes. 

Diagnosis. — The  symptoms  are  fairly  characteristic,  but  a  positive  recog- 
nition of  the  disease  is  rendered  easy  by  lumbar  puncture,  centrifugaliza- 
tion  of  the  cerebrospinal  fluid,  and  demonstration  of  the  parasites  by  a 
microscopic  examination  of  the  sediment. 

Prognosis. — The  course  of  the  disease  is  chronic.  Cases  may  last  from 
three  to  four  years.  The  prognosis  is  bad.  There  is  no  record  of  the 
recovery  of  an  authentic  case  of  African  lethargy. 

Treatment. — With  regard  to  treatment  it  has  been  found  that  purging 
in  the  early  stages  does  good  and  in  some  cases  temporarily  arrests  or  delays 
the  disease.  Massive  doses  of  arsenic  are  of  some  service  and  should  be  used 
on  account  of  their  supposed  value  in  trypanosoma  fever. 


KALA-AZAR. 

Definition. — Kala-azar  or  Tropical  Splenomegaly,  sometimes  called  Dum 
Dum  Fever,  is  a  chronic  infectious  disease,  characterized  by  long-con- 
tinued fever,  extreme  emaciation,  profound  ansemia,  marked  enlargement  of 
the  liver  and  spleen,  and  a  characteristic  pigmentation  of  the  skin. 

Much  uncertainty  has  existed  as  to  the  nature  of  kala-azar,  and  our 
present  knowledge  rests  largely  upon  the  investigation  of  Leishman,  who 
showed  that  it  is  a  form  of  trypanosomiasis.  (See  Trypanosomiasis.) 
This  investigator,  with  Marchand,  James,  Bentley,  Rogers  and  others,  has 
found  the  so-called  Leishman  bodies  in  persons  sufl'ering  from  typical 
kala-azar  in  various  parts  of  the  world,  as  in  the  Egyptian  Soudan,  Algiers, 
and  in  Assam.  Airde  has  also  made  confirmatory  investigations  in  China. 
These  Leishman  bodies  are  minute,  spherical,  oval  forms  closely  resem- 
bling the  chromatin  masses  seen  in  stained  trypanosomes.  They  are 
found  chiefly  in  the  spleen  and  liver,  and  can  be  obtained  during  life  by 
puncturing  the  spleen  with  a  fine  exploring  needle,  the  fluid  contained  in 
them  being  expelled  upon  a  glass  slide  and  stained  by  the  Romanowsky 
method. 

The  Leishman  bodies  or  parasites  are  capable  of  developing  into  flag- 
ellated organisms  closely  resembling  trypanosomes,  but  differing  somewhat 
in  the  position  of  the  flagellum. 

Manson  believes  that  the  intermediate  host  of  this  parasite  is  some 
scavenger-fly  which  derives  the  parasite  from  the  intestinal  or  other  dis^ 
charges  of  the  patient  and  then  infects  the  human  being  by  a  bite.    There 


g84  DISEASES  DUE   TO  ANIMAL  PARASITES 

may  be  a  sexual  multiplication  in  the  fly,  but  in  the  human  host  the  para- 
site multiplies  by  fission,  and  Manson  thinks  that  this  multiplication  is 
asexual. 

Pathology  and  Morbid  Anatomy. — The  autopsy  in  a  case  of  kala-azar  shows' 
enormous  enlargement  of  the  spleen,  which  is  firm  and  friable.  The  Hver 
is  also  greatly  enlarged  and  toughened  in  texture.  The  bone-marrow  and 
the  organs  just  named  are  crowded  with  the  parasites.  Leishman  bodies 
can  also  be  found  in  the  lymphatic  glands,  the  suprarenal  capsules,  in  the 
testicles,  and  in  the  inflammatory  exudates  in  the  pleura  and  peritoneum. 
The  direct  cause  of  death  seems  to  be  an  associated  dysentery  or  pneu- 
monia. 

Sjrmptoms. — -The  symptoms  in  onset  resemble  those  of  malarial  fever, 
being  characterized  by  daily  chills  and  fever,  followed  by  free  sweating, 
these  symptoms  recurring  about  the  same  time  every  afternoon.  After  a 
period  of  ten  days  or  two  weeks  these  symptoms  diminish  and  a  period  of 
remission  occurs  followed  after  another  period  of  ten  days  or  two  weeks  by 
a  return  of  the  paroxysm.  This  may  last  for  weeks  or  months.  Occasion- 
ally the  remissions  already  spoken  of  fail  to  occur,  and  profound  inanition 
develops  after  some  months.  In  still  other  cases  the  febrile  movements  are 
exceedingly  irregular  and  varied.  Enlargement  of  the  liver  and  spleen 
begin  early.  The  patient  complains  of  languor,  dyspnoea,  and  the  general 
manifestations  of  profound  anaemia.  The  constant  symptoms  are  fever, 
enlargement  of  the  liver  and  spleen,  the  progressive  emaciation,  and  grave 
anaemia. 

Treatment. — No  method  of  treatment  has  as  yet  been  discovered  which 
produces  any  good  results. 


NEMATODES. 

Ascariasis. — Ascaris  lumbricoides,  or  round  worms,  are  found  in  the  small 
intestine  of  man  more  commonly  than  any  other  parasite. 

They  are  not  segmented  as  are  the  cestodes,  but  occur  as  smooth  worms, 
not  unlike  an  ordinary  earth-worm,  except  that  they  are  provided  with 
small  papillae  or  hairs.  The  worm  also  possesses  longitudinal  striae  and 
transverse  rings,  a  mouth,  and  an  anus.  They  are  not  hermaphroditic,  but 
occur  in  the  form  of  the  male  and  female  worm. 

They  are  met  with  far  more  frequently  in  children  than  in  adults.  The 
female  worm  is  of  a  light-brown,  or  red,  color,  and  is  usually  about  10  to  20 
cm.  long  and  0.5  cm.  thick.    The  male  is  about  one-half  the  size  of  the  female. 

How  these  worms  gain  access  to  the  body  is  not  known,  although  it 
may  be  by  ingestion.  While  they  most  commonly  are  found  in  the  small 
intestine,  they  occasionally  find  their  way  from  the  intestine  into  the  stom- 
ach, and  cases  are  on  record  in  which  they  have  wandered  into  the  oesoph- 
agus and  mouth,  and  even  into  the  nose  and  bronchial  tubes.  Cases  have 
also  been  reported  in  which  the  migration  of  a  worm  into  the  gall  passages 
has  produced  obstruction,  and  still  other  instances  are  recorded  in  which 
they  have  found  their  way  through  an  ulcer,  or  through  a  perforation  in  the 


NEMATODES  885 

appendix  vermiformis,  into  the  peritoneal  cavity.  As  a  rule  they  are  present 
in  the  intestines  in  numbers  and  do  not  occur  singly.  In  rare  cases  coiled, 
mottled  masses  of  lumbricoids  have  caused  intestinal  obstruction. 

A  form  of  round  worm,  somewhat  like  that  found  in  man,  is  found  in  the 
intestine  of  cats  and  dogs,  but  it  is  considerably  smaller  in  size  and  does 
not  infest  man. 

Symptoms. — The  symptoms  of  the  presence  of  this  worm  do  not  differ 
materially  from  those  produced  by  the  tapeworm  (which  see).  Occasionally, 
however,  this  worm  seems  to  have  the  power  of  producing  an  irritant  poison 
which  not  only  causes  intestinal  irritation,  but  when  absorbed  may  cause 
great  nervous  irritation  and  apparently  be  responsible  for  convulsions  in 
young  children. 

Treatment. — The  treatment  of  a  patient  suffering  from  Ascaris  lumhri- 
coides  is  abstinence  from  food  for  twelve  or  eighteen  hours  and  the  admin- 
istration of  1  drachm  of  the  fluid  extract  of  spigelia,  or  2  drachms  of  the 
more  old-fashioned,  but  efficacious,  fluid  extract  of  spigelia  and  senna.  In 
other  cases,  5  to  15  minims  of  the  oil  of  chenopodium  in  capsule  or  emulsion, 
or  on  sugar,  may  be  administered.  In  still  other  cases  from  2  to  5  grains 
of  santonin  may  be  given  in  tablets  or  troches.  All  of  these  drugs  should 
be  followed  by  castor  oil  or  a  saline  purge  in  order  to  sweep  out  the  worms 
while  they  are  poisoned  by  the  drug. 

Ox5niris  Vermicularis. — Under  the  name  Oxyuris  vermicularis  or  thread- 
worm, sometimes  called  pin-worm,  a  very  small  nematode  worm  exists  in 
the  rectum  of  young  children  and  is  sometimes  found  in  adults.  Occasionally 
it  infests  the  entire  colon.  The  length  of  the  female  is  about  10  mm.,  and 
of  the  male  about  4  mm.  This  worm  may  be  present  in  great  numbers 
without  producing  any  symptoms  whatever.  Some  irritation  about  the 
anus  may  be  the  only  disturbance  produced  by  their  presence. 

Seat-worms  are  to  be  removed  by  the  injection  into  the  bowel  of  soap  and 
water,  which,  after  it  is  passed,  is  to  be  followed  by  a  pint  of  warm  water 
which  has  been  medicated  by  boiling  in  it  from  ^  to  1  ounce  of  quassia  chips. 

Trichina  Spiralis. — A  patient  infected  by  the  parasite  known  as  the 
Trichina  spiralis  is  said  to  suffer  from  trichiniasis.  This  parasite  was  first 
described  by  Owen  in  1835.  It  was  found  in  the  flesh  of  the  hog  by  Leidy 
in  1847,  and  in  a  human  being  by  Zenker  in  1860,  the  patient,  a  young  girl, 
being  thought  to  be  a  sufferer  from  enteric  fever  until  at  autopsy  the 
parasites  were  found  free  in  the  bowel  and  encapsulated  in  the  mus- 
cles. 

Etiology. — In  practically  every  case  the  infection  of  a  human  being  comes 
from  eating  the  flesh  of  an  infected  hog.  It  is  scarcely  necessary  to  state 
that  infection  does  not  occur  if  the  pork  has  been  well  cooked. 

The  frequency  with  which  the  disease  occurs  is  not  known,  but  it  is  not 
as  rare  as  some  have  thought.  Williams  found  it  present  27  times  in  505 
unselected  autopsies  in  Buffalo,  New  York. 

If  the  muscle  of  a  man  infected  by  this  parasite  is  examined,  tiny  little 
white  or  gray  dots  will  be  found  upon  its  surface  and  through  its  texture; 
later  the  parasites  encapsulate  and  look  like  deposits  of  calcareous  material 
of  about  the  size  of  miliary  tubercles.     If   such  a  calcareous  deposit  be 


886  DISEASES  DUE   TO  ANIMAL  PARASITES 

opened  it  may  be  found  to  contain   the  embryo  of  the  parasite,  or  if  the 
worm  be  dead  a  granular  detritus  only  is  present. 

When  uncooked  meat  containing  this  parasite  is  swallowed,  the  digestive 
juices  dissolve  the  capsule  of  the  parasite,  and  in  this  way  the  embryos 
are  set  free  in  the  stomach.  Here  they  rapidly  develop  and  become  sexually 
mature  in  about  seven  days.  The  female  parasite  gives  off  an  immense 
number  of  embryos,  so  that  it  is  estimated  that  one  parasite  may  throw 
off  from  one  to  two  thousand  young.  These  parasites  soon  find  their 
way  through  the  wall  of  the  intestine,  enter  the  lymph  spaces,  and  so  reach 
the  circulation,  by  which  they  pass  to  the  muscles.  Their  favorite  position 
for  settlement  is  the  striated  muscles.  They  enter  the  muscular  connective 
tissue  and  then  the  sarcolemma,  where  they  coil  themselves  and  cause  a 
disintegration  of  the  contractile  substance.  Here  they  become  encapsu- 
lated in  about  six  weeks,  partly  by  the  inflammatory  exudate  which  is 
produced  by  their  presence,  and  partly  by  the  calcareous  material  which 
they  seem  to  have  the  power  of  collecting.  In  these  capsules  the  para- 
site remains  alive  for  a  very  long  period  of  time,  possibly  for  twenty-five 
years.  Occasionally,  however,  it  dies,  and  the  entire  mass  undergoes 
calcification. 

When  one  of  the  domestic  animals  swallows  meat  infected  in  this  way, 
the  same  process  takes  place  in  the  muscles  as  occurs  in  the  muscles  of 
man.  In  the  muscles  of  the  hog  the  parasite  may  escape  notice,  as  it 
often  lacks  the  calcified  capsule.  Moreover,  an  infected  hog  may  be  in 
excellent  health. 

Pathology  and  Morbid  Anatomy. — The  lesions  of  trichiniasis  consist  in 
gastrointestinal  irritation,  overgrowth  of  the  lymph  nodes  in  the  abdominal 
cavity,  occasionally  bronchopneumonia  with  great  swelling  of  the  bronchial 
glands,  still  more  rarely  fatty  degeneration  of  the  liver,  and  constantly  a 
parasitic  myositis  due  to  the  embryos  invading  the  muscles.  Almost  every 
muscle  of  the  body  may  be  found  infected;  but  where  the  number  of 
trichinae  is  not  very  great,  the  muscles  of  the  neck,  the  intercostal  muscles, 
and  the  diaphragm  seem  to  be  the  parts  in  which  the  greatest  aggregations 
occur.  Furthermore,  the  greatest  number  of  trichinse  are  usually  found 
near  the  insertions  of  the  muscles. 

Symptoms. — The  symptoms  consist  in  muscular  soreness  and  fain,  and 
disinclination  to  move.  A  diagnosis  of  muscular  rheumatism  is  often  made 
because  of  these  symptoms.  Headache,  puffiness  of  the  skin  about  the  eyes 
and  nose,  and  moderate  fever  are  also  present.  Not  rarely  the  symptoms 
may  closely  resemble  those  of  typhoid  fever,  with  great  prostration  and 
emaciation.  For  some  unknown  reason  a  marked  leukocytosis  develops, 
which  is  peculiar  in  the  fact  that  the  eosinophile  corpuscles  are  chiefly 
increased.  From  investigations  made  by  Opie  it  would  appear  probable 
that  this  eosinophilia  is  of  some  value  from  both  a  diagnostic  and  prognostic 
standpoint.  The  eosinophiles  are  not  greatly  increased,  if  the  infection  by 
trichinse  is  excessive,  and  their  greatest  development  seems  to  occur  at  about 
the  time  that  the  embryonal  trichinse  are  passing  from  the  intestine  by  way 
of  the  lymphatics  and  blood  to  the  muscular  tissues — that  is,  during  the 
third  week  after  the  ingestion  of  the  trichinatous  meat. 


NEMATODES  887 

Diagnosis. — In  a  suspected  case  the  diagnosis  may  be  reached  by  taking 
a  small  piece  of  muscle  and  examining  it  with  a  microscope.  The  stools 
of  the  patient  should  be  flattened  to  a  thin  layer  between  two  sheets  of 
glass  resting  upon  a  black  background,  and  then  examined  by  means  of  a 
hand  magnifying  glass,  when  the  parasite  may  be  found  as  small,  short, 
glistening,  thread-like  bodies. 

Prognosis. — The  prognosis  depends  largely  upon  the  severity  of  the  infec- 
tion. In  the  worst  outbreaks  the  mortality  may  be  as  high  as  70  per  cent. 
Many  cases  recover  by  the  end  of  a  fortnight.  Others  remain  ill  for  weeks 
or  months  before  recovery  takes  place. 

Treatment. — There  is  no  treatment  which  can  be  directed  to  the  removal 
of  the  parasite  after  it  has  entered  the  muscles.  The  only  thing  the  physician 
can  do  is  to  give  a  nutritious  diet,  and  relieve  pain  or  other  symptoms  by 
symptomatic  remedies.  If  the  discovery  is  made  that  the  patient  has 
swallowed  trichinatous  pork  within  a  few  hours,  then  5  grains  of  thymol 
followed  by  a  dose  of  castor  oil  or  sulphate  of  magnesium  should  be  ordered 
to  kill  the  parasite  and  sweep  it  out  of  the  intestines  before  it  can  migrate 
into  the  tissues. 

Uncinariasis  (Ankylostomiasis).  Definition. — Uncinariasis  is  an  infec- 
tion by  different  varieties  of  worm  of  the  uncinaria  species;  it  occurs  not 
only  in  man,  but  in  many  of  the  lower  animals.  The  parasite  is  often 
called  the  Ankylostomum  duodenale,  or  hook-worm.  The  chief  symptoms 
are  severe  anemia,  abdominal  pains,  asthenia  without  emaciation,  and 
oedema.  The  parasite  was  described  as  uncinaria  by  Froelich  in  1789; 
Dubini  in  1843  gave  it  the  name  ankylostoma. 

The  condition  is  also  known  as  "  brickmakers'  anaemia,"  "  Egyptian 
chlorosis,"  "  miners'  anaemia,"  "  miners'  cachexia,"  "  miners'  disease," 
"  Porto  Rican  anaemia,"  "  St.  Gothard's  tunnel  disease,"  "  tunnel  dis- 
ease," "tunnel  anamia,"  "tropical  chlorosis,"  and  "hook-worm  disease," 
besides  a  host  of  local  names.  It  is  one  of  the  most  ancient  diseases 
known  to  man,  for  it  was  described  by  the  Egyptians  3500  years  ago. 

Frequency. — Uncinariasis  occurs  in  all  the  tropical  and  practically  all 
the  subtropical  world.  According  to  Thornton  it  is  the  greatest  enemy  of 
the  human  race  in  the  tropics;  greater  even  than  plague  or  cholera.  In 
portions  of  India  75  per  cent,  of  the  population  are  said  to  be  affected. 
In  Egypt  this  worm  is  found  at  nearly  every  postmortem.  It  has  been 
the  most  disabling  of  all  diseases  in  the  Egyptian  army,  as  well  as  the 
greatest  cause  for  the  rejection  of  recruits.  In  Ceylon  its  ravages  are 
said  to  be  more  serious  than  those  of  cholera.  Harris  has  found  it  in 
Georgia  and  Florida,  and  believes  it  is  the  common  cause  of  the  severe 
anaemias  of  the  Southern  United  States  that  have  hitherto  been  re- 
garded as  malarial.  Stiles  has  also  made  very  valuable  studies  of  its 
characters  and  recurrence  in  the  Southern  United  States.  In  Assam 
it  is  almost  universal,  299  cases  having  been  found  in  300  postmortems. 
According  to  Alden,  22.5  per  cent,  of  the  total  death  rate  of  Porto  Rico 
is  ascribed  to  tropical  anaemia  due  to  uncinaria.  In  more  temperate  re- 
gions it  has  been  found  in  nearly  all  our  States  as  far  north  as  New  York. 
In  the  Cornwall  and  Westphalian  mines  the  disability  caused  by  this  para- 


DISEASES  DUE   TO  ANIMAL  PARASITES 


Fig.  112 


Male  of  Ankylostoma  duodenale  :  a,  head ;  &,  oesophagus ;  c, 
gut ;  d,  anal  glands ;  e,  cervical  glands  ;/,  skin  ;  g,  muscular  layer; 
hi  excretory  pore  ;  i,  tri-lobed  bursa  ;  k,  ribs  of  bursa ;  I,  seminal 
duct  ;  m,  vesicula  seminalis  ;  n,  ductus  ejaculatorius  ;  o.  its  groove; 
p,  penis;  q,  penile  sheath.  Magnification,  20.  (After  Schulthess, 
from  Ziegler.) 


site  has  become  so  great  as  to  threaten  the 
existence  of  these  industries. 

Etiology. — The  uncinaria  is  a  nematode 
worm  of  the  family  Strongylidce.  It  is  very 
widely  distributed  in  the  animal  world,  in 
distinct  species.  In  man  two  species  are 
recognized,  viz.,  Uncinaria  duodenale  (Dubini) 
and  Uncinaria  Americana  (Stiles),  commonly 
spoken  of  as  the  old-world  and  the  new- 
world  uncinaria,  or  hook-worm.  The  two 
sexes  are  distinct;  the  male  worm  is  from  8 
to  10  mm.  long  and  the  female  slightly 
longer,  10  to  18  mm.  They  are  grayish-white 
in  color,  cylindrical  in  shape,  with  a  con- 
tracted head,  and  in  the  female  a  broad 
caudal  bursa.  When  male  and  female  worms 
are  present,  as  they  usually  are  in  the  propor- 
tion of  one  male  to  three  females,  the  female 
produces  an  enormous  number  of  ova.  When 
deposited  in  favorable  surroundings  these  ova 
develop  into  embryos  in  twenty-four  hours. 
The  embryo  grows  rapidly,  passing  through 
two  ecdyses  in  about  five  days.  The  second 
ecdysis  is  the  termination  of  the  extra-cor- 
poreal phase,  and  the  embryo  is  now  infec- 
tive for  man.  When  taken  into  its  appropriate 
host  the  worm  goes  through  three  more  ecdyses, 
making  five  in  all;  the  fourth  marking  the 
formation  of  a  provisional  buccal  armature; 
the  fifth,  the  appearance  of  the  definite  arma- 
ture. It  then  reaches  an  adult  or  mature 
form  in  from  five  to  six  weeks. 

The  sources  of  infection  are  the  ingestion 
of  infected  water  or  food,  the  accidental  inges- 
tion of  infected  earth  from  soiled  hands, 
and  infection  through  the  skin  during  or  after 
the  second  ecdysis  of  the 
worm.  The  mode  of  in- 
fection by  earth  is  obvi- 
ous. In  all  regions  af- 
fected by  uncinaria,  dirt 
and  clay  eating  are  very 
common  habits.  There 
is  no  doubt  that  geophagy 
in  infected  areas  is  a 
common  manner  of  tak- 
ing the  disease;  but  it  is 
also  true  that  this  habit 
does  not   show   itself,  in 


NEMATODES 


889 


many  cases,  until  the  disease  is  fully  developed.  In  these  cases  it  seems 
clear  that  the  earthy  matter  is  eaten  in  obedience  to  an  instinctive  craving, 
and  that  it  brings  relief  by  mechanically  loosening  a  number  of  the  para- 
sites. That  infection  may  take  place  through  the  skin,  the  experiments  of 
Looss  and  many  clinical  observations,  as  well  as  accidental  laboratory  infec- 
tions, have  made  quite  apparent.  It  has  often  been  observed  that  children, 
v^alking  barefooted  through  infected  ground,  became  infected.  The  disease 
known  as  Pani-Ghao,  and  the  "ground  itch"  of  the  South,  are  probably  skin 
infections  by  this  parasite,  the  lesions  representing  the  point  of  entrance  of 
the  parasite  into  the  human  host.  Looss  experimented  with  the  young 
worms  in  a  mixture  of  earth  and  charcoal.  This  mixture  was  placed  on  the 
skin  of  dogs  without  scarification  or  friction.  The  parasites  were  found  in 
the  intestines  as  rapidly  as  when  experimental  infection  by  the  mouth  was 


Fig.  113 


Ova  and  embryo  of  Uncinaria  AEoericana  :  a,  unicellular  ovum ;  6,  c,  d,  e,  ova  showing  various  stages 
of  segmentation ;  /,  g,  ova  containing  larval  uncinarise  ;  h,  peculiarly  shaped  ovum ;  i,  larval  worm 
just  emerged  from  shell ;  j,  larva  extended  after  emergence.    (Stiles.) 


made.  While  making  these  experiments  he  accidentally  allowed  some  of 
the  mixture  to  remain  on  his  own  hand  and  himself  became  infected. 
Air-borne  infection  occurs  very  rarely,  if  ever. 

Prophylaxis. — Prophylaxis  of  uncinariasis  demands  the  exclusion  of  all 
infected  persons  from  earth-workings.  Where  large  bands  of  laborers  are 
collected  in  districts  in  which  the  disease  is  prevalent,  in  mines,  in  tunnels, 
and  in  excavations  of  all  kinds,  systematic  examination  of  all  cases  of  anaemia 
should  be  made.  Defecation  in  the  workings  or  tunnels  should  be  rigorously 
prohibited.  Water-tight  latrines  should  be  provided,  and  the  contents 
rendered  harmless  by  a  cheap  disinfectant.  In  the  Arlberg  tunnels  the 
pail  system  has  been  recently  used  with  good  effect.  Personal  prophylaxis 
should  include  careful  washing  of  the  hands  before  eating,  and  the  wearing 
of  sound  shoes  when  working  in  suspected  soils. 


890  DISEASES  DUE   TO  ANIMAL  PARASITES 

Pathology  and  Morbid  Anatomy. — Postmortem  the  subcutaneous  fat,  the 
panniculus  adiposus,  and  the  mesenteric  fat  are  fairly  well  preserved.  The 
parasites  are  found  in  the  jejunum,  still  attached  to  the  bowel  wall  if  the 
section  is  early,  or  free  in  the  intestinal  contents  if  the  section  is  delayed. 
They  vary  in  number  from  100  to  600  or  more.  The  jejunum  is  covered 
with  old  and  recent  pinhead  bloody  extravasations.  The  bowel  is  thickened 
in  spots,  and  there  may  be  small  cavities  in  the  bowel  wall  filled  with  blood 
and  containing  the  heads  of  one  or  two  parasites.  The  liver  and  kidneys 
commonly  show  some  degree  of  fatty  degeneration.  The  cause  of  the  anaemia 
is  probably  twofold — the  mechanical  abstraction  of  a  considerable  amount  of 
blood  by  the  parasites,  and  a  hsemolytic  effect  from  a  toxin  elaborated 
by  the  worm.  That  haemolysis  occurs  is  indicated  by  increased  iron  in  the 
liver,  the  occurrence  of  haematoidin  in  the  liver  and  kidneys,  as  well  as  free 
iron  in  the  stools. 

The  blood  shows  the  ordinary  changes  similar  to  those  observed  in 
pernicious  anaemia.  In  early  cases  the  color-index  may  be  low,  the  loss  of 
haemoglobin  being  more  rapid  at  first  than  the  red-cell  loss.  As  the  case 
advances,  however,  the  haemoglobin  index  rises  and  may  be  plus.  Megalo- 
blasts  are  not  seen  in  as  large  numbers  as  in  other  pernicious  anaemias. 
There  is  no  marked  leukocytosis;  there  is,  however,  a  fairly  constant  rela- 
tive increase  in  the  eosinophiles,  ranging  from  3  to  30  per  cent. 

The  feces  contain  the  ova.  They  also  contain  considerable  blood,  in 
which  differential  staining  will  demonstrate  a  great  many  eosinophiles, 
showing  that  there  is  not  only  a  general  increase  in  these  cells  in  the  circu- 
lation, but  that  there  is  an  active  determination  of  them  to  the  intestinal 
lesions.     Charcot-Leyden  crystals  are  constantly  present. 

Symptoms. — The  symptoms  vary  with  the  number  of  parasites  in  the 
intestines  and  with  the  general  condition  of  the  patient.  Recent  obser- 
vations seem  to  make  it  clear  that  the  new-world  hook-worm  is  not  nearly 
so  fatal  as  the  old-world  hook-worm.  If  there  be  but  a  few  worms,  the 
general  symptoms  produced  are  very  mild.  If,  on  the  other  hand,  the 
worms  run  up  into  the  hundreds,  or  thousands,  the  blood  destruction  is 
extensive.  In  conditions  of  great  deterioration,  in  the  half-starved  or  ill- 
nourished,  in  acute  or  chronic  dysentery  the  presence  of  only  a  few  of 
these  parasites  may  act  as  a  very  dangerous  complication. 

In  well-developed  cases  the  symptoms  are  those  of  pernicious  anoemia. 
The  principal  phenomena  are  dyspeptic  symptoms  with  colicky  pains  in  the 
early  stages,  followed  by  progressive  ancemia  with  little  or  no  emaciation, 
and  with  terminal  oedema.  The  pain  in  uncinariasis  is  colicky  in  character, 
is  one  of  the  earliest  symptoms,  and  is  fairly  constant  throughout  the  disease. 
In  cases  in  which  only  a  few  parasites  are  present,  it  may  amount  only  to 
uneasiness;  when  there  are  many,  it  may  be  severe.  Like  all  abdominal 
pains  due  to  intestinal  parasites  it  is  relieved  by  food  for  the  time  being. 
The  appetite  is  very  variable;  it  may  be  voracious  or  it  may  be  diminished, 
and  curious  perversions  of  taste,  such  as  earth-eating,  may  develop. 

Following  the  development  of  the  colic,  ancemia  appears  and  rapidly 
becomes  profound.  There  is  very  little  wasting,  the  subcutaneous  fat  being 
fairly  well  preserved.    The  skin  is  a  lemon-white  color;  the  conjunctivae  and 


NEMATODES  891 

lips  are  exsanguinated;  the  sclerse  pearly  or  muddy-white.  All  the  subjec- 
tive phenomena  of  profound  anaemia  become  marked.  There  is  lassitude, 
breathlessness  on  the  slightest  exertion,  vertigo,  and  occasionally  dimness 
of  vision  from  retinal  hemorrhages.  Crises  of  fever  occur  that  may  last 
for  days  or  weeks.  Auscultation  over  the  prsecordial  area  reveals  soft 
haemic  bruits,  propagated  to  a  remarkable  distance  into  the  great  vessels. 
The  face  and  ankles  become  puffy,  and  there  may  be  a  slight  general  oedema. 
Harris  has  reported  a  case  of  uncinariasis  with  symptoms  resembling 
pellagra.  When  the  disease  attacks  children  before  the  age  of  puberty, 
bodily  and  mental  growth  are  stunted.  The  pubic  hair,  the  axillary  hair,  and 
the  hair  on  the  face  is  scanty  or  absent,  the  limbs  are  thin  and  undeveloped, 
and  the  children  are  markedly  pot-bellied.  Stiles  describes  a  fish-like, 
staring  expression  of  the  eyes  in  these  cases. 

Diagnosis. — ^The  diagnosis  is  easy,  once  the  attention  is  directed  to  the 
intestinal  parasites.  The  occupation  of  the  patient,  if  it  be  one  that  predi- 
cates working  in  earth,  is  very  suggestive.  The  anaemia  is  very  commonly 
diagnosticated  as  malarial.  There  really  is  no  diagnostic  difiiculty  between 
malarial  anaemia  and  the  parasitic  anaemia.  This  very  common  error  has 
been  made  because,  in  the  intensely  malarial  regions,  the  existence  of  this 
parasite  has  not  been  generally  known.  The  disease  has  also  been  mistaken 
for  beriberi,  but  there  is  a  complete  absence  of  paralytic  symptoms  in 
uncinariasis. 

A  diagnostic  sign,  recently  described,  is  the  occurrence  of  triangular  black 
or  bluish  patches  on  the  dorsum  of  the  tongue,  looking  as  though  a  pen 
had  been  wiped  on  it.  This  appearance  is  quite  striking.  Recent  obser- 
vations have  shown  that  it  is  very  constant;  that  it  appears  early,  even 
before  the  advent  of  pronounced  anaemia,  and  persists  to  the  end  of  the 
disease. 

The  diagnosis  is  definitely  made  by  the  demonstration  of  the  ova  or 
parasites  in  the  feces.  Search  should  be  made  in  as  fresh  specimens  as 
possible,  to  avoid  confusion  in  case  embryos  have  occurred  and  quitted  the 
ova.  A  small  amount  of  the  material  is  placed  on  a  large  glass  slide  diluted 
with  distilled  water,  and  pressed  down  with  a  thick  cover.  The  ova  of 
uncinaria  are  very  striking  bodies.  They  are  clear,  transparent,  light  gray 
in  color;  they  have  a  delicate,  transparent  capsule,  containing  in  its  centre 
from  one  to  six  gray  yolk  segments  with  granular  nuclei.  In  shape,  they 
are  regularly  oval,  with  an  average  length  of  60  microns  and  an  average 
width  of  35  microns.  Leichtenstern  has  found  as  many  as  4,216,930  ova 
in  a  single  stool.  Care  must  be  taken  not  to  mistake  the  egg  of  the  Ascaris 
lumbricoides  for  the  egg  of  the  uncinaria.  The  former  have  a  thick,  gela- 
tinous, often  mammillated  covering,  and  unsegmented  protoplasm.  So,  too, 
the  egg  of  the  Oxyuris  vermicular  is,  which  is  a  thin,  symmetrical  shell,  one 
side  of  which  is  almost  straight  and  which  contains  an  embryo,  may  be 
mistaken  for  the  ova  of  the  uncinaria.  The  egg  of  the  whip-worm,  Triclio- 
cephalus  dispar,  possesses  a  smooth,  thick  shell,  apparently  perforated  at 
each  end,  with  unsegmented  protoplasm. 

Stiles  has  recently  described  a  rapid  and  effective  test,  where  micro- 
scopic evidence  cannot  be  obtained.    The  stool  is  placed  on  ordinary  white 


892  DISEASES  DUE   TO  ANIMAL  PARASITES 

blotting-paper,  and  allowed  to  stand  for  one  hour.  A  rusty-red  discoloration 
or  stain  develops  along  the  edge  of  moisture,  resembling  somewhat  that 
due  to  the  presence  of  blood  and  the  probable  presence  of  uncinaria.  Stiles 
directs  that  if  uncinariasis  is  suspected,  and  it  is  not  practicable  either  to 
make  a  microscopic  examination  or  to  delay  matters  until  a  specimen  can 
be  sent  away  for  examination,  still  another  method  of  diagnosis  is  possible. 
Give  a  small  dose  of  thymol,  followed  by  Rochelle  salts,  and  collect  all  of 
the  stools  passed.  Wash  the  stools  thoroughly  several  times  in  a  bucket, 
and  examine  the  sediment  for  worms  about  half  an  inch  long,  about  as 
thick  as  a  hairpin  or  hatpin,  and  with  one  end  curved  back  to  form  a  hook. 

Treatment. — In  the  treatment  of  uncinariasis  there  are  two  drugs  of  value: 
male  fern  and  thymol.  Of  the  two  the  most  effective  is  thymol  or  its  deriva- 
tive, thymol  urethane  (thymol  carbonic  ether).  Thymol  should  be  given 
in  capsule,  or  in  emulsion  with  acacia,  in  30  grain  doses  repeated  in  two 
hours  for  an  adult.  In  these  doses  the  drug  occasionally  causes  vertigo, 
excitement,  and  smoky  urine.  For  one  or  two  days  prior  to  the  administra- 
tion of  the  remedy  patients  should  be  put  on  liquid  diet  and  given  a  brisk 
saline  purge  the  night  before.  On  account  of  the  high  location  of  the  para- 
sites in  the  intestinal  tract,  it  will  not  be  necessary  to  restrict  the  quantity 
of  food.  In  administering  thymol,  it  is  essential  that  none  of  the  solvents 
of  the  drug  be  given  either  with  it  or  immediately  after.  Several  cases  of 
poisoning  have  occurred  when  alcohol  or  alcohohc  drinks  have  been  given 
with,  or  closely  after,  a  dose  of  thymol.  Similarly,  ether,  chloroform, 
glycerin,  and  most  oils  act  as  solvents,  and  may  cause  severe  toxic  symptoms 
owing  to  the  absorption  of  the  drug  in  bulk.  In  order  to  prevent  poisoning, 
therefore,  thymol  should  be  followed  by  a  saline  purge,  and  castor  oil  should 
not  be  used.  Weekly  examinations  of  the  stools  should  be  made,  and  as  long 
as  ova  or  Charcot-Leyden  crystals  are  found  the  use  of  this  remedy  must  be 
repeated.  Sometimes  thymol  is  vomited,  and  in  rare  cases  proves  inactive. 
In  these  the  male  fern  should  be  administered  in  the  usual  way.  After  the 
expulsion  of  the  worm,  the  therapeutic  indications  are  the  same  as  for 
advanced  ancemia  from  any  other  cause. 

Filariasis  (Filaria  Sanguinis  Hominis).  Definition  and  History. — The 
group  of  Filarice  includes  a  number  of  species.  The  human  parasite  was 
first  discovered  by  Demarquai  in  1863  in  a  chylocele  and  demonstrated  in 
the  peripheral  circulation  by  Lewis  in  1872.  The  principal  varieties 
affecting  man  are  the  following:  Filaria  nocturna,  Filaria  diurna,  Filaria 
"per starts,  Filaria  Demarquaii,  Filaria  Ozzardi,  Filaria  Magalhaesi,  and 
Filaria  loa.  Of  this  group  the  Filaria  nocturna  and  the  Filaria  loa  are 
the  only  ones  known  to  cause  definite  pathological  conditions. 

The  geographical  distribution  of  the  Filaria  nocturna  is  very  extensive. 
It  is  found  in  all  tropical  and  in  most  subtropical  countries.  Its  southerly 
limit  of  observation  is  Brisbane.  In  the  United  States  it  has  been  found  in 
Alabama,  Louisiana,  South  Carolina,  Pennsylvania,  Illinois,  and  New  York. 
In  the  Samoan  Islands  from  10  per  cent,  to  50  per  cent,  of  the  inhabitants 
are  said  to  be  infected,  and  in  the  Friendly  Islands  32  per  cent.  In  Porto 
Rico  the  native  troops  showed  12  per  cent.,  and  small  communities  may 
have  as  high  as  70  per  cent,  of  the  total  population  infected. 


NEMATODES  893 

Filaria  Noctuma. — This  parasite  has  two  corporeal  and  one  extra- 
corporeal phase.  First,  the  parent  worm,  whose  normal  habitat  is  the 
lymphatic  system;  second,  the  embryo  found  in  the  circulating  blood,  and 
third,  the  intermediary  stage  in  the  body  of  the  mosquito,  which  has  been 
definitely  shown  to  be  the  intermediary  host  for  this  parasite.  When 
examined  in  a  drop  of  peripheral  blood  the  embryonic  form  is  found  as  a 
minute  transparent  worm,  one-eightieth  of  an  inch  in  length  and  about  the 
diameter  of  a  red  blood  corpuscle.  It  has  a  transparent  sheath,  or  sac, 
somewhat  longer  than  the  body  of  the  embryo,  and  is  usually  present  in 
very  great  numbers. 

The  most  striking  characteristic  of  this  filaria  is  the  periodicity  of  its  appear- 
ance. They  are  found  only  at  night  in  the  peripheral  circulation,  hence  the 
name  Filaria  noctuma.  In  the  daytime  they  entirely  disappear  and  retire  to 
the  larger  vessels,  particularly  the  vessels  of  the  lungs.  The  periodicity  may 
be  reversed  by  causing  the  patient  to  sleep  in  the  daytime,  when,  after  a 
few  days,  the  embryos  are  found  in  the  peripheral  blood  during  the  day 
and  are  absent  at  night. 

The  microscopic  demonstration  of  the  worm  is  easy.  The  blood  should 
be  drawn  near  midnight,  when  the  parasites  are  most  numerous.  A  large 
drop  of  blood  should  be  taken  and  a  thick,  coarse  spread  made.  The  slides 
are  dried  in  air  without  covers,  or,  if  it  is  desired  to  study  the  parasite  in 
motion,  the  blood-drop  is  covered  with  a  cover-slip  and  ringed  with  vaselin. 
In  such  a  preparation  the  filaria  retains  its  motility  for  days.  The  worms 
are  quite  large;  an  inch  objective  will  be  ample  for  the  search  and  demon- 
stration. 

As  already  stated  the  mosquito  is  the  intermediary  host.  When  a  mos- 
quito sucks  the  blood  of  a  patient  containing  filarise  the  parasites  escape 
from  their  sheath  while  the  blood  is  still  in  the  stomach  of  the  insect. 
Thence  they  pass  to  the  thoracic  muscles.  In  this  location,  in  from  six  to 
seven  days,  the  metamorphosis  from  embryo  to  the  young  of  the  adult  form 
takes  place.  The  minute  filarise  migrate  to  the  proboscis  and  are  found 
lying  in  pairs  in  the  labia,  whence  they  are  undoubtedly  carried  into  the 
circulation  of  the  first  warm-blooded  animal  bitten  by  the  insect.  The 
possibility  of  the  filariae  being  passed  into  water  when  the  mosquito  lays  her 
eggs,  and  being  carried  thence  into  the  stomach  in  drinking  water,  is  also 
to  be  remembered.  Female  mosquitoes,  both  of  the  culex  and  anopheles 
species,  are  capable  of  acting  as  the  intermediary  host. 

The  adult  form  of  the  parasite,  commonly  known  as  the  Filaria  Bancrofti, 
is  a  long,  delicate,  nematode  worm.  It  is  from  three  to  four  inches  in  length 
and  the  thickness  of  a  coarse  hair  or  bristle.  The  sexes  are  distinct.  The 
habitat  of  the  parent  worms  is  the  lymphatic  system,  commonly  the  thoracic 
duct,  although  any  portion  of  the  peripheral  lymphatics  may  be  invaded. 
There  may  be  only  one  worm  of  each  sex  or  there  may  be  many. 

The  Filaria  diurna  presents  minor  differences  in  structure  and  appearance 
from  the  Filaria  noctuma.  The  chief  difference  is  in  the  periodicity,  this 
parasite  being  found  in  the  peripheral  circulation  only  in  the  daytime.  It 
is  supposed  that  the  Filaria  diurna  is  the  embryonic  form  of  the  Filaria  ha. 
Nothing  is  known  of  its  pathological  significance, 


894  DISEASES  DUE   TO  ANIMAL  PARASITES 

The  Filaria  ferstans  is  common  in  certain  districts  of  West  Africa,  where 
it  occurs  in  as  much  as  50  per  cent,  of  the  population.  This  parasite  is 
found  in  the  peripheral  circulation  at  all  times,  day  and  night;  hence  its 
name.  The  pathological  significance  of  this  filaria  is  unknown.  It  was 
for  a  time  supposed  to  be  the  cause  of  sleeping  sickness,  and  was  also 
found  very  commonly  in  association  with  crawcraw,  an  itching,  pustular 
affection  of  the  skin. 

Pathology  and  Morbid  Anatomy. — Filariasis  causes  no  symptoms  in  the 
large  majority  of  cases.  The  embryos  are  innocuous.  When  symptoms 
develop  they  are  due  to  the  parent  worm  or  an  immature  product  of  the 
parent  worm.  The  lesions  produced  are  divided  into  two  broad  classes, 
namely,  those  which  are  due  to  lymphatic  varix  from  stasis,  and  those  due 
to  oedema  from  lymphatic  obstruction.  The  parent  worms,  when  present 
in  numbers,  may  mechanically  plug  the  thoracic  duct  or  one  of  the  larger 
lymphatic  trunks.  They  may  also  initiate  a  lymphangitis,  with  thickening 
and  occlusion  of  the  lymphatics.  Under  either  circumstance,  stasis  and 
retrograde  movement  of  the  lymph  current  are  inaugurated  and  eventually 
a  compensatory  lymph  circulation  is  established.  The  result  is  engorgement 
of  some  portion  of  the  lymphatic  system  and  the  development  of  a  peculiar 
group  of  phenomena:  lymph  scrotum,  lymphatic  groin  glands,  varices  of 
the  pelvic  or  lumbar  lymphatic  trunks  or  of  the  lymphatics  of  the  bladder, 
ureter,  or  kidney.  As  these  varicosities  grow,  they  become  more  extensive, 
and  rupture.  If  the  rupture  be  in  the  genito-urinary  tracts,  chyluria 
develops;  if  into  the  tunica  vaginalis,  a  chylocele;  if  into  the  abdominal 
cavity,  chylous  ascites.  These  are  the  lesions  due  to  lymph  stasis  and 
lymphatic  varices. 

In  the  second  group  the  lymph  stasis  is  associated  with  lymphangitis 
followed  by  obstruction,  resulting  in  the  formation  of  the  peculiar  solid 
oedema  and  the  huge  hypertrophies  of  the  affected  tissues  known  as  elephan- 
tiasis. 

The  majority  of  cases  of  elephantiasis  are  clearly  due  to  filarial  disease. 
The  geographical  distribution  of  elephantiasis  and  filariasis  are  identical; 
elephantiasis  is  most  common  in  the  areas  most  severely  affected  by  filaria. 
Lymphatic  varix  and  lymph  scrotum  are  not  only  found  in  the  same  districts 
as  elephantiasis,  but  very  commonly  terminate  in  elephantiasis.  The  disease 
is  also  seen  in  cases  of  operative  removal  of  lymphatic  varices.  In  a  large 
number  of  these  cases  the  embryo  filarise  cannot  be  demonstrated  in  the 
peripheral  circulation.  This  is  due  to  the  fact  that  the  parent  female  worm 
lies  in  the  centre  of  the  inflamed  tissue  and  because  the  embryos  cannot 
pass  through  the  occluded  portion  of  the  lymphatic  circulation.  Manson's 
theory  as  to  the  direct  causation  of  elephantiasis  is  that  the  parent  female 
worm  migrates  to  one  of  the  peripheral  trunks.  While  in  this  position  she 
receives  an  injury  which  is  followed  by  premature  parturition  and  the 
expulsion  of  ova  instead  of  embryos.  These  ova  are  five  times  the  diameter 
of  the  embryos,  so  that  although  the  embryos  pass  freely  through  the  finer 
lymphatic  radicles  the  ova  block  up  the  smaller  lymph  channels,  forming 
minute  emboli. 

Following  this  stage  of  embolism,  lymphangitis  with  inflammatory  thick- 


NEMATODES  895 

ening  occurs.  When  the  inflammatory  process  subsides  the  deposit  is  in 
small  part  absorbed,  but  when  the  inflammation  recurs  an  additional  deposit 
is  added  to  the  remnant  of  the  first.  This  concurs  with  the  commonly 
observed  clinical  history  of  elephantiasis,  which  advances  by  crises  of 
inflammation  and  a  general  symptom-complex  known  as  elephantoid 
fever. 

As  already  stated,  filariasis  may  occur  without  any  symptoms  being 
present  until  the  lesions  just  described  develop. 

Symptoms.  Elephantiasis. — The  most  common  location  of  elephantiasis 
is  in  the  legs;  next  in  the  scrotum  of  the  male  and  the  labia  of  the  female. 
It  occurs  in  the  breast,  in  the  arms,  and  as  interstitial  or  pedunculated 
masses  in  other  parts  of  the  body.  These  tumors  occasionally  grow  to 
enormous  dimensions.  A  scrotal  tumor  of  50  pounds  is  not  at  all  uncommon, 
and  one  has  been  reported  weighing  224  pounds.  These  large  tumors 
develop  as  described  with  elephantoid  fever.  With  each  crisis  of  fever  and 
lymphangitis  there  is  not  only  an  increase  in  the  size  and  bulk  already 
affected,  but  an  extension  into  new  territory. 

Elephantoid  fever  is  the  systemic  expression  of  the  lymphangitis  origin- 
ating in  filarial  varices  or  in  tissues  already  the  seat  of  elephantiasis.  The 
attacks  recur  at  varying  intervals  of  weeks  or  months.  Exciting  causes  may 
be  slight  traumatism  such  as  friction  of  the  clothing  over  the  occluded  lymph 
channels..  The  attack  begins  with  rigor  and  high  fever,  with  all  the  usual 
manifestations  of  febrile  disturbance,  as  anorexia,  nausea,  and,  in  severe 
cases,  delirium.  The  skin  over  the  inflamed  lymphatic  area  is  hot,  tense, 
and  red,  with  a  marked  degree  of  inflammatory  thickening.  After  persisting 
a  few  days,  the  attack  ends  in  a  critical  sweat.  The  inflammatory  thickening 
remains.  The  attack  may  be  so  intense  as  to  result  in  the  formation  of 
abscess.  When  this  takes  place  in  superficial  lesions,  the  condition  is  readily 
recognized  and  the  treatment  is  obvious.  When  it  occurs  in  the  deeper 
varices,  as  in  the  pelvis  or  loin,  there  will  be  deep-seated  pain,  tenderness, 
and  rapidly  developing  sepsis. 

HcBmatochyluria  is  usually  paroxysmal  and  is  due  to  the  leakage  of  chyle 
into  some  portion  of  the  genito-urinary  tract.  The  common  location  of  the 
leak  is  in  the  lymphatics  surrounding  the  pelvis  of  the  kidneys  or  the  lymph- 
atics of  the  bladder.  The  appearance  of  chyle  in  the  urine  is  intermittent 
and  is  not  accompanied  by  any  increase  of  symptoms.  The  urine  is  opaque 
and  varies  in  color  from  a  milky-white  to  a  deep  red  in  proportion  to  the 
amount  of  blood  that  may  be  mixed  with  the  chyle.  Chylous  urine  coagu- 
lates on  standing  into  a  soft,  jelly-like  clot.  In  a  few  hours  the  clot  contracts 
and  forms  a  firm,  white  ball  floating  in  a  milky  fluid.  Microscopically,  the 
urine  contains  fat,  blood  cells  in  varying  amount,  and  occasionally  embryo 
filaria.  Chyluria  may  persist  for  many  years  without  great  deterioration  of 
health.  The  only  symptoms  may  be  a  dull  pain  in  the  loins  or  pelvis.  Osier 
reports  a  case  of  intermittent  chyluria  which  persisted  for  eighteen  years 
without  any  special  discomfort.  When  chyle  escapes  in  large  quantities, 
clots  are  occasionally  formed  in  the  bladder  and  may  cause  urinary  retention. 
Medical  treatment  is  of  no  avail  in  this  condition,  but  the  patient  should  be 
put  at  rest  on  dry  diet,  with  as  great  restriction  as  possible  in  the  fatty 


896  DISEASES  DUE  TO  ANIMAL  PARASITES 

elements  of  his  food.  Under  this  regimen  the  amount  of  chyle  may  be 
notably  diminished. 

Varicose  groin  glands  is  a  varicose  condition  of  the  superficial  and  deep 
inguinal  lymphatics,  and  it  is  usually  bilateral.  It  gives  rise  to  doughy, 
soft,  painless  swellings  in  both  groins.  They  cause  little  trouble  until 
lymphangitis  develops,  when  they  may  become  very  painful.  They  have 
been  mistaken  for  the  buboes  of  plague,  and  are  commonly  mistaken  for 
hernia. 

Lymph  Scrotum. — In  this  condition  the  filarial  varix  is  situated  in  the 
lymphatics  of  the  scrotum  and  is  usually  bilateral.  It  may  be  associated 
with  the  enlargement  of  the  groin  glands,  and,  Uke  that  state,  it  is  prone  to 
accessions  of  lymphangitis.  When  the  deeper  lymphatics  are  involved,  the 
lymphangitis  may  extend  to  the  testicle,  forming  what  is  known  as  filarial 
orchitis. 

Treatment. — The  treatment  of  these  conditions  is  surgical.  When  the 
tumors  become  so  large  as  to  be  a  burden  to  the  patient,  or  when  the  inflam- 
matory symptoms  cause  great  pain,  their  removal  should  be  undertaken. 
The  removal  of  an  enormous  scrotum  or  the  amputation  of  a  gigantic  limb 
may  be  done  to  rid  the  patient  of  a  drag  that  has,  by  its  sheer  weight,  anchored 
him  to  his  bed  or  chair  for  years.  These  growths  may  be  removed  with 
comparatively  little  risk.  All  surgical  treatment  in  filarial  disease  must 
be  regarded  as  palliative  unless  the  parent  female  worm  is  included  in  the 
excised  tissues,  when  the  cure  will  be  a  definite  one. 

As  far  as  any  plan  of  treatment  aimed  at  the  destruction  of  this  parasite, 
adult  or  embryo,  is  concerned,  there  is  no  remedy  of  even  the  slightest 
value.  During  the  attacks  of  filarial  or  elephantoid  fever  the  affected  part 
should  be  elevated,  coohng  lotions  should  be  applied,  and  the  patient  freely 
purged.  After  the  acute  symptoms  subside  elastic  bandages  should  be 
tried,  and  frequently  give  great  relief. 

In  countries  where  filarial  diseases  are  common  segregation  is  impracti- 
cable, but  the  danger  of  dissemination  would  be  greatly  lessened  if  patients 
harboring  the  parasites  would  so  live  as  to  avoid  mosquitoes;  such  pre- 
cautions might  be  advisable  for  sporadic  cases  in  countries  wherein  filariasis 
is  only  occasionally  introduced. 

Guinea-worm  Disease  (Dracontiasis).  Definition. — Guinea  worm  is 
sometimes  called  Dracunculus  medinensis,  or  Medina  worm. 

Distribution. — This  parasite  is  distributed  throughout  the  tropics.  It  was 
known  in  medicine  long  before  the  Christian  era,  and  there  is  some  reason 
for  believing  that  the  Biblical  mention  of  the  serpents  affecting  the  IsraeUtes 
near  the  Red  Sea  were  these  parasites.  Though  very  widely  distributed, 
the  infection  occurs  in  sharply  defined  areas.  It  exists  on  the  west  coast  of 
Africa,  particularly  on  the  Gold  Coast,  in  Abyssinia,  Southern  Egypt,  and 
the  Soudan.  In  Asia  it  occurs  along  the  Caspian  Sea,  the  Gulf  of  Persia, 
and  in  some  sections  of  British  India.  It  was  common  enough  in  the  West 
Indies  and  Tropical  America  during  the  days  of  the  slave  trade,  but  seems 
to  have  estabhshed  a  permanent  hold  only  in  a  few  South  American  Islands 
and  in  isolated  spots  in  Brazil.  In  the  United  States  this  parasite  is  encoun- 
tered from  time  to  time  in  imported  cases,  although  at  least  three  cases  have 


NEMATODES  '  897 

been  recorded  in  persons  who  had  never  lived  in  or  visited  tropical  regions. 
Thus,  Van  Harlingen  reports  it  as  occurring  in  a  case  of  a  man  who  had 
never  Hved  outside  of  Philadelphia ;  Jarvis,  in  the  case  of  a  man  who  lived 
at  Fortress  Monroe,  Va.,  for  thirty  years;  and  Walker,  in  a  case  from  Georgia. 

The  Dracunculus  medinensis  is  a  nematode  worm.  We  have  definite 
knowledge  of  the  female  only.  The  adult  female  worm  is  cylindrical  in  form, 
from  60  to  80  cm.  in  average  length  and  about  2  mm.  in  thickness.  The 
head  of  the  worm  is  blunt,  with  a  triangular  mouth  and  eight  papillae.  The 
tail  is  tapered  and  recurvated  ventrally.  The  vascular  tube  and  alimentary 
canal  extend  as  straight  canals  the  length  of  the  worm,  ending  as  blind 
pouches. 

Charles  found  in  the  mesentery  of  a  cadaver  two  female  guinea  worms 
in  conjugation  with  two  smaller  worms.  These  worms  were  about  4  cm. 
long  and  attached  to  the  females,  which  were  quite  small,  about  14  cm. 
from  the  head  end.  It  is  assumed  that  these  were  males.  In  the  adult 
female  the  uterus  occupies  almost  the  entire  body  and  is  filled  with  myriads 
of  tightly-coiled  embryos  averaging  0.6  mm.  in  length. 

Fedschenko  and  Manson  have  shown  that  the  intermediate  host  of  the 
guinea  worm  is  a  minute  water  flea  (Cyclops  quadricornis).  The  recently 
escaped  embryos  penetrate  the  cyclops,  in  which  they  pass  through  one  stage 
of  larval  development  lasting  about  six  weeks. 

It  is  assumed  that  infection  occurs  through  swallowing  the  cyclops  itself 
or  the  larva  in  drinking  water.  While  this  intermediate  stage  in  cyclops 
is  the  usual  history,  Plehn  has  shown,  experimentally,  in  monkeys,  that 
direct  infection  by  the  embryos  may  also  take  place. 

Negroes  and  the  laboring  classes  are  more  frequently  attacked  than  others, 
and  usually,  in  each  small  area,  the  infected  well  or  spring  may  be  identified. 
The  greater  number  of  cases  occur  at  the  close  of  the  heavy  rains,  probably 
because  these  conditions  are  then  more  favorable  to  the  development  of  cyclops. 

The  worm  is  taken  into  the  body  through  the  stomach.  The  males  and 
females  probably  pass  through  the  intestine  to  the  mesentery,  where  conjuga- 
tion takes  place.  The  male  dies  and  becomes  calcified  or  absorbed  and  the 
female  migrates  into  the  connective  tissue  of  the  host.  In  these  migrations 
she  usually  tends  toward  the  lower  extremity  and  appears  in  the  foot  or  the 
leg,  although  she  may  appear  in  the  subcutaneous  tissues  of  the  trunk,  arm, 
or  even  the  head.  When  the  subcutaneous  tissue  is  reached  complete 
development  takes  place,  and  when  the  embryos  are  ready  for  expulsion  a 
small  boil  or  vesicle  forms,  which  bursts  and  leaves  a  small  sinus  leading 
down  to  the  head  of  the  worm.  The  period  of  incubation  from  the  ingestion 
of  the  embryo  to  the  appearance  of  the  adult  embryo-bearing  female  in  the 
subcutaneous  tissue  is  about  one  year.  The  migrations  of  the  worm  are  not 
attended  by  pain  or  any  other  symptoms. 

Symptoms. — At  the  time  of  development  of  the  vesicle  or  boil  there  may 
be  some  slight  febrile  disturbance,  and  there  is  slight  pain  from  the  local 
irritation  and  inflammation.  The  rupture  of  the  vesicle  leaves  a  flattened, 
shallow  ulcer,  at  the  bottom  of  which  is  a  small  opening.  At  this  opening 
the  head  of  the  worm  may  appear.  If  the  ulcer  be  douched  or  sprayed 
with  cold  water  a  small  quantity  of  a  milky  fluid  exudes  from  the  orifice, 
57 


DISEASES  DUE   TO  ANIMAL  PARASITES 

or  the  uterus  of  the  worm  may  be  protruded  as  a  deHcate  tube  which  is 
seen  to  fill  up  and  suddenly  empty  itself  of  a  few  drops  of  milky  fluid  which, 
examined  microscopically,  contains  myriads  of  embryos.  Usually  when 
parturition  is  completed,  or  nearly  so,  the  worm  spontaneously  leaves  her 
host.  In  a  case  reported  by  Francis,  in  which  five  worms  were  observed  in 
the  feet,  one  complete  worm  containing  its  embryos  and  measuring  twenty-six 
inches  was  passed  in  about  half  an  hour.  Usually  a  much  longer  period 
is  required  (fifteen  or  twenty  days)  before  the  worm  emerges.  Exception- 
ally, parturition  being  completed,  the  worm  dies,  becomes  encysted,  and  can 
be  felt  as  a  firm,  fibrous  cord  under  the  skin. 

Treatment. — The  older  method,  and  the  popular  one  with  the  natives,  is 
to  grasp  the  presenting  head  of  the  worm,  fix  it  to  a  smooth  stick,  and  gradu- 
ally wind  her  out  by  twisting  out  a  few  inches  every  day.  By  this  method 
the  worm  may  easily  be  torn  and  a  swarm  of  embryos  liberated  in  the 
subcutaneous  tissues.  In  the  case  reported  by  Francis,  a  temperature,  with 
morning  and  evening  variation  between  98.8°  and  104.5°  lasting  several 
days,  occurred  after  rupture  and  retraction  of  a  worm.  These  accidents 
have  occasioned  severe  infections,  resulting  in  death.  Manson  advises 
douching  with  cold  water,  application  of  a  cold  pack  or  cold  baths  to  hasten 
expulsion  of  the  embryos  and  the  spontaneous  emergence  of  the  worm. 
Massage  and  electricity  have  been  used  with  success.  The  best  methods 
of  treatment  we  owe  to  the  suggestion  of  Emily.  He  advises  injection  of 
0.1  per  cent  solution  of  mercuric  chloride  into  the  head  of  the  worm  or  into 
the  swelling.  This  solution  causes  death  of  the  worm,  which  may  then  be 
easily  extracted.  Similarly,  Aoulkes  advises  injection  of  alcohol,  and 
Tufnel,  pure  carbolic  acid. 

Prophylaxis  consists  in  careful  filtration  or  sterilization  of  drinking 
water. 

Strongyloides  Intestinalis.  Definition. — Strongyloides  stercoralis  is  a 
nematode  worm  infecting  the  intestinal  canal.  When  present  in  large 
numbers  it  causes  a  chronic  diarrhoea,  with  anaemia  and  emaciation. 

Distribution. — This  parasite  is  widely  distributed  throughout  the  tropical 
and  subtropical  countries.  It  is  extremely  common  in  Cochin  China,  where 
it  is  supposed  to  be  the  cause  of  the  severe  diarrhoea  of  that  country  known 
as  Cochin  China  diarrhoea.  Powell  has  found  it  in  India,  in  15  out  of  20 
cases  of  anaemia.  It  has  been  observed  in  Martinique,  Sicily,  Egypt,  India, 
Porto  Rico,  and  the  Philippine  Islands.  In  Italy,  Germany,  Brazil,  and 
California  it  has  been  frequently  observed  in  association  with  uncinaria. 
It  was  first  reported  in  the  United  States  by  Thayer,  and  is  now  known  to 
be  fairly  common  in  all  our  Southern  States. 

Much  confusion  has  arisen  over  the  various  nematode  worms  resembling 
this  parasite.  These  are  now  believed  by  the  majority  of  observers  to 
represent  morphological  variations  of  the  same  worm.  The  following 
classification  is  given  by  M.  L.  Price: 

1.  The  rhabditiform  embryo,  formerly  known  as  ^w^'mZ/wk  stercoralis. 
found  in  the  fresh  stools,  is  a  slender,  active  nematode  worm,  0.3  mm.  long 
and  0.04  mm.  broad. 

2.  Filariform  embryo  found  in  the  stools  after  standing  one  or  two  days, 


NEMATODES 


899 


and  supposed  to  develop  from  the  rhabditiform  embryos.     This  embryo 
is  twice  as  long  as  the  preceding  form,  and  is  also  actively  motile. 


Fig.   114 


A.  Egg  of  Coehin-China  diarrhoea  worm  (Strongyloides  stercoralis)  found  in  stools.  B.  Rhabditiform 
embryo  of  same,  from  the  stools.  C.  Filariform  larva  of  same  derived,  by  direct  transformation,  from  a 
rhabditiform  embryo.  The  figures  were  drawn  from  life,  as  seen  under  Leitz,  objective  7,  ocular  3. 
Bulletin  of  the  United  States  Marine  Hospital  Service,  No.  10, 1903.    (After  Thayer.) 

3.  The  sexually  differentiated  form,  Rhabditis  stercoralis,  which  may  be 
developed  from  the  preceding  in  five  days.    The  male  is  a  fine  nematode 


900  DISEASES  DUE  TO  ANIMAL  PARASITES 

worm  0.7  mm.  in  length,  the  female  1  mm.  in  length,  which,  when  cultivated 
extracorporeally,  produces  filariform  embryos.    Finally  there  is: 

4.  The  parthenogenetic  mother-worm,  Anguillula  iniestinalis,  found  in  the 
intestinal  canal  at  autopsy.  A  slender  worm,  2  mm.  in  length,  easily  recog- 
nized by  the  string  of  five  or  six  eggs  in  the  centre  of  the  body.  Infection 
probably  takes  place  by  the  ingestion  of  the  filariform  embryo  in  water  or 
on  uncooked  vegetables.  Leichtenstern  has  experimentally  shown  the 
incubation  period  to  be  seventeen  days. 

Later  researches  have  disproved  much  of  the  pathological  importance 
previously  attached  to  this  parasite.  It  is  a  mistake,  however,  to  say  that 
the  worm  has  no  clinical  significance.  The  principal  symptom  is  a  continuous 
diarrhoea,  without  pain  or  temperature  disturbance.  Secondarily,  intestinal 
indigestion  develops  and  nutrition  is  very  much  lowered.  As  a  consequence, 
there  is  anoemia  and  wasting.  Blood  examination  shows  an  ordinary  anaemia 
and,  in  marked  contrast  with  other  verminous  anaemias,  shows  neither 
leukocytosis  nor  eosinophilia. 

Treatment. — Thymol,  given  fasting,  in  the  same  manner  as  for  uncina- 
riasis, is  the  best  remedy  for  expulsion  of  strongyloides.  If,  for  any  reason, 
thymol  should  fail  or  if  it  should  be  rejected,  or  the  patient  show  any  intoler- 
ance to  the  drug,  male  fern  should  be  used  in  large  doses. 

Trichocephalus  Dispar. — The  Trichocephalus  dispar,  sometimes  called 
a  "whip-worm,"  is  occasionally  found  in  the  intestinal  canal  of  man.  The 
male  and  female  worms  are  about  equal  in  size.  The  male  is  usually 
coiled  in  a  spiral  form,  but  the  female  is  nearly  straight.  The  posterior 
portion  of  the  body  is  thicker  than  the  anterior  part,  and  by  the  slim 
anterior  filament  the  parasite  embeds  itself  in  the  mucous  membrane  of  the 
intestine.  This  parasite  is  not  common  in  the  United  States,  but  is  frequently 
observed  in  France  and  Southern  Italy.  Its  chief  area  of  development  is  in 
the  csecum,  and  more  than  one  worm  is  usually  present.  Sometimes  very 
large  numbers  are  found.  It  is  supposed  to  possess  no  pathological  signifi- 
cance and  to  be  incapable  of  producing  serious  symptoms,  but  some  writers 
have  claimed  that  it  may  cause  diarrhoea  and  anaemia  of  a  serious  character. 
We  know  little  about  its  history  of  development. 


CESTODES  OR  TAPEWORMS. 

Tapeworms  are  very  frequently  found  in  the  intestinal  canal  of  man. 
As  their  name  indicates,  they  are  flat,  broad,  white  parasites,  which  consist 
of  segments,  each  of  which  is  rectangular  in  shape,  but  somewhat  elongated. 
Each  of  these  segments  represents  a  single  individual.  From  the  head  the 
segments  just  named  develop.  The  technical  name  for  the  head  and  neck 
is  the  "scolex,"  and  for  the  segment  "proglottis."  By  means  of  the  head 
the  worm  is  attached  to  the  mucous  membrane  of  the  intestine,*  but  there 
is  no  mouth  in  the  sense  that  an  opening  exists  which  communicates  with 
an  intestinal  canal.  Each  segment  of  the  worm  is  hermaphroditic;  that  is 
to  say,  each  segment  contains  male  and  female  organs  of  reproduction. 

There  are  several  varieties  of  tapeworms.     The  most  frequently  found 


CESTODES  901 

are  the  Toenia  mediocanellata,  sometimes  called  the  TcEnia  saginata,  or 
unarmed  tapeworm,  or  beef-worm,  the  Tosnia  solium  (pork-worm),  and  the 
TcBnia  echinococcus.  Less  common  forms  are  the  Dibothriocephalus  latus, 
or  Russian  tapeworm,  derived  from  eating  infected  fish;  the  Taenia  nana, 
the  Tcenia  confusa,  and  the  "double-pored  dog  tapeworm,"  Dipylidium 
caninum.  The  TcBuia  nana  is  sometimes  called  the  Hymenolepis  nana,  or 
dwarf  tapeworm. 

The  Tcsnia  solium  usually  gains  its  entrance  into  the  intestinal  canal 
of  man  by  the  ingestion  of  imperfectly  cooked  pork,  the  Tcenia  medio- 
canellata by  the  eating  of  uncooked  beef,  and  the  Tania  echinococcus  by 
the  ingestion  of  food  which  has  been  fouled  by  the  excrement  of  the  dog. 

All  tapeworms  pass  through  three  stages  of  existence.  The  segments 
of  the  worm  give  off  eggs  which  are  discharged  from  the  intestinal  canal 
of  the  host,  enter  the  alimentary  canal  of  some  animal,  and  are  hatched 
out  as  parasites  which  pass  through  the  wall  of  the  intestine,  gain  a  place 
of  rest  in  the  muscles  or  other  tissues,  and  there  form  cysts.  When  these 
muscular  tissues  are  eaten,  the  parasite  in  the  cyst  once  more  enters  the 
alimentary  canal,  becomes  attached  to  its  mucous  membrane,  and  from  it 
is  developed  the  adult  worm. 

The  Taenia  solium  may  be  several  yards  in  length.  At  one  time  it  was 
thought  to  be  solitary;  hence  its  name.  It  not  infrequently  happens,  how- 
ever, that  more  than  one  worm  is  present.  The  head,  which  is  very  small, 
scarcely  larger  than  a  pinhead,  has  a  proboscis,  or  rostellum,  about  which 
is  arranged  a  double  row  of  horny  booklets.  The  booklets  in  the  anterior 
row  are  larger  than  those  in  the  posterior  row.  Below  these  are  four  sucking 
disks  at  the  sides  of  the  head.  By  these  means  the  worm  attaches  itself 
to  the  bowel.  The  segments  of  the  worm  are  about  10  to  12  mm.  in  length 
and  from  5  to  60  mm.  wide,  but  they  vary  considerably  in  size;  those  nearest 
the  neck  of  the  worm  being  shorter  and  narrower  than  those  which  develop 
several  feet  away  from  the  neck.  When  the  egg  of  the  Tcenia  solium  is 
hatched  out  so  that  a  scolex  (or  head)  is  set  free,  and  this  parasite  becomes 
encysted  in  the  muscles  of  a  pig,  the  pork  is  said  to  be  "  measly."  When  it 
finds  a  resting  place  in  the  muscles  of  the  brain,  or  other  parts  of  the  human 
being,  it  is  known  as  the  Cysticercus  cellulosa.  These  cysts  vary  in  size  from 
that  of  a  small  pea  to  that  of  a  bantam's  egg,  and  are  separated  from  the 
surrounding  tissues  by  a  formation  of  connective  tissue  which  acts  as  a 
capsule. 

The  T(Bnia  mediocanellata  possesses  a  head  which  differs  materially 
from  the  head  of  the  Tcenia  solium.  There  is  no  rostellum  or  booklets, 
but  there  are  four  sucking  disks,  which  are  much  nearer  the  point  of  the 
head  than  they  are  in  the  Tcenia  solium.  This  worm  further  differs  from  the 
T(Bnia  solium  in  addition  in  that  its  segments  are  generally  broader  and 
shorter,  and  the  entire  worm  is  usually  much  longer. 

This  worm  may  reach  the  length  of  about  25  or  30  feet,  and  it  is  not 
very  rare  for  from  15  to  20  feet  of  a  worm  to  be  passed  intact.  When  the 
scolex  of  this  worm  is  found  in  the  muscles  of  cattle  it  is  called  the  Cysti- 
cercus mediocanellata. 

In  Germany,  where  imperfectly  cooked  pork  is  largely  eaten,  the  Taenia 


902  DISEASES  DUE   TO  ANIMAL  PARASITES 

solium  is  most  frequently  met  with,  but  in  this  country,  where  the  people  eat 
largely  of  beef,  the  Taenia  mediocanellata  is  much  more  common. 

The  Tcenia  echinococcus  is  very  rarely  met  with  in  the  United  States.  It 
is,  however,  exceedingly  common  in  Australia.  This  worm  possesses  a 
double  row  of  booklets  and  four  sucking  disks.  It  is  rare  for  more  than 
three  or  four  segments  to  be  attached  to  any  one  head,  but  as  the  para- 
site is  often  present  in  numbers  many  disconnected  segments  may  be 
discharged.  Like  the  other  forms  of  tapeworm,  the  segments  increase 
in  size  as  the  distance  from  the  head  is  increased.  This  worm  does 
not  inhabit  the  intestine  of  man,  but  produces  its  evil  influence  by 
reason  of  the  entrance  of  its  eggs  into  his  alimentary  canal,  from  which 
place  they  wander  into  other  parts  of  the  body,  forming  what  are  known 
as  hydatid  cysts.  In  other  words,  the  infection  of  human  beings  by  the 
Tcenia  mediocanellata  and  the  Taenia  solium  is  quite  different  from  the 
infection  of  human  beings  by  the  Taenia  echinococcus,  for  in  the  first  cases 
the  patient  swallows  the  parasite  when  it  has  reached  the  second  stage  of 
its  existence  and  is  prepared  to  develop  its  segments;  whereas,  in  the  case 
of  the  Taenia  echinococcus  the  patient  takes  food  which  has  in  some  way 
become  contaminated  by  the  fecal  discharges  of  the  dog,  which  fecal  dis- 
charges contain  the  eggs  of  the  parasite,  and  from  these  eggs  are  developed 
cysts.  A  patient  infected  by  the  Taenia  echinococcus  therefore  suffers  from 
the  cystic  stage  of  development  of  the  worm. 

The  hydatid  cysts  formed  in  this  manner  most  frequently  infest  the 
liver,  but  almost  any  portion  of  the  body  may  be  affected.  Such  cysts,  in 
the  liver  in  particular,  are  always  surrounded  by  a  layer  of  connective  tissue 
which  is  thrown  out  in  an  endeavor  to  circumscribe  the  invading  parasite. 
The  wall  of  hydatid  cysts,  therefore,  is  formed  of  two  layers;  the  outside 
layer  is  lamellated  and  is  sometimes  called  the  cuticula.  The  inner  wall 
of  the  cyst  often  contains  muscular  fibres  and  bloodvessels,  and  is  called 
the  parenchymatous  layer.  Not  rarely  the  primary  cysts  give  rise  to  sec- 
ondary cysts  called  daughter-cysts,  and  these  daughter-cysts  may  develop 
in  themselves  cysts  which  are  called  granddaughter-cysts. 

On  the  inner  surface  of  these  cysts  the  scolices,  or  heads,  of  the  worm 
are  formed.  At  the  posterior  end  of  the  scolex  is  a  stem,  or  pedicle,  by 
which  it  is  attached  to  the  wall  of  the  brood  capsule.  In  some  instances  the 
scolex  may  be  found  free  inside  of  this  capsule.  In  most  cases,  after  the 
cyst  has  existed  for  a  long  period  of  time,  the  scolices  die,  the  fluid  is 
absorbed,  and  a  granular  mass  remains.  This  granular  mass  may  contain 
the  booklets,  or  the  booklets  may  be  found  free  in  the  contents  of  the  cap- 
sules, or  in  the  primary  cyst  itself.  Occasionally,  a  hydatid  cyst  is  found 
which  is  sterile,  that  is,  in  which  neither  sub-cysts  nor  scolices  are  devel- 
oped. 

In  addition  to  the  scolices,  the  cysts  contain  a  clear,  limpid  fluid 
which  sometimes  becomes  turbid  after  the  cyst  has  existed  for  a  con- 
siderable period  of  time,  the  turbidity  being  due  to  disintegration  of  the 
lining  layer  of  the  cysts  and  the  formation  of  crystals  of  cholesterin,  and  to 
the  presence  of  lime-salts.  Occasionally  the  cyst  shrinks,  its  contents 
become  inspissated  or  thickened,  and  the  entire  mass,  including  the  con- 


CESTODES  903 

nective  tissue  which  has  been  formed  around  the  cyst,  may  become  calcified. 
Sometimes,  too,  the  daughter-cysts  instead  of  growing  inside  grow  outside. 
Indeed,  this  variation  is  more  commonly  seen  in  man  than  it  is  in  animals 
that  are  affected  by  this  parasite.  This  is  called  the  echinococcus 
exogena. 

Under  the  name  of  echinococcus  multilocularis  a  variety  of  echinococcus 
cyst  is  found  in  the  liver,  which  is  characterized  by  a  somewhat  irregular 
distribution  of  groups  of  small  cysts  walled  off  by  connective  tissue,  as 
are  the  larger  cysts  already  described.  These  cysts  are  often  sterile; 
that  is  to  say,  they  do  not  contain  scolices  or  booklets.  It  is  probable  that 
this  formation  is  due  to  a  somewhat  different  parasite  from  the  ordinary 
Toenia  echinococcus. 

The  Bothriocephalus  lotus,  or  Dibothriocephalus  lotus,  is  the  largest  of  all 
human  tapeworms,  and  has  very  broad,  square  segments.  The  head  is 
egg-shaped,  but  possesses  no  disks  or  booklets.  On  the  contrary,  its  head 
is  marked  by  long  grooves  by  v/hich  it  attaches  itself  to  the  intestine.  Its 
neck  is  longer  and  more  slender  than  that  of  other  tapeworms.  Two 
species  have  been  described,  the  Bothriocepholus  cordatus  and  the  Bothrio- 
cephalus  cristatus.  Infection  by  this  parasite  occurs  most  frequently  by  the 
eating  of  imperfectly  cooked  fish,  probably  because  the  eggs  develop  to 
some  extent  in  water  and  are  swallowed  by  various  fish,  in  whose  flesh  the 
cysts  are  formed  just  as  the  other  scolices  already  described  form  in  the 
flesh  of  the  hog  or  ox. 

TcBnia  nona,  or  dwarf  tapeworm,  Hymenolepis,  is  only  from  one-fifth 
to  two  inches  in  length.  It  has  four  suckers  and  a  single  row  of  booklets  on 
its  head.  Stiles  states  that  it  may  be  present  singly  or  by  thousands,  and 
is  probably  more  frequent  than  is  generally  thought.  Its  intermediate  host 
is  usually  the  rat,  from  the  stools  of  which  food  is  infected.  In  the  rat  the 
cyst  stage  may  occur  in  the  intestinal  wall  and  is  called  a  cercocystis. 
Like  other  tapeworms,  the  embryos  burrow  into  the  wall  of  the  intestine, 
but  do  not  remain  there,  falling  back  into  the  lumen  of  the  bowel  to  reach 
adult  development  with  eggs  in  about  fifteen  days.  The  only  taeniafuge 
which  has  proved  effective  for  the  removal  of  this  worm  is  aspidium. 

The  TcBnia  cucumerina  is  slightly  larger  than  the  Toenia  nana,  and  its 
head  possesses  four  rows  of  booklets.  It  is  not  infrequently  found  in  the 
ileum  of  dogs  and  cats,  but  rarely  affects  man.  Its  scolices  inhabit  the 
dog-louse  and  by  means  of  this  parasite,  or  by  the  carrying  of  the  embryos 
to  the  mouth  by  the  hands  after  handling  a  dog  or  cat,  infection  of  a  human 
being  may  take  place. 

Symptoms. — The  symptoms  produced  by  the  presence  of  tapeworms  in 
the  alimentary  canal  are  not  pathognomonic.  Not  infrequently  the  worms 
exist  for  a  long  period  of  time  without  their  host  having  any  knowledge 
of  their  presence,  and  the  infection  is  only  discovered  by  the  chance  observa- 
tion of  one  or  more  segments  in  a  stool.  The  patient  may  suffer  from 
symptoms  of  gastrointestinal  catarrh  produced  by  the  irritation  caused  by 
the  worm,  and  sometimes  an  inordinate  appetite  is  present,  but  this  is  by 
no  means  as  constant  a  symptom  of  tapeworm  as  most  persons  imagine. 
Not  infrequently,  the  host  of  a  tapeworm  suffers  from  anorexia  rather  than 


904  DISEASES  DUE   TO  ANIMAL  PARASITES 

from  excessive  hunger.  In  children  there  may  be  a  good  deal  of  nervous 
irritation  and  peevishness. 

In  some  instances,  however,  the  presence  of  a  tapeworm  produces  a  very 
much  more  serious  train  of  symptoms,  which  consist  in  an  intense  anceviia 
that  may  be  so  severe  as  to  give  rise  to  the  suspicion  that  pernicious  anaemia 
is  present.  The  Bothriocephalus  latus  is  said  to  be  more  prone  to  produce 
grave  anaemia  than  any  other  of  the  tapeworms. 

Treatment. — ^The  treatment  of  a  patient  infected  by  tapeworm  consists 
in  the  abstinence  of  all  food  for  eighteen  hours  prior  to  the  administration 
of  one  of  the  following  drugs,  which  are  known  to  possess  the  power  of  so 
paralyzing  or  killing  the  worm  that  it  lets  go  its  hold,  and  then  is  readily 
passed  from  the  bowel  under  the  influence  of  a  purge.  One-half  to  one 
drachm  of  the  oleoresin  of  aspidium  may  be  given  in  capsule  or  emulsion 
to  an  adult,  and  followed  in  four  or  five  hours  by  a  saline  purgative,  such 
as  citrate  or  sulphate  of  magnesium  or  Rochelle  salts.  In  other  instances 
pelletierine  given  in  the  dose  of  3  to  5  grains  may  be  used  under  the  same 
conditions.  It  is  commonly  given  in  syrupy  solution,  and  this  syrupy  solution 
is  put  up  in  a  small  container  which  holds  one  dose.  If  it  is  desired  pelle- 
tierine may  be  followed  by  castor  oil  in  place  of  the  other  purgatives  named, 
but  castor  oil  must  not  be  used  after  aspidium  is  given,  as  it  aids  in  the 
absorption  of  the  drug  into  the  body  and  so  tends  to  poison  the  individual. 
A  less  agreeable  method  of  destroying  the  worm  is  to  administer  a  confection 
made  of  pepo,  or  pumpkin  seeds  which  have  been  deprived  of  their  hard 
coverings  by  the  process  of  bruising.  Several  drachms  of  these  seeds  are, 
without  doubt,  very  efficacious.  The  patient  should  always  be  instructed 
to  pass  the  stool  through  a  sieve  and  not  to  seek  so  much  for  the  segments 
of  the  worm  as  for  the  small  head.  The  mere  passage  of  a  large  number 
of  feet  of  segments  does  not  indicate  in  any  way  that  the  patient  is  perma- 
nently relieved  unless  the  head,  from  which  other  segments  will  grow  if  it 
remains  in  the  bowel,  is  also  passed. 


TREMATODES. 

Definition. — A  large  number  of  worms  belonging  to  the  Trematodes  live 
as  parasites  in  the  body  of  man  or  of  the  lower  animals.  When  the  body 
is  so  infested  the  condition  is  said  to  be  one  of  Distomatosis,  this  term 
arising  from  the  fact  that  the  word  Distoma  is  oftentimes  applied  to  these 
parasites. 

Up  to  the  present  time  no  less  than  thirteen  species  of  Trematodes  or 
Flukes  have  been  described  as  occurring  in  human  beings.  Eleven  of  these 
belong  to  the  family  of  the  Fasciolidoe,  one  to  the  family  Paramphiscus,  and 
one  to  the  family  Schistosomidoe. 

When  the  human  being  is  attacked  the  parasite  is  usually  found  in  the 
genito-urinary  tract,  when  it  causes  what  is  known  as  Bilharzia  Disease  or 
Endemic  Hcematuria.  Less  commonly  it  infests  the  lung  and  the  condition 
is  then  called  Distomatosis  of  the  Lung,  Endemic  or  Parasitic  Hoemoptysis 
or  Lung  Fluke;  and  it  is  also  met  with  in  the  liver,  forming  the  so-called 


TREMATODES 


905 


Liver  Fluke  or  Distomatosis  of  the  Liver.  The  fluke  found  in  the  genito- 
urinary tract  is  the  Schistosoma  hcematobium,  that  met  with  in  the  lung  is 
the  Paragonimus  Westermanni,  sometimes  called  the  Distoma  Ringeri  or 
Distoma  pulmonale,  and  that  discovered  in  the  liver  the  Fasciola  hepatica 
or  instead  Dicrococlium  lanceatum,  Opisthorchis  sinensis,  the  Opisthorchis 
felineus,  and  the  Opisthorchis  noverca. 

Bilharzia  Disease. — Bilharzia  disease,  or  endemic  haematuria,  is  due  to 
the  development  in  the  body  of  the  Schistosoma  hcematobium,  and  is  charac- 
terized by  hsematuria  and  the  formation  of  papillomatous  tumors  in  the 
genito-urinary  tract. 

Etiology. — The  male  worm  is  about  4  to  15  mm.  in  length  and  0.6  mm.  in 
breadth.  The  female  averages  15  to  20  mm.  in  length  and  0.28  mm.  in 
breadth.  The  male  has  flattened  sides,  rolled  up  on  both  edges  so  as  to 
form  a  deep  groove,  the  gynecophoric  canal,  in  which  the  female  lies  during 
conjugation  (Fig.  115). 


Fig.  115 


Male  bilharzia  worm  carrying  the  female,  showing  the  papillae  on  his  skin.    The  small  figure  is  a 
cross-section  showing  relative  position  of  the  sexes.    (Looss.) 


History  and  Distribution. — Endemic  hsematuria  has  been  observed  in 
Egypt  for  centuries.  At  the  present  day  it  is  said  to  be  present  in  fully  one- 
half  of  the  population.  According  to  Looss  it  is  equally  frequent  in  Uganda. 
It  is  practically  limited  to  the  African  continent,  although  cases  have  been 
reported  from  Cyprus  and  Sicily,  and  Manson  reports  a  case  from  the  West 
Indies.  It  occurs  frequently  in  British  India,  but  always  as  an  imported 
infection.  A  few  cases  have  been  reported  in  the  United  States,  The 
parasitic  nature  of  the  disease  was  discovered  in  1851  by  Bilharz. 

The  ova  of  these  worms  are  found  in  very  great  numbers  in  the  urine. 
They  are  oval,  and  have  a  marked  terminal  spine  and  contain  a  ciliated 
embryo.  It  is  supposed  that  the  spine  is  the  organ  by  means  of  which 
the  embryo  bores  through  the  peripheral  tissues.     Ova  with  lateral  implan- 


906  DISEASES  DUE  TO  ANIMAL  PARASITES 

tation  of  the  spine  are  frequently  observed.  Looss  supposes  these  are 
examples  of  faulty  development,  and  that  the  faulty  position  of  the  spine, 
limiting  the  mobility  of  the  ovum,  is  the  reason  many  more  of  this  form 
are  found  in  sections  than  free.  In  urine  or  in  water  the  embryos  very 
soon  escape  from  the  ovum  and  move  about  very  actively  by  means  of  their 
cilia.  In  undiluted  urine  they  die  when  it  cools.  In  water  they  remain 
active  for  a  long  time. 

The  embryos  are  probably  taken  into  the  stomach  in  drinking-water, 
penetrate  the  gastric  or  intestinal  wall,  and  they  develop  into  mature  worms. 
Looss  surmises  and  brings  some  evidence  to  show  that,  like  the  uncinaria, 
this  parasite  may  also  penetrate  the  skin. 

Pathology. — The  affected  bladder  is  covered  with  a  bloody,  tenacious, 
mucous  layer;  the  submucosa  is  greatly  thickened;  the  muscular  and  serous 
coats,  as  a  rule,  are  unchanged.  In  older  cases  papillomata  are  found,  vary- 
ing in  size  from  a  small  pea  to  large  tumors  filling  the  entire  bladder.  Micro- 
scopically the  changes  consist  in  marked  degeneration  of  the  epithelial 
layers,  going  on  to  complete  destruction  of  the  mucosa.  The  pseudomem- 
branous covering  then  consists  of  ova,  leukocytes,  and  urinary  salts.  In 
the  submucosa  enormous  masses  of  ova  are  found,  many  of  them  calcified. 
The  papillomatous  tumors  spring  from  this  layer,  and  are  very  similar  in 
their  histological  structure  to  nasal  polypi.  Similar  changes  occur  in  the 
rectum,  urethra,  ureter,  seminal  vesicles,  prostate,  and  uterus.  Second- 
arily these  lesions  produce  stricture,  urinary  fistulse,  pyelitis,  prostatitis, 
and  urethritis. 

The  papillomatous  tumors  show  some  tendency  to  undergo  malignant 
change,  but  by  far  the  commoner  complication  of  the  disease  is  stone  forma- 
tion. In  old  cases  a  beginning  deposit  of  lime-salts  is  found  in  the  mucus 
covering  the  bladder  wall,  as  small  calculi  embedded  in  the  folds  and  loculi. 
In  other  cases  large,  free  calculi  are  found  with  clumped  masses  of  calcified 
ova  as  their  nucleus. 

Tumors  and  ma,sses  of  ova  are  sometimes  found  in  the  pelvis  of  the  kid- 
ney, rarely  in  its  parenchyma. 

Symptoms. — The  symptoms  vary  with  the  intensity  of  the  infection,  the 
number  of  adult  worms,  and  the  location  and  extent  of  the  lesions  already 
described.  The  only  constant  symptom  is  hcematuria.  The  amount  of 
blood  present  in  the  urine  may  be  so  small  as  only  to  be  evident  on  micro- 
scopic examination,  or  so  large  as  to  form  clots  of  appreciable  size  in  the 
bladder.  As  a  rule,  the  blood  is  passed  at  the  end  of  urination.  The  micro- 
scopic examination,  in  doubtful  cases,  should  therefore  be  directed  to  the 
last  few  drops  of  urine  expelled.  In  the  large  majority  of  cases  hsematuria 
will  be  the  only  symptom.  In  the  severe  infections,  however,  cystitis  usually 
develops  and  becomes  very  troublesome.  Following  the  development  of 
inflammation  the  ordinary  symptoms  of  tumor  or  stone  develop.  In  severe 
cases,  with  diminished  resistance,  suppuration  of  these  lesions  occurs,  with 
formation  of  extensive  fistulous  tracts.  When  the  lesions  are  confined  to  or 
are  most  marked  in  the  bowel,  the  early  symptoms  may  resemble  acute 
dysentery  and,  in  older  cases,  chronic  dysentery,  with  pain,  tenesmus,  and 
bloody  and  mucous  stools.    When  tumors  occur  in  the  bowel  they  are  readily 


TREMATODES  907 

recognized,  although  when  situated  low  in  the  rectum  they  have  been  mis- 
taken for  hemorrhoids. 

The  urine  contains  red  blood  cells,  leukocytes,  principally  eosinophiles  and 
polynuclear  cells,  besides  large  numbers  of  ova.  With  these  the  ordinary 
evidences  of  an  extensive  chronic  cystitis  are  also  found.  The  number  of 
ova  present  varies  very  widely  and  bears  no  relation  to  the  amount  of  blood 
in  the  urine.  When  they  are  very  few  in  number  they  may  only  be  found 
in  the  last  few  drops  of  urine  passed. 

The  blood  changes,  in  severe  cases,  are  marked.  There  is  a  pronounced 
fall  in  the  number  of  red  cells  and  a  still  greater  reduction  of  haemoglobin. 
With  this  there  is  a  moderate  degree  of  leukocytosis,  the  increase  consisting 
almost  entirely  of  eosinophile  cells,  which  are  present  in  proportion  varying 
from  9  per  cent,  to  as  high  as  52  per  cent. 

Diagnosis. — ^The  blood  condition  pointing  to  a  toxic  or  parasitic  anaemia, 
with  the  demonstration  of  the  ova  in  the  urine,  make  the  diagnosis  of  Bil- 
harzia  disease. 

Prognosis  depends  on  several  factors,  namely,  the  extent  of  the  infec- 
tion, the  number  of  adult  worms  present,  and,  more  important  still,  the 
conditions  favoring  reinfection.  When  all  opportunity  for  reinfection  is 
avoided,  as  by  removal  from  the  endemic  area,  after  a  time  the  adult 
worms  die,  and  eventually  all  the  ova  are  evacuated.  This  process  may 
be  a  very  long  one.  In  some  observed  cases  it  has  extended  up  to  eight 
years.  The  prognosis  also  depends  on  the  character  and  extent  of  the 
surgical  complications  and  sequelae. 

Treatment. — ^There  is  no  treatment  that  will  influence  either  the  worm 
or  the  ova  in  the  slightest  degree.  All  the  anthelmintics  have  been  tried 
and  found  useless.  Similarly,  local  application  of  antiseptics  and  proto- 
plasmic poisons  to  the  bladder  have  failed.  In  most  cases  the  haematuria 
does  not  require  treatment.  When  it  becomes  severe,  rest  in  bed  should  be 
enjoined.  Cystitis  should  be  treated  on  general  lines  by  local  medication, 
as  well  as  the  internal  administration  of  urotropin,  salol,  benzoic  acid, 
and  remedies  of  this  group.  The  complications  of  the  disease,  such  as 
stricture,  extensive  tumors  of  the  bladder  and  rectum,  accessible  ulcera- 
tions of  the  vagina  or  cervix,  and  prostatic  involvement,  call  for  appropriate 
surgical  measures.  In  a  general  way,  all  the  conditions  which  predispose 
to  or  aggravate  cystitis  should  be  avoided.  These  are  exposure,  chill,  violent 
muscular  effort,  alcohohc  debauches,  spices,  and  highly  seasoned  food. 
With  a  view  to  obtaining  an  eventual  cure,  patients  should  if  possible  be 
removed  from  the  endemic  area.  When  this  is  not  possible,  proper  means 
should  be  taken  to  ensure  a  good  water  supply.  In  this  manner  the  constant 
reinfection  of  the  patient  is  avoided.  Similarly,  in  view  of  the  possibility 
of  infection  through  the  skin,  sound  shoes  should  be  insisted  on  and  work 
in  alluvial  oozes  should  be  avoided. 

Distomatosis  of  the  Lung  (Lung  Flukes;  Endemic  or  Parasitic  Hcemop- 
tysis). — The  lung  fluke  {Faragonimus  Westermanni)  is  widely  distributed 
in  Japan,  Formosa,  Corea,  and  North  China.  It  has  been  carried  by  Oriental 
emigrants  to  many  other  countries.  Isolated  cases  have  been  reported  from 
the  United  States  and  Mexico. 


DISEASES  DUE  TO  ANIMAL  PARASITES 

The  parasite  is  a  small,  fleshy,  trematode  worm  or  fluke.  It  is  8  to 
20  mm.  long  and  6  mm.  in  its  transverse  diameter.  It  is  usually 
found  in  the  lungs,  but  has  been  observed  in  other  organs,  notably 
the  liver  and  brain.  The  worms  discharge  a  vast  number  of  ova.  These 
ova  are  dark  brown,  oval,  0.08  mm.  long  by  0.05  mm.  wide,  possess  a  small 
operculum,  and  contain  a  ciliated  embryo.  They  are  found  in  great  numbers 
in  the  sputum.  Infection  probably  takes  place  through  contaminated  water, 
although  nothing  is  known  of  the  extracorporeal  phases  of  the  parasites. 
By  far  the  larger  percentage  of  cases  is  observed  in  young  males.  Alcoholism 
is  supposed  to  predispose  to  the  disease. 

Pathology. — Patches  are  scattered  all  over  the  lungs,  but  particularly  in 
the  periphery,  resembling  hemorrhagic  infarcts.  On  section  these  patches 
are  found  to  be  infiltrated  and  honeycombed  with  small  tunnels  and 
cavities,  each  of  which  contains  one  or  more  distoma  and  masses  of  eggs. 
Occasionally  large  cavities  are  formed  by  coalescence  of  the  smaller 
lesions. 

In  cases  in  which  the  parasite  invades  the  brain,  analogous  conditions  are 
found,  but  they  are  almost  entirely  limited  to  the  cortical  areas. 

Symptoms. — The  commonest  symptom  is  chronic  morning  cough,  with  a 
rusty,  prune-juice,  or  bloody  sputum.  The  amount  of  blood  in  the  sputum 
may  be  so  small  as  to  be  only  demonstrable  by  the  microscope,  or  there  may 
be  periodical  and  severe  hemorrhages  from  the  lungs.  The  rusty  color  of 
the  sputum  is  due  not  only  to  the  blood  and  the  bloody  pigments  contained 
in  it,  but  also  to  the  large  numbers  of  dark-brown  ova.  The  sputum  also 
contains  eosinophile  cells,  Charcot-Leyden  crystals,  and  elastic  fibres.  The 
course  of  the  disease  is  essentially  chronic.  Cases  last  from  ten  to  twenty 
years  without  much  discomfort  and  without  much  deterioration  in  the 
general  health,  excepting  where  marked  secondary  anaemia  results  from 
repeated  and  severe  hemorrhages. 

Prognosis. — ^The  prognosis  is  good,  excepting  in  the  rare  instances  in 
which  hemorrhage  is  sufiiciently  severe  to  cause  a  fatal  ending.  When  the 
parasite  attacks  the  brain,  epileptic  symptoms  have  been  observed  and  the 
prognosis  is  grave. 

Treatment. — A  large  numer  of  drugs  have  been  administered  to  patients 
suffering  from  this  condition,  both  by  the  mouth  and  by  inhalation, 
in  the  hope  that  benefit  might  accrue.  It  is  evident  that  the  nature  of 
the  lesions  renders  any  therapeutic  measure  of  little  value. 

Distomatosis  of  the  Liver  (Liver  Flukes). — Liver  flukes  occur  endem- 
ically  in  certain  sections  of  Japan.  For  instance,  Baelz  estimates  that  20 
per  cent,  of  the  inhabitants  of  Okayama  Province  are  infected  with  the  liver 
fluke.  Inouye  found  in  various  sections  from  19  per  cent,  to  71.9  per  cent, 
of  the  population  infected.  Infection  has  been  carried  all  over  the  world  by 
Oriental  emigrants.  In  the  United  States  an  entirely  analogous  affection  is 
seen  in  cats  and  cattle  and  several  cases  have  been  met  with  in  man. 

The  parasite  commonly  invades  the  biliary  tract  or  the  pancreatic  duct, 
and  is  also  found  in  the  duodenum,  the  stomach,  and  spleen.  The  obstruc- 
tion of  the  biliary  ducts  by  the  parasites  causes  dilatation  and  chronic 
catarrh.     There  is  also  overgrowth  of  the  hepatic  connective  tissue,  with 


DHOBIE  ITCH  909 

atrophy  of  the  parenchyma.  Small  but  constant  hemorrhage  from  the 
biliary  passage  may  cause  a  grave  anaemia. 

Postmortem  the  parasites  are  found  in  great  numbers  in  the  walls  of 
the  gall-bladder  and  biliary  ducts,  or  free  in  the  ducts.  They  lie  in  small, 
cyst-like  cavities  connecting  with  the  gall-bladder  or  ducts. 

Symptoms. — The  symptoms  depend  on  the  number  of  worms.  The  first 
symptom  is  rapid  enlargement  of  the  liver,  with  voracious  appetite.  The 
liver  may  reach  to  the  umbilicus,  it  is  tender  on  palpation,  and  there  are 
recurring  attacks  of  jaundice.  Sooner  or  later  diarrhea  begins,  and  with 
it  marked  failure  of  nutrition.  The  patient  becomes  weak,  emaciated,  and 
anaemic.  The  diarrhoea  in  marked  cases  is  severe,  and  the  movements 
contain  much  blood  besides  the  ova  of  the  parasites.  Later,  dropsy  of  the 
legs  and  belly  develop,  and  the  patient  dies  exhausted.  The  course  of  the 
disease  is  very  chronic,  and  likewise  depends  on  the  number  of  parasites. 
Recovery  never  takes  place. 

Treatment. — There  is  no  treatment  save  the  use  of  stimulants  and  good 
food. 

With  the  idea  of  prophylaxis  Inouye  advises  against  drinking  or  swim- 
ming in  canal  water  or  eating  raw  fish  or  mussels.  He  states  that  in  one 
region  notably  infected  with  the  disease  the  mortality  from  distomiasis  has 
been  reduced  to  zero  by  following  these  simple  precautions. 


PARASITIC  INFUSORIA. 

The  parasitic  infusoria  which  are  found  in  man  are  protozoa  of  the  sub- 
class flagellata.  They  are  rarely  met  with.  The  Plagiomonas  urinaria 
has  been  found  in  the  urine  of  a  man  who  suffered  from  chronic  suppura- 
tion. The  Trichomonas  vaginalis  is  found  in  acid  vaginal  mucus,  and  the 
Trichomonas  hominis  has  been  found  in  the  bowels  and  stools.  They  all 
possess  but  little  clinical  interest. 

DHOBIE  ITCH. 

Definition. — Dhobie  itch  is  a  term  applied  to  a  large  group  of  mycotic  and 
bacterial,  itching  skin  diseases  affecting  persons  living  in  hot  climates.  These 
eruptions  may  occur  anywhere  on  the  body,  but  usually  in  the  crotch, 
axilla,  on  the  soles  of  the  feet,  and  between  the  toes.  The  term  dhobie 
is  derived  from  the  "dhobie"  or  washerman,  owing  to  the  widespread 
belief  that  the  contagion  is  conveyed  by  the  clothing  passing  through  his 
hands. 

Etiology. — Epiphytic  skin  diseases  are  exceedingly  connnon  in  the 
tropics,  and  all  forms  of  ringworm  grow  with  the  greatest  freedom  under  the 
exceedingly  favorable  conditions  of  heat  and  moisture  afforded  by  the  climate. 
Three  types  of  the  disease  are  recognized.  The  first  is  thought  to  be 
due  to  the  Microsporon  minuiissimum;  the  second  type  probably  represents 
a  very  extensive  group  of  different  varieties  of  tricophyton,  or  ringworms. 
The  third  type,  classed  as  dhobie  itch,  is  that  described  by  Manson  as 


910  DISEASES  DUE  TO  ANIMAL  PARASITES 

Pemphigus  contagiosus,  in  which  he  has  isolated  a  diplococcus,  the  exact 
significance  of  which  has  not  yet  been  fully  determined. 

These  skin  diseases  have  all  been  imported  into  the  United  States  by 
soldiers  returning  from  the  Philippines,  and  there  is  every  possibility  of 
spreading  them  in  the  States  that  lie  in  the  subtropical  belt.  Tropical  skin 
infections  of  this  type  are  usually  spread  by  direct  contact  with  infected 
persons  or  their  clothing.  In  many  instances  sexual  intercourse  serves  as  a 
means  of  spreading  the  disease.  Bathing  in  the  waters  of  sluggish  streams 
and  tanks  sometimes  causes  dhobie  itch.  The  natives  of  Luzon  believe 
that  sea  bathing  is  one  of  the  common  causes,  and  among  men  who  habit- 
ually bathed  in  the  sea  I  (Kieffer)  saw  a  larger  proportion  of  itch  cases 
than  in  those  who  did  not.  The  washing  of  underclothing  in  cold  water, 
and  without  boiling,  must  also  be  considered  a  cause.  Clothing  washed  in 
cold  water  invariably  becomes  overgrown  with  moulds  when  laid  aside  for 
a  day  or  two.  These  mouldy  clothes  frequently  cause  ringworm  infection. 
Ringworms  are  also  very  common  among  the  domestic  animals  in  the  tropics, 
and  are  undoubtedly  conveyed  from  them  to  man. 

In  the  two  mycotic  forms  the  disease  usually  attacks  the  crotch  and 
axilla.  The  appearance  of  the  lesion  is  that  of  an  ordinary  ringworm  with 
festooned,  scaly  margins.  The  interior  of  the  patch  is  red,  glossy,  and  bare. 
Secondary  infections  frequently  occur  from  scratching  or  chafing,  or  from 
simple  contact  with  the  denuded  epithelium.  These  diseases  affect  almost 
all  ages,  and  are  found  in  the  native  as  well  as  in  the  foreigner.  In  the  Philip- 
pines very  few  Americans  escape  without  contracting  one  or  another  of  them. 
The  smarting  and  itching  are  very  severe.  The  suffering  from  the  chafing 
of  the  clothing  may  be  so  great  as  to  entirely  prevent  the  patient  from 
moving  about.  Unless  vigorously  treated  the  disease  persists  until  the  cool 
season,  when  the  patch  heals  up,  leaving  a  scaly,  pigmented  area  which 
breaks  out  again  with  the  approach  of  the  hot  weather. 

Pemphigus  contagiosus  occurs  in  the  form  of  vesicles,  or  blebs,  which 
break  and  leave  a  raw,  red,  and  shiny,  denuded  surface,  with  a  sharp,  clear- 
cut  zone  one-sixteenth  to  one-eighth  inch  in  width  of  undermined  epithe- 
lium surrounding  them.  When  the  blebs  are  small  its  resemblance  to 
varicella  may  be  very  close.  The  disease  occurs  in  foreigners  of  all  ages. 
Among  the  natives  adults  are  as  a  rule  immune,  and  it  is  principally  seen 
in  children.  The  eruption  may  be  scattered  over  the  entire  body  or  may 
be  limited  to  the  crotch  and  axilla. 

When  any  doubt  exists  of  the  nature  of  these  eruptions,  the  mycotic 
elements  can  be  readily  demonstrated  microscopically.  Pemphigus  con- 
tagiosus is  to  be  differentiated  from  varicella  in  that  the  constitutional 
symptoms  of  the  latter  are  wholly  lacking. 

Treatment.— The  parts  should  be  thoroughly  cleaned  with  green  soap, 
following  which  a  parasiticide  remedy  should  be  used.  Manson  advises 
Vleminck's  solution  of  the  sulphuret  of  calcium,  applied  every  night  for 
three  or  four  times.  Tincture  of  iodine  painted  over  the  area  daily  is  a  valu- 
able remedy.  Similarly,  an  ointment  of  chrysophanic  acid  or  the  oleate  of 
mercury  is  very  efficient.  A  saturated  solution  of  salicylic  acid  in  collodium, 
applied  twice  daily,  is  a  convenient  and  excellent  remedy.    The  main  diffi- 


MYIASIS  911 

culty  is  that  in  the  majority  of  cases,  as  soon  as  the  diseased  area  is  sterilized 
by  these  remedies,  it  becomes  reinfected  by  the  clothing  or  hands  of  the 
patient.  Pemphigus  contagiosus  should  be  treated  by  bichloride  of  mercury 
washes  and  a  dusting  powder.  Prophylaxis  includes  careful  boiling  of  the 
underclothing,  and  keeping  the  crotch  and  axilla  as  dry  as  possible  with  a 
good  dusting  powder. 


CHIGGER  (SAND  FLEA). 

The  chigger,  or  sand  flea  (Pulex  'penetrans),  is  distributed  widely  over 
tropical  and  many  parts  of  subtropical  America  and  the  West  Indies.  It 
is  supposed  to  have  been  carried  in  1872  from  South  America  to  Africa. 
At  present  it  is  widely  distributed  on  both  African  coasts  and  in  certain  sec- 
tions of  India.  It  is  a  very  common  pest  in  the  Philippine  Islands,  where 
it  is  known  as  "  tungau."  The  chigger  is  a  minute,  reddish-brown  flea,  and 
attacks  both  man  and  animal.  When  impregnated  the  female  attaches 
herself  to  the  skin  surfaces  and  burrows  under  the  skin,  head  first.  Ovula- 
tion takes  place  in  the  cutaneous  tissue  and  the  female  increases  to  the  size 
of  a  small  pea.  If  unmolested  the  ova,  when  mature,  are  expelled  through 
the  point  of  entrance,  through  which  also  the  female  is  ultimately  extruded. 
The  chiggers  may  vary  in  number  from  one  to  several  hundred.  They 
usually  lodge  in  the  feet  and  legs,  but  the  hands,  arms,  genitals,  and  face 
may  also  be  invaded.  The  bite  of  the  insect  causes  little  pain,  and  the  female 
is  usually  detected  when  she  commences  to  enlarge  beneath  the  skin.  There 
is  then  intolerable  itching,  with  formation  of  small  papules,  with  red,  in- 
flamed heads,  and  a  black  spot  on  the  summit.  The  papules  become  pustu- 
lar, discharge,  form  small  ulcers,  and  eventually  heal,  leaving  small,  pitted 
scars.  When  the  lesions  are  numerous,  particularly  when  neglected  in  the 
unclean  and  the  physically  deteriorated,  extensive  infections  and  sloughing 
wounds  may  occur.     Rarely  tetanus  and  phagedenic  areas  develop. 

Treatment. — Treatment  consists  in  complete  enucleation  with  a  needle  or 
the  point  of  a  fine  scalpel.  Chloroform,  turpentine,  infusion  of  tobacco, 
mercurial  ointment,  and  the  essential  oils  allay  the  itching  and  kill  the  para- 
sites. The  essential  oils,  particularly  the  oil  of  eucalyptus,  act  not  only  as  a 
cure,  but  also  as  a  preventive  against  the  bites  of  the  insects. 


MYIASIS. 

Infection  by  Larvae  of  the  Diptera. — Screw-worm  (Lucilia  Macellaria), 
the  larva  of  the  common  blue-bottle  flesh  fly,  a  very  common  fly  in 
the  United  States,  West  Indies,  and  South  America,  causes  infection  in 
man  through  the  female  laying  her  eggs  on  wounds  in  the  skin  and  in  the 
noses  or  ears  of  people  sleeping  in  the  open.  During  the  campaign  at  San- 
tiago de  Cuba,  in  1898,  numerous  cases  of  infection  by  this  larva  w^ere  seen 
in  wounds  and  abrasions  about  the  feet  of  the  men  and  horses.  In  the 
tropics  they  have  also  been  seen  attacking  the  vagina  of  recently  delivered 


912  DISEASES  DUE   TO  ANIMAL  PARASITES 

women.  The  eggs  deposited  in  these  locations  hatch  out  in  a  few  hours 
into  the  larva,  known  as  the  screw-worm  on  account  of  the  circles  of  minute 
spines  running  around  the  body  of  the  worm  very  much  as  does  the  thread 
of  a  screw.  The  larvse  are  about  three-quarters  of  an  inch  in  length.  They 
are  extremely  active,  and  burrow  widely,  causing  extensive  destruction  of 
all  the  tissues.  On  account  of  the  circles  of  spines  they  are  extremely  diffi- 
cult to  extract  from  their  burrows  in  firm  tissue.  Screw-worm  infections  of 
the  nose  are  very  painful  and  exceedingly  fatal.  The  larvae  bore  into  the  frontal 
and  ethmoidal  sinuses,  and  eventually  may  even  enter  the  brain.  There  is 
intolerable  pain  at  the  bridge  of  the  nose,  with  a  bloody,  fetid  discharge  from 
the  nostrils.  A  very  large  percentage  of  the  cases  die  from  extension  of  the 
infection  into  the  sinuses  or  meninges.  When  the  larvse  develop  in  the  ear 
they  penetrate  the  tymy)anic  cavity,  causing  severe  otitis  media  and  even  fatal 
meningitis.  Numbers  of  such  cases  have  been  reported  by  army  surgeons 
from  the  Rio  Grande  border. 

Treatment. — Treatment  consists  in  the  injection  of  strong  parasiticides, 
such  as  carbolic  acid  and  chloroform.  Better  still,  chloroform  is  taken  up 
on  a  small  probe  tipped  with  absorbent  cotton,  and,  with  a  good  light,  the 
nose  or  ear  is  explored  and  each  worm  as  it  hes  embedded  in  the  tissues 
is  touched  with  the  chloroform-saturated  cotton.  This  kills  them  immedi- 
ately and  they  may  then  be  readily  extracted  with  small  forceps.  In  super- 
ficial wounds  the  destruction  of  the  larvae  is  much  more  simple. 

Intestinal  Myiasis. — The  larvae  of  diptera  are  very  frequently  found  in 
the  alimentary  canal  of  man.  They  usually  gain  entrance  by  being  swal- 
lowed on  fly-blown  food.  No  less  than  nineteen  different  species  have  been 
identified  in  human  evacuations.  As  a  rule  no  symptoms  are  produced, 
and  the  first  the  patient  knows  of  the  existence  of  the  larvae  is  to  find  per- 
haps a  copious  mass  of  them  in  the  stools.  In  tropical  climates  the  passage 
of  larvae  is  very  much  more  frequent  than  in  temperate  countries,  for 
obvious  reasons  connected  with  the  difficulty  of  preserving  food  supplies. 
The  appearance  of  the  larvae  is  usually  viewed  with  the  greatest  alarm  by 
the  patients,  but,  as  a  rule,  they  are  entirely  harmless.  Occasionally  they 
produce  some  symptoms  of  gastrointestinal  disturbance,  such  as  vomiting, 
diarrhoea,  and  abdominal  pains.  Free  purgation  is  indicated  whenever 
larvae  are  seen  in  the  stools,  to  ensure  evacuation  of  those  remaining.  For 
this  purpose  calomel  is  the  best  drug,  as  it  exercises  not  only  an  evacuant 
but  a  toxic  effect  on  the  larvae. 

Dermatobia  Cyaniventris. — This  common  American  fly  deposits  its  eggs 
on  the  skin  of  man  and  cattle.  The  larvae  penetrate  the  cutaneous  structure, 
producing  large  pustular  lesions  (locally  known  as  ver  macaque).  Besides 
this  fly  there  are  great  numbers  of  diptera  whose  larvae  attack  the  skin  of 
man.  In  all  of  them  the  lesions  are  similar  to  that  above  described.  In 
America  these  are  principally  the  Musca  vomitoria.  the  ordinary  blue-bottle 
fly,  and  the  bot-fly  of  the  ox  and  sheep. 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


DISEASES  IN  WHICH   THE   CHIEF   MANIFESTATIONS   ARE  IN 
THE  BRAIN  AND  ITS  MEMBRANES. 


HEMORRHAGE  INTO  THE  BRAIN,  CEREBRAL  THROMBOSIS, 
AND  EMBOLISM. 

Definition. — Apoplexy  consists  in  the  sudden  onset  of  paralysis  and  loss 
of  consciousness  from  an  abrupt  intracranial  lesion.  In  its  most  typical 
form  it  is  due  to  hemorrhage  in  the  cerebrum,  but  it  may  also  be  due  to 
hemorrhage  into  the  cerebellum,  into  the  brain-stem,  or  into  the  meninges, 
and  it  may  result  from  embolism  or  from  thrombosis.  When  it  arises 
without  being  accompanied  by  a  demonstrable  brain  lesion  it  is  spoken 
of  as  an  "  apoplectiform  attack."  An  inflammatory  process  in  the  central 
nervous  system,  so  acute  that  minute  hemorrhages  occur  in  the  affected 
area,  is  also  spoken  of  as  apoplectiform,  as,  for  example,  "apoplectiform 
bulbar  paralysis." 

The  term  "apoplexy,"  as  commonly  employed,  is  nearly  equivalent  to 
the  popular  term  "stroke,"  and  is  used  so  indefinitely  that  it  is  better  to 
use  the  more  accurate  terms  cerebral  hemorrhage,  cerebral  thrombosis,  or 
embolism  when  describing  the  condition  present.  The  symptoms  pro- 
duced by  thrombosis  and  embolism  are  almost  identical  with  those  due 
to  hemorrhage,  and  will  be  found  discussed  in  the  consideration  of  the 
differential  diagnosis  of  the  disease. 

Etiology. — As  already  stated,  the  usual  cause  of  apoplexy  is  the  rupture 
of  a  bloodvessel  in  the  brain  or  its  meninges.  This  is  due  in  the  great 
majority  of  cases  to  changes  in  the  bloodvessel  produced  by  disease  or  bv 
injury.  These  changes  are  described  in  the  article  on  Arteriosclerosis. 
The  immediate  causes  which  produce  rupture  of  an  intracranial  vessel  are 
numerous,  for  all  factors  which  cause  a  sudden  increase  in  blood  pressure 
may  result  in  so  great  a  strain  on  a  weakened  vessel  wall  that  it  gives 
way.  Thus,  apoplexy  not  rarely  follows  a  paroxysm  of  rage,  a  severe 
nervous  shock,  a  sudden  muscular  effort,  as  in  running  for  a  car,  in 
straining  at  stool,  and  during  sexual  intercourse.  The  use  of  alcoholic 
and  other  stimulants  may  also  cause  rupture. 

Frequency. — Men  are  more  frequently  attacked  by  apoplexy  than  are 
women,  because  they  suffer  so  much  more  commonly  from  arteriocapillary 
fibrosis.  The  ratio  is  about  as  80  to  20  per  cent.,  according  to  Starr,  but 
68  ( 913 ) 


914  DISEASES  OF   THE  NERVOUS  SYSTEM 

Gintrac  puts  it  at  56.6  to  43.4  per  cent.  Of  816  cases  of  cerebral  hemorrhage 
collected  by  me  from  various  sources,  454  occurred  in  men  and  362  in  women. 
The  period  of  life  at  which  cerebral  hemorrhage  most  commonly  occurs  is 
from  fifty  to  eighty  years  of  age.  This  is  the  age  period  during  which  the 
patient  is  actually  most  liable  to  this  accident;  but  if  the  ages  of  the  entire 
number  of  persons  dying  of  apoplexy  in  a  given  series  of  statistics  be  added 
together  and  an  average  obtained,  the  largest  number  of  cases  is  found 
between  forty  and  sixty  years,  because  so  few  persons  live  to  eighty  years 
that  not  many  persons  of  that  age  are  to  be  found  in  such  a  series.  The  fol- 
lowing table  is  a  combination  of  the  cases  of  Gintrac  and  Breese,  and  shows 
the  age  incidence  of  cerebral  hemorrhage  by  decades  from  thirty  to  eighty 
years. 

Between  30  and  40  years  of  age 74 

"       40    "    50      "           "             98 

"       50    "     60      "           "             138 

"       60    "    70      "           "  ......  172 

"       70    "     80      "           "             124 

The  question  of  age  in  its  relation  to  apoplexy  is,  however,  more  dependent 
upon  the  state  of  the  bloodvessels  than  upon  the  actual  years  of  existence, 
for  not  infrequently  a  syphilitic  of  thirty  years  of  age  may  suffer  more  from 
degeneration  of  the  arteries  than  another  man  at  seventy. 

Available  statistics  do  not  show  any  increase  in  the  frequency  of  cerebral 
hemorrhage.  Thus,  from  1879  to  1884,  12,408  patients  were  admitted  to 
the  medical  wards  of  St.  Bartholomew's  Hospital,  London,  and  of  this  num- 
ber 79  were  affected  with  cerebral  hemorrhage.  During  the  five  years  from 
1897  to  1902,  12,089  medical  patients  were  admitted  to  the  hospital,  and 
among  them  there  were  62  cases  of  cerebral  hemorrhage. 

Pathology. — The  changes  which  take  place  in  the  bloodvessels  of  the 
brain  which  result  in  apoplexy  are  those  of  arteriosclerosis  as  we  meet  it  in 
other  parts  of  the  body;  the  intima  becomes  roughened  and  eroded,  the 
muscular  sheath  undergoes  fatty  degeneration,  and  the  fibrous  sheath 
becomes  less  elastic  than  in  health.  Aneurysmal  dilatations  frequently 
develop,  and  these  are  the  parts  of  the  vessel  from  which  hemorrhage  often 
ensues.  In  the  article  on  Arteriosclerosis  it  was  shown  that  the  causes  of 
this  state  are  syphilis,  lead,  gout,  renal  disease,  and,  not  least  important, 
advanced  years;  but  of  all  these  causes  renal  disease  is  probably  the  one 
which  most  frequently  produces  vascular  rupture,  because  it  is  usually 
associated  with  cardiac  hypertrophy  and  a  high  arterial  tension,  which 
increases  the  stress  on  the  weakened  vessel  wall. 

Rupture  of  a  vessel  occurs  very  much  more  frequently  in  certain  areas 
than  in  others,  as  already  pointed  out.  This  is  because  certain  vessels 
suffe  from  arterial  sclerosis  earlier  than  others,  and  also  because  of  the 
anatomical  relationship.  Thus,  the  blood  current  reaches  the  left  middle 
cerebral  artery  more  directly  from  the  heart  than  it  does  on  the  right  side, 
where  it  first  passes  through  the  innominate  artery,  which  diminishes  its 
force.  Durand  Fardel  states  that  75  per  cent,  of  the  miliary  aneurysms 
which  affect  cerebral  vessels  involve  the  branches  of  the  middle  cerebral 


HEMORRHAGE  INTO   THE  BRAIN  915 

artery  which  enter  the  anterior  perforated  space,  namely,  the  lenticulo- 
striate  and  the  lenticulo-thalamic  vessels.  For  this  reason  the  lenticulo- 
striate  branch  was  called  by  Charcot  the  "artery  of  cerebral  hemorrhage." 
About  50  to  60  per  cent,  of  all  cerebral  hemorrhage  is  from  this  vessel,  and 
therefore  occurs  in  the  internal  capsule  or  near  it.  (See  Hemiplegia.)  The 
sharp  spurt  of  blood  which  follows  rupture  of  the  vessel  wall  may  break 
through  the  corpus  striatum  in  either  direction,  often  internally  through 
the  caudate  nucleus,  or  it  may  break  through  the  optic  thalamus;  and  when 
the  rupture  is  large  and  the  blood  pressure  high,  the  blood  thus  finds  its 
way  into  the  lateral  ventricles  (see  Fig.  118),  into  the  third  ventricle, 
and  even  into  the  fourth  ventricle,  where  it  causes  death  by  pressure  on  the 
vital  centres,  if  death  has  not  already  ensued  from  shock  and  the  damage 
to  the  cerebral  tissues. 

When  these  "  capsulo-ganglionic  "  vessels  do  not  give  way  the  cause  of  the 
symptoms  is  usually  rupture  of  some  of  the  outer  branches  of  the  Sylvian 
artery,  producing  lesions  in  the  cortex.  In  still  other  cases,  which  are  less 
frequent,  the  hemorrhage  takes  place  into  the  pons  and  still  more  rarely 
into  the  cerebellum. 

Cerebellar  hemorrhages  are  especially  prone  to  inundate  the  fourth  ventricle. 

A  very  much  rarer  form  of  apoplexy  is  that  in  which  by  reason  of  disease 
of  the  blood,  or  of  the  vessels,  small  oozings  or  extravasations  take  place 
through  the  vessel  walls,  which  on  subsequent  examination  do  not  reveal 
any  rupture.  This  extra vasated ,  fluid  finds  its  way  alongside  the  vessels, 
and  so  does  damage  to  a  wide  area  without  causing  any  very  gross  lesion 
in  the  brain  tissues.  Such  a  state  may  develop  in  the  course  of  purpura  or 
leukocythemia.  Extravasations  of  blood  into  the  meninges  and  cortex  also 
occur  as  the  result  of  injury. 

In  those  cases  in  which  the  hemorrhage  is  arrested  before  it  does  great 
damage  much  depends  upon  the  part  of  the  brain  which  is  affected. 

If  the  hemorrhage  occurs  on,  or  in,  the  cortex,  and  is  small  in  amount, 
the  convulsions  and  paralysis  which  ensue  may  only  involve  part  of  the 
arm,  or  leg,  or  face,  or  one  of  the  special  senses,  or  a  particular  function 
controlled  by  the  centre  that  has  been  destroyed,  or  such  a  monoplegia  may 
be  due  to  a  small  hemorrhage  in  the  subcortex  cutting  off  the  fibres  of  the 
corona  radiata  descending  from  the  cortical  centre.  But  an  equally  small 
hemorrhage  still  lower  down,  where  the  fibres  from  the  entire  cerebral 
hemisphere  come  together  in  the  internal  capsule,  will  produce  a  complete 
hemiplegia  (Fig.  116,  lesion  of  ordinary  hemiplegia).  On  the  other  hand, 
if  the  lesion  occurs  still  lower  down — that  is,  in  the  brain-stem,  where 
bundles  of  fibres  are  separating  from  the  main  paths  and  crossing  to 
the  opposite  sides  to  connect  with  cranial  nerves — it  will  produce  crossed 
paralysis — for  example,  the  face  is  paralyzed  on  one  side  and  the  body  on 
the  other.  Ordinary  "crossed  paralysis"  indicates  a  lesion  in  the  lower 
third  of  the  pons  because  at  this  point  the  motor  fibres  for  the  face  have 
crossed  but  the  fibres  for  the  limbs  have  not  done  so  (Fig.  117,  lesion  of 
crossed  paralysis).  If  the  posterior  third  of  the  internal  capsule  is  affected 
as  well  as  the  anterior  and  middle  thirds,  we  find  hemiansesthesia  as  well 
as  motor  paralysis  on  the  opposite  side  (Fig.  118);  and  if  the  very  posterior 


916 


DISEASES  OF   THE  NERVOUS  SYSTEM 


portion  of  this  limb  is  affected  the  optic  radiations  are  impHcated  and 
hemianopsia  is  added  to  the  symptoms.  (See  Fig.  118,  "optic")  If  the 
patient  survives  the  attack  the  extravasated  blood  coagulates  and  is  sur- 
rounded by  a    protective    wall  of  lymph,    which   undergoes    organization 


Fig.  116 

LIMB 


Diagram  sbowing  the  fibres  from  the  cortex  forming  the  corona  radiata,  which  after  they  are  approxi- 
mated pass  into  the  internal  capsule.  It  also  shows  the  decussation  of  the  pyramid  of  the  left  side,  which 
passes  to  the  right  side  of  the  spinal  cord,  and  the  direct  or  uncrossed  tract  (Turck's  column).  Finally,  it 
also  shows  the  secondary  degeneration  which  occurs  after  cerebral  hemorrhage  or  softening,  and  which 
follows  the  course  of  the  motor  tracts  into  the  spinal  cord.  H.  Site  of  lesion.  The  continuous  lines  are 
fibres  going  to  the  legs,  the  dotted  are  those  going  to  the  arms  and  motor  cranial  nerves.  The  Koman 
numerals  refer  to  the  origins  of  the  cranial  nerves.    (Modified  from  Van  Gehuchten.) 


HEMORRHAGE  INTO    THE  BRAIN 


917 


while  the  clot  softens,  and  contracts  as  its  contents  are  being  absorbed. 
The  permanent  lesion  of  apoplexy  is  thus  commonly  a  cyst,  but  some- 
times, absorption  having  been  complete,  only  a  scar  remains.  Not  only  do 
these  changes  take  place  at  the  site  of  the  hemorrhage,  when  it  affects  the 
the  cortex  or  motor  fibres  in  the  corona  radiata  or  in  the  internal  capsule, 
but  degenerative  alterations  follow  along  the  motor  pathways  through  the 
peduncles  of  the  cerebrum,  the  pons,  the  pyramids  of  the  medulla,  and  so 
on  into  the  direct  and  crossed  pyramidal  tracts  of  the  cord.    (See  Fig.  116.) 


Fig.  117 


Lesion  of  cerehral-mo- 
noplegia  {brachial) 


Lesion  of  ordinary 
hemiplegia 


Lesion  of  cross  paralysis 
{face  of  same  side  with 
limbs  of  other  side) 


A  lesion  causing  paraplegia. 


A  lesion  causing  hetni- 
paraplegia 


Vortical  centre  for  op- 
posite leg 


-Cortical  centre  for  op- 
posite arm, 


Cortical  centre  for  op- 
posite side  of  face 


ntenial  capsule  (pos- 
terior limb  ) 


-Motor  nerve  to  face 


Decussation  of  pyra- 
mids 


Crossed  pyramidal  tract 


Motor  nerves  to  upper 
limb 


Crossed  pyramidal  tract 


Sensory  nerves  entering 
cord,  and  decussating 
soon  after  entry 


Motor  nerves  to  lower 
limb 


Diagram  showing  the  general  arrangement  of  the  motor  tract  and  the  efiect  of  lesions  at 
various  points.    (Ormerod.) 

Symptoms.— The  symptoms  of  apoplexy  depend  upon  the  site  of  the  lesion 
and  upon  the  suddenness  and  severity  of  the  hemorrhagic  extravasation, 
as  already  stated.  A  few  cases  have  some  premonitory  sym-ptoms  such  as 
numbness  or  tingling  in  the  part  of  the  body  about  to  be  affected,  but  most 
cases  are  attacked  without  warning.  When  the  hemorrhage  takes  place 
from  the  middle  cerebral  artery  the  symptoms  are  usually  as  follows: 


918 


DISEASES  OF   THE  NERVOUS  SYSTEM 


An  individual  who  is  apparently  in  his  normal  health  is  suddenly  seized 
with  vertigo,  which  causes  him  to  stagger  and  fall.  The  face  is  at  first  pallid 
and  later  somewhat  congested.  The  respiration  is  altered  almost  imme- 
diately. At  first  it  may  be  slightly  gasping  and  irregular,  but  soon  becomes 
full  and  deep.     The  air  is  drawn  into  the  lungs  with  considerable  force 


Fig.  118 


Cross-section  of  the  brain,  showing  the  lateral  ventricles,  the  cerebellum,  and,  most  important,  the  cross- 
section  of  the  motor  fibres  in  the  internal  capsule.    (Modified  from  Fuller.) 

and  then  equally  forcibly  expelled.  As  it  enters  it  causes  the  relaxed  soft 
palate  to  vibrate  and  as  it  escapes  through  the  angle  of  the  mouth,  which 
is  paralyzed,  it  produces  a  noise  to  which  the  term  "stertorous  breathing" 
has  been  applied.  The  pulse  is  slow  and  full  and  its  tension  high  except 
for  a  few  moments  after  the  onset  of  the  symptoms,  when  it  may  be  rapid 


HEMORRHAGE  INTO   THE  BRAIN  919 

and  irregular  from  the  shock.  In  some  cases,  too,  in  which  the  hemorrhage 
into  the  brain  is  very  great  and  death  imminent,  the  pulse  may  not 
become  full  and  strong. 

An  examination  of  the  patient's  limbs  may  show  that  both  sides  are  almost 
equally  relaxed  and  powerless,  but  this  is  usually  a  temporary  state  due  to 
shock,  and  in  a  very  short  time  it  will  be  found  that  the  limbs  on  one  side 
are  moved,  or  at  least  are  not  quite  powerless,  while  those  on  the  opposite 
side  are  paralyzed.  In  other  words,  the  typical  paralysis  of  cerebral  hemor- 
rhage called  hemiplegia  is  present. 

The  muscles  of  the  trunk  are  never  as  completely  paralyzed  as  those  of 
the  limbs.  The  muscles  of  the  lower  part  of  the  face  share  in  the  paralysis, 
and  for  this  reason  the  features  will  be  drawn  away  from  the  paralyzed  side 
because  the  normal  balance  between  the  muscles  on  the  two  halves  of  the 
face  has  been  destroyed.  Unlike  the  facial  paralysis  due  to  a  lesion  in  the 
facial  nucleus  in  the  pons  or  in  the  facial  nerve  itself,  the  upper  muscles 
escape,  and  so  we  find  that  the  muscles  of  the  forehead  and  eyes  are 
not  paralyzed;  the  forehead  can  be  wrinkled  and  the  eyes  can  be  closed. 

In  the  stage  of  onset  we  sometimes  find  the  head  and  eyes  turned 
sharply  to  one  side  (conjugate  deviation),  usually  away  from  the  para- 
lyzed side.  When  this  occurs  it  is  said  that  the  eyes  "look  at  the  lesion." 
The  pupils  are  sometimes  contracted,  but  more  conimonly  are  dilated, 
the  pupil  on  the  side  upon  which  the  hemorrhage  has  taken  place  being 
more  dilated  than  its  fellow. 

Pricking  or  pinching  the  skin  of  the  paralyzed  side  is  not  followed  by 
any  reflex  contraction  soon  after  the  onset,  though  the  deep  reflexes  may 
be  present,  but  later,  when  the  primary  shock  has  passed  away,  it  will  be 
found  that  the  skiyi  reflexes  as  well  as  the  knee-jerk  and  other  deep  reflexes 
are  exaggerated,  particularly  upon  the  paralyzed  side.  Irritation  of  the  sole 
of  the  foot  almost  invariably  causes  extension  of  the  big  toe  (Babinski's 
reflex),  a  reversal  of  the  normal  plantar  reflex,  which  is  flexion  of  the 
toes.     Ankle-clonus  is  also  frequently  present. 

In  cases  in  which  the  bladder  and  the  bowel  are  full  at  the  time  of  the 
"stroke,"  the  shock  of  the  hemorrhage  may  result  in  involuntary  evacua- 
tions, but  in  some  cases  the  bladder  and  rectum  are  not  only  retentive,  in 
the  ordinary  sense,  but  fail  to  empty  themselves  when  they  become  full.  The 
bladder  of  an  apoplectic  patient  should,  therefore,  be  frequently  examined, 
and  if  the  urine  accumulates  in  excess  it  must  be  withdrawn  by  the  catheter. 
If  the  urine  is  examined  a  trace  of  albumin  is  usually  found  in  it,  even  if 
actual  renal  disease  is  not  present.  The  temperature  of  the  body  immediately 
after  a  hemorrhage  is  usually  subnormal.  With  reaction  from  the  primary 
shock,  which  is  often  of  brief  duration,  the  temperature  rises  from  one 
to  three  degrees,  the  chief  change  being  on  the    paralyzed  side. 

The  unconsciousness  of  the  early  stage  of  apoplexy  may  last  from  a  few 
hours  to  several  days,  according  to  the  severity  of  the  lesion.  When  it 
persists  for  any  length  of  time  the  prognosis  is  correspondingly  bad. 
In  some  cases  the  depth  of  the  coma  decreases  and  the  patient  emerges 
to  some  extent,  only  to  sink  back  again  into  deep  coma  and  high  fever  a  few 
days  later  when  a  secondary  hemorrhage  takes  place,  perhaps  bursting  into 


920  DISEASES  OF   THE  NERVOUS  SYSTEM 

the  ventricle,  or  secondary  irritation  of  the  brain,  produced  by  the  pres- 
ence of  the  extravasated  blood,  develops.  In  other  cases  in  which  the 
extravasation  of  blood  has  been  hmited,  and  the  parts  damaged  are  not  of 
vital  importance,  the  patient  gradually  improves  in  his  mental  state  and 
progresses  toward  recovery.  In  most  cases,  however,  the  mind  never  com- 
pletely recovers  its  previous  acuity. 

The  persistency  of  the  hemiplegia  also  varies  greatly  in  different  cases.  It 
may  remain  absolutely  unchanged,  one-half  of  the  body  being  helpless,  or 
it  may  diminish  in  severity  and  even  greatly  improve  to  the  extent  that  the 
patient  can  walk  about  and  write.  In  most  of  the  cases,  however,  in  which 
this  much  to  be  desired  result  is  attained,  the  lesion  has  probably  been  due 
to  embolism  or  thrombosis   rather  than  to  an  actual  hemorrhage. 

Many  patients  after  an  attack  of  apoplexy  not  only  suffer  from  a  degree 
of  mental  failure,  but  in  addition  become  exceedingly  irritable  or  emotional, 
crying,  laughing,  or  getting  into  a  furious  temper  at  slight  causes.  Distinct 
loss  of  emotional  control  has  been  said  to  be  particularly  prone  to  occur 
when  the  lesion  involves  the  frontal  lobes. 

There  still  remain  to  be  considered  several  additional  symptoms  of  apo- 
plexy which  are  often  present.  The  most  important  of  these  is  aphasia. 
It  is  most  common  in  cases  in  which  the  right  side  is  paralyzed,  because  the 
speech  centre  is  chiefly  in  the  third  left  frontal  convolution.  If  the  patient 
is  left-handed,  however,  the  aphasia  is  present  when  the  left  side  is  paralyzed. 
The  symptom  aphasia  varies  very  greatly  in  the  time  at  which  it  is  first 
evident  and  in  its  severity.  Not  infrequently  it  is  one  of  the  first  signs  of 
a  beginning  apoplexy,  the  speech  becoming  suddenly  confused  and  indis- 
tinct. In  most  cases,  however,  the  aphasia  is  first  noticed  after  the  patient 
recovers  from  the  immediate  effects  of  the  stroke.  The  persistency  of  the 
aphasia  varies  greatly.  In  some  cases  it  remains  so  severe  that  the  patient 
has  great  difficulty  in  making  himself  understood.  In  others  it  improves 
so  greatly  that  it  may  entirely  disappear,  or  only  be  present  when  the  patient 
becomes  very  tired  or  excited. 

Another  special  symptom  is  hemianopsia,  which  is  of  the  homonymous 
type,  that  is,  the  corresponding  halves  of  the  visual  fields  are  darkened 
because  the  temporal  half  of  one  retina  and  the  inner  or  nasal  half  of  the 
other  retina  has  lost  its  visual  function. 

Hemianoesthesia  persisting  after  recovery  from  the  primary  shock  is  a  rare 
symptom  and  is  never  complete,  thereby  differing  from  the  hemianeesthesia 
of  hysteria.  The  sense  of  heat  or  cold  or  touch  may  be  impaired,  but  total 
loss  of  the  senses  does  not  take  place. 

When  the  power  of  recognizing  objects  placed  in  the  hand  is  lost  (astereog- 
nosis)  it  indicates  a  lesion  in  the  superior  parietal  portion  of  the  cortex 
on  the  opposite  side.      (See  Fig.  121.) 

In  some  cases  of  hemiplegia  of  a  severe  type  bed-sores  develop  on  the  heel 
or  buttock  of  the  affected  side.  The  tendency  to  this  accident  can  be  greatly 
decreased  if  the  patient  is  not  permitted  to  lie  in  one  position  for  long  periods 
of  time,  and  if  great  care  is  taken  as  to  the  cleanliness  of  the  skin  in  the 
places  where  pressure  is  marked. 

As  a  sequence  to  an  apoplexy  we  find  not  only  persistent  paralysis,  but 


HEMORRHAGE  INTO   THE  BRAIN  921 

as  time  goes  on  contractures  occur  in  the  affected  limbs.  The  forearm 
and  hand,  however,  suffer  far  more  than  the  leg.  The  flexor  muscles 
being  stronger  than  the  extensors,  the  hand  is  usually  found  in  marked 
flexion  upon  the  wrist,  and  the  fingers  are  turned  into  the  palm  of  the  hand. 
The  leg  is  usually  held  in  the  position  of  extension  so  that  it  cannot  be  bent 
at  the  knee,  and  for  this  reason  it  is  often  swung  with  a  lateral  movement 
from  the  hip  when  the  patient  attempts  to  walk.  These  contractures  are 
usually  much  diminished  when  the  patient  is  asleep,  and  are  due  to 
degenerative  changes  in  the  crossed  pyramidal  tracts.  (See  Fig.  116.) 
Occasionally,  that  curious  mobile  spasm  of  the  fingers  or  other  members, 
called  "  athetosis,"  is  a  sequence  of  apoplexy  and  posthemiplegic  chorea 
may  develop.  This  is  commonest  in  the  hemiplegias  of  childhood,  but 
occurs  in  adults.  Full  doses  of  strychnine  may  produce  spastic  contractions 
in  old  cases  of  hemiplegia.  Next  to  signs  of  spasm  the  most  common 
symptom  as  a  sequel  is  muscular  atrophy,  which  is  due  in  part  to  disuse 
of  the  muscles  in  the  paralyzed  limbs  and  does  not  develop  till  some 
time  after  the  acute  stage  of  the  attack.  Charcot  has  reported  instances  in 
which  true  trophic  joint  changes  took  place,  but  they  are  exceedingly 
rare. 

The  symptoms  of  an  attack  of  apoplexy  in  which  the  lesion  has  been  due 
to  rupture  of  a  branch  of  the  middle  cerebral  artery  having  been  described, 
there  still  remain  to  be  considered  those  additional  symptoms  which  develop 
when  other  parts  of  the  cranial  contents  are  affected  by  the  giving  way  of 
other  vessels. 

When  a  vessel  in  the  dura  mater  is  ruptured,  usually  as  the  result  of  an 
injury,  it  is  the  middle  meningeal  artery  or  vein  which  suffers  as  a  rule. 
The  clot  which  is  formed  is  either  outside  the  dura  mater  (extradural) 
or  beneath  it  (subdural).  The  noteworthy  peculiarity  of  these  cases  is 
that  the  primary  unconsciousness  due  to  a  blow  speedily  disappears,  the 
patient  may  recover  his  normal  mental  state,  and  then,  after  an  interval 
varying  from  some  minutes  to  several  hours  or  days,  becomes  heavy  and 
dull,  and  finally  comatose.  Spasmodic  movements  of  the  muscles  on  one 
side  of  the  body,  followed  by  paralysis,  may  develop.  If  the  extravasation 
of  blood  is  large,  the  pupil  on  the  paralyzed  side  is  contracted  and  that  on  the 
side  of  the  hemorrhage  is  dilated.  This  is  called  the  "Hutchinson  pupil." 
The  eyes  are  turned  away  from  the  lesion,  whereas  in  the  acute  stage  of  an 
ordinary  apoplexy  they  are  turned  toward  it.  It  is  in  this  form  of  apoplexy 
that  surgical  interference  is  absolutely  essential  to  save  life.  Such  hemor- 
rhages sometimes  occur  in  the  insane  without  a  history  of  injury,  particularly 
in  paretics  and  in  chronic  alcoholics. 

In  hemorrhage  from  a  vessel  upon  the  cortex,  as  one  of  the  branches  of 
the  Sylvian  artery,  it  is  important  to  recall  the  fact  that  muscular  spasm,  or 
a  convulsion,  usually  ushers  in  the  attack  due  to  the  disturbance  of  the 
cells  in  the  motor  area. 

When  the  blood  finds  its  way  into  the  lateral  ventricles,  a  general  convul- 
sion affecting  the  entire  body  may  develop.  Such  cases  usually  pass  into 
deep  coma  and  soon  die. 

When  the  lesion  is  in  the  pons  the  temperature  is  usually  soon  hyperpyretic, 


922  DISEASES  OF   THE  NERVOUS  SYSTEM 

the  pupils  are  tightly  contracted,  siuallowing  is  difficult,  and  the  respiration 
is  very  slow.    Death  comes  rapidly  in  these  cases  as  a  rule. 

Under  the  name  of  "ingravescent  apoplexy"  a  condition  is  met  "sivith  in  which 
the  symptoms  develop  very  gradually,  beginning,  it  may  be,  by  an  attack 
of  vertigo  or  aphasia,  followed  by  the  slow  development  of  the  other 
symptoms  already  described,  so  that  several  days  may  elapse  before  the 
entire  symptom-complex  of  apoplexy  is  present. 

Diagnosis. — An  attack  of  apoplexy,  or  hemorrhage  into  the  brain,  must 
be  separated  from  a  number  of  conditions  which  may  closely  resemble  it. 
Two  conditions  which  resemble  it  so  closely  as  to  be  inseparable  in  some 
cases  are  thrombosis  and  embolism  of  the  cerebral  vessels.  The  symptoms 
produced  by  these  accidents  will  be  found  described  below. 

An  ordinary  attack  of  syncope  can  readily  be  differentiated  by  the  pallor, 
the  feeble  pulse,  the  weak  heart  of  a  fainting  attack,  and  the  quick  recovery 
of  the  patient  after  receiving  some  rapidly  acting  diffusible  stimulant. 

In  epilepsy  the  peculiar  initial  cry,  the  bloody  froth  at  the  mouth,  the  general 
convulsion,  and  the  deep  unconsciousness  are  more  constant  and  severe  than 
in  apoplexy,  even  if  the  hemorrhage  takes  place  in  the  cortex.  Epilepsy  is  more 
common  in  the  young,  apoplexy  in  those  of  advanced  years,  and  there  may 
be  scars  to  indicate  previous  severe  falls  in  epileptics.  A  history  of  epilepsy 
will  practically  settle  the  diagnosis,  although  the  epileptic  is  liable  to  apoplexy. 
The  respiration  in  the  coma  of  apoplexy  continues  deep  and  noisy,  the 
lips  and  cheeks  of  one  side  flap  in  the  air  current,  showing  paralysis, 
and  weakness  of  one  arm  and  leg  may  be  ascertained.  In  the  coma  of 
epilepsy  the  breathing  soon  becomes  quiet.  Rarely  in  epilepsy  weakness 
of  one  side  of  the  body  or  of  one  limb  may  appear  as  the  patient  emerges 
from  the  coma;  this  postepileptic  hemiplegia  is  ascribed  to  exhaustion,  for 
it  passes  off  in  a  few  hours  or  days,  but  it  may  put  the  diagnosis  in  doubt 
for  a  time. 

From  the  stupid  stage  of  acute  alcoholism  apoplexy  can  be  differentiated 
by  the  history  of  the  patient,  by  the  odor  of  alcohol  on  his  breath,  by  the  fact 
that  both  legs  are  moved  if  they  are  irritated  by  pricking,  proving  the  absence 
of  hemiplegia,  and  by  the  cool  skin  as  compared  to  the  hot,  dry  skin  of 
apoplexy.  It  is,  however,  possible  for  an  apoplectic  to  have  induced  an 
attack  by  the  use  of  alcohol,  and  therefore  the  odor  of  alcohol  on  his 
breath  is  not  of  great  importance  from  a  diagnostic  standpoint. 

Opium  poisoning  is  differentiated  by  the  presence  of  contracted  pupils,' 
by  the  fact  that  by  shouting  the  patient  can  be  aroused,  by  the  absence 
of  paralysis,  and  by  the  presence  of  the  corneal  reflexes. 

The  coma  of  urjemia  and  of  diabetes  may  also  be  mistaken  for  apoplexy, 
but  in  uraemia  there  may  be  oedema  of  the  lower  extremities,  and  there  is  a 
urinous  odor  about  the  body  and  breath  of  the  patient.  If  the  renal  disease 
is  of  the  parenchymatous  type,  the  peculiar  waxen  appearance  of  the  patient 
and  the  urine  heavily  loaded  with  albumin  will  make  the  diagnosis  clear. 
If  the  uraemia  is  of  the  type  caused  by  chronic  contracted  kidney,  these  latter 
signs  will  not  be  present  nor  will  oedema  be  found,  and  as  apoplexy  often 
complicates  this  disease  the  diagnosis  may  be  most  difficult.  Unless  the 
coma  is  very  deep  one  side  may  be  moved  far  more  than  the  other,  reveal- 


HEMORRHAGE  INTO   THE  BRAIN  923 

ing  the  hemiplegia  of  apoplexy.  However,  in  uraemia  the  cerebral  affection 
may  be  more  pronounced  in  one  hemisphere,  thus  causing  a  hemiplegia 
("ursemic  apoplexy").  In  diabetic  coma  the  sweet  odor  of  the  breath  and 
the  presence  of  sugar  and  acetone  in  the  urine  will  make  the  diagnosis 
possible. 

In  sunstroke  likewise  hemiplegia  may  be  found,  which  is  not  an  apoplexy 
in  the  ordinary  sense. 

Finally,  it  must  not  be  forgotten  that  apoplectiform  attacks  not  rarely 
develop  in  the  course  of  general  paralysis  of  the  insane.  In  this  disease  the 
speedy  return  to  consciousness  and  recovery  of  power  in  the  affected  limbs, 
with  the  physical  signs  of  this  disease  and  the  mental  symptoms,  will 
render  a  diagnosis  possible. 

The  separation  of  the  paralysis  due  to  hemorrhage  from  that  due  to 
thrombosis  depends  more  upon  the  history  of  the  patient  than  upon  the 
symptoms  actually  present.  As  already  stated,  hemorrhage  usually  fol- 
lows some  effort  and  takes  place  during  waking  hours,  whereas  the  paralysis 
of  thrombosis  develops  during  periods  of  quiet  and  rest,  as  during  sleep,  so 
that  the  patient  wakes  to  find  the  palsy  present.  In  cases  of  hemorrhage 
premonitory  symptoms  are  not  common,  but  in  thrombosis  they  are  nearly 
constant.  Thrombosis  is  most  frequent  in  the  aged  or  prematurely  senile, 
and  in  syphilitics.  i\.gain,  thrombosis  does  not  cause  such  violent  symp- 
toms nor  is  the  onset  of  the  symptoms  so  sudden,  but  consciousness  is  pre- 
served or  is  not  so  completely  lost,  or  if  moderate  coma  is  present  it  is 
brief  in  duration  and  is  followed  by  mental  clearness.  Finally,  in  cases  of 
thrombosis,  the  recovery  of  power  in  parts  of  the  paralyzed  side  may  be 
quite  rapid,  and  at  the  end  of  a  few  days  only  a  few  muscles,  as  one  arm  or 
leg,  are  affected.  Such  cases  are,  however,  often  mentally  feeble,  emotional, 
and  forgetful  after  the  attack.  There  is  often  to  be  found  a  history  of 
syphilis,  of  arteriosclerosis,  or  an  infectious  disease,  which  has  predisposed 
the  patient  to  a  formation  of  a  clot  by  causing  disease  in  the  lining  of  the 
bloodvessel  or  producing  changes  in  the  blood. 

Embolism  can  be  determined  by  the  sudden  onset  of  symptoms  during 
the  waking  hours,  as  a  rule,  and  by  the  discovery  of  some  source  of  clot  or 
foreign  body,  as  in  an  endocarditis  with  vegetations  or  a  septic  focus  else- 
where. Unconsciousness,  when  it  develops,  may  be  as  profound,  but  is 
usually  more  transient  than  in  hemorrhage  (Mills),  and  is  often  entirely 
absent.  The  appearance  of  the  patient  is  not  so  alarming  as  in  hemor- 
rhage, and  localized  or  general  twitching  may  be  present  in  the  affected 
limbs.  Not  rarely  as  a  collateral  circulation  is  established,  the  symptoms 
improve  with  great  rapidity  and  after  a  few  days  may  amount  to  only  a 
partial  monoplegia.  It  must  be  recalled,  however,  that  in  some  cases  of 
thrombosis  and  embolism  the  symptoms  may  be  so  like  those  due  to  hemor- 
rhage that  a  differentiation  is  almost  impossible. 

The  chances  of  the  case  being  one  of  hemorrhage  rather  than  embolism 
or  thrombosis  is  as  6  to  1,  according  to  Dana. 

Prognosis. — Many  cases  of  hemorrhage  into  the  brain  survive  the  first 
rupture,  but  if  so  they  nearly  always  fall  victims  to  subsequent  attacks.  Out 
of  441  cases  occurring  in  St.  Thomas'  and  St.  Bartholomew's  Hospitals, 


924  DISEASES  OF   THE  NERVOUS  SYSTEM 

London,  375  proved  fatal,  a  mortality  percentage  of  85.  This  per- 
centage is,  however,  far  too  high  for  private  practice,  where  milder  cases 
are  often  seen.  In  the  severe  cases  in  which  the  coma  is  profound,  the 
temperature  low  and  then  quite  high,  the  paralysis  severe,  and  control 
of  the  bladder  or  bowels  impaired,  death  will  probably  occur  in  the  first 
attack,  and  if  Cheyne-Stokes  breathing  is  present  death  nearly  always  takes 
place  within  a  few  hours.  If  the  hemorrhage  affects  the  pons  or  cerebellum 
death  may  come  on  speedily,  but  when  the  hemorrhage  is  small  the  patient 
often  survives.  When  the  hemorrhage  is  cortical  the  prognosis  is  better 
than  in  the  other  forms  unless  the  pressure  symptoms  are  severe.  The 
patient  not  rarely  dies  from  pulmonary  oedema  or  pneumonia  as  an  inter- 
current disease. 

Treatment. — Apoplexy,  like  other  forms  of  internal  hemorrhage,  cannot 
be  materially  benefited  by  medicinal  treatment.  If  nature  does  not  form 
a  clot  to  plug  the  bleeding  vessel,  the  hemorrhage  must  continue  until  it 
has  done  so  much  damage  that  death  is  inevitable  unless  the  vessel  is  on  the 
surface  or  in  the  meninges,  when  surgical  relief  should  be  given.  Again,  the 
pressure  with  which  the  blood  escapes  into  the  soft  textures  of  the  brain  is 
so  great  that  if  the  leak  is  of  any  size  the  mechanical  injury  to  the  cerebral 
tissues  must  be  very  great,  and  for  this  reason  the  organ  is  permanently 
disabled. 

Until  the  recent  researches  of  Gushing,  of  Baltimore,  in  regard  to  the 
significance  of  high  arterial  pressure  in  cases  of  hemorrhagic  extrava- 
sations inside  the  skull,  it  was  universally  taught  that  the  presence  of 
a  full,  bounding  pulse  in  a  case  of  apoplexy  indicated  venesection,  par- 
ticularly if  at  the  same  time  there  was  distinct  venous  engorgement,  the 
thought  being  that  by  this  means  the  blood  pressure  would  be  lowered,  and 
that  there  would  be  a  corresponding  decrease  in  the  leakage  from  the  rup- 
tured vessel.  Cushing's  investigations  have  apparently  shown  beyond  all 
doubt  that  the  high  arterial  pressure  which  is  so  constantly  found  in  persons 
who  suffer  from  hemorrhage  inside  the  skull  is  an  effort  of  nature  to  main- 
tain the  blood  supply  to  the  vital  centres  at  the  base  of  the  brain,  and  that 
if  this  blood  supply  cannot  be  maintained  because  of  a  fall  in  arterial  pressure 
death  speedily  ensues.  In  other  words,  the  maintenance  of  a  high  arterial 
pressure  in  these  cases  is  an  advantageous  sign,  and  any  marked  diminution 
in  arterial  tension  is  an  indication  that  the  vasomotor  centre  is  becoming 
paralyzed  and  that  the  blood  supply  to  the  centres  at  the  base  of  the  brain 
is  becoming  impaired.  If  Cushing's  studies  are  correctly  interpreted  by  him, 
venesection  or  the  administration  of  vascular  sedatives,  with  the  purpose 
of  lowering  tension,  is  therefore  a  distinctly  harmful  method  of  treatment, 
and  truth  demands  that  we  should  admit  that  the  physician  can  do  little 
if  anything  in  the  way  of  controlling  the  escape  of  blood. 

For  the  purpose  of  apparently  making  an  effort  to  do  good  for  the  sake  of 
the  friends  who  may  demand  activity  rather  than  masterly  inactivity,  a  hot 
mustard  foot-bath  may  be  given,  and  some  diffusible  stimulant  like 
Hoffmann's  anodyne  may  be  used  if  the  patient  is  able  to  swallow,  or 
atropine  may  be  given  if  arterial  tension  falls  and  the  surface  becomes  cold 
and  clammy. 


INFANTILE  CEREBRAL  PARALYSIS  925 

If  vomiting  occurs,  the  patient  should  be  promptly  turned  on  one  side 
so  that  free  drainage  from  the  mouth  may  take  place,  and  in  order  that 
particles  of  food  may  not  be  drawn  into  the  respiratory  passages. 

If  the  tongue  falls  back  in  such  a  manner  as  to  make  the  breathing 
difficult  it  should  be  drawn  forward  by  means  of  the  fingers  covered  with 
a  towel.  If,  by  chance,  the  patient  is  convulsed,  his  tongue  should  be  pro- 
tected from  damage  by  placing  between  the  teeth  a  penholder  or  tooth-brush 
handle  covered  with  a  piece  of  muslin. 

The  patient's  body  should  always  be  put  in  that  position  in  which  breathing 
is  most  easily  carried  on. 

The  treatment  after  the  hemorrhage  has  ceased  consists  in  absolute 
rest,  in  the  application  of  an  ice-bag  to  the  head,  and  attention  to  the 
bowels  and  bladder  to  prevent  them  from  becoming  overdistended. 
Gentle  purgation  is  probably  advantageous  for  its  influence  upon  the 
brain.  If  any  evidence  of  nervous  excitation  exists,  it  may  be  controlled 
by  small  doses  of  the  bromides  or  morphine.  If  any  tendency  to  sec- 
ondary reaction  develops  in  the  course  of  a  few  days,  cold  to  the  head 
and  small  doses  of  aconite  to  quiet  the  circulation  may  be  administered. 
Later  on,  with  the  hope  of  diminishing  the  paralysis,  iodide  of  potassium 
may  be  given  in  moderate  doses  in  order  that  it  may  aid  in  the  absorption 
of  the  extra vasated  blood  and  remove  products  of  inflammation.  There  is 
little  use  in  giving  the  iodide  of  potassium  for  the  purpose  of  causing  absorp- 
tion earlier  than  two  or  three  weeks  after  the  hemorrhage.  Strychnine  is 
usually  not  valuable  in  these  cases,  as  it  is  very  apt  to  produce  spasm  or 
contracture  in  the  parts  which  are  paralyzed  by  irritating  the  motor  tracts 
in  the  spinal  cord. 

From  three  to  four  weeks  after  the  hemorrhage  it  is  often  advantageous  to 
apply  a  slowly  interrupted  faradic  current  to  the  paralyzed  muscles,  with 
the  object  of  maintaining  their  nutrition  by  exercise  and  keeping  them  in 
the  best  possible  condition,  in  the  hope  that  eventually  they  may  receive  a 
sufficient  amount  of  nervous  impulse  from  the  cerebral  centres  to  be  able 
to  respond  sufficiently  to  permit  the  patient  to  move  his  limbs.  Massage  is 
another  excellent  means  to  combat  the  loss  of  power.  Passive  and  active 
movements  followed  by  a  course  of  systematic  exercises  will  render  valuable 
service  in  combating  secondary  contractures  of  the  paralyzed  extremities. 
Great  care  should  be  taken  that  all  stimulants  which  increase  circulatory 
activity,  and  all  foods  which  readily  cause  indigestion,  be  avoided,  as  these 
two  factors  tend  to  produce  that  most  unfortunate  complication,  another 
hemorrhage. 

INFANTILE  CEREBRAL  PARALYSIS. 

Definition. — As  a  result  of  injury  or  disease  of  the  brain  during  fetal  life 
or  soon  after  birth,  it  not  rarely  happens  that  certain  portions  of  the  cere- 
brum fail  to  develop,  and  as  a  consequence  a  number  of  very  characteristic 
conditions  are  produced,  which  depend  in  their  nature  upon  the  site  and 
size  of  the  atrophied  region. 

These  conditions  can  be  grouped  in  three  divisions:    In  the  first  there  is 


926  DISEASES  OF   THE  NERVOUS  SYSTEM 

a  spastic  paralysis  which  may  be  limited  to  one  side  of  the  body  (spastic 
hemiplegia),  or  it  may  be  bilateral  (spastic  diplegia).  In  spastic  diplegia 
the  legs  may  be  affected  alone  or  the  arms  and  legs  may  both  be  involved. 
The  second  class  is  chiefly  characterized  by  mental  failure  varying  in  severity 
from  slight  intellectual  deficiency  to  absolute  idiocy.  In  some  instances  the 
defect  is  manifested  by  epileptic  attacks.  The  third  class  presents  disorders 
of  the  special  senses,  such  as  blindness,  deafness,  mutism  from  deafness, 
and  it  may  be  epileptic  seizures  as  well. 

Etiology. — Acute  infectious  disease  occurring  in  the  mother  during  preg- 
nancy may  result  in  lesions  in  the  fetal  brain.  Syphilis  may  also  act  in 
this  manner.  It  is  probable,  too,  that  definite  developmental  defects 
may  be  hereditary,  as  when  the  parent  or  parents  are  epileptics,  neurotic, 
alcoholic,  or  otherwise  degenerate.  Premature  labor  is  a  frequent  cause  of 
diplegia.  A  very  large  proportion  of  cases  develop  as  a  result  of  injury 
during  birth  because  of  a  meningeal  or  cerebral  hemorrhage.  In  a  few 
cases  the  damage  is  due  to  a  fall  in  early  infancy,  and  in  still  others  there 
develops  some  time  during  the  first  three  years  of  life  a  cerebral  thrombosis, 
a  hemorrhage,  an  encephalitis,  or  a  meningitis  which  is  followed  by  the 
brain  symptoms  about  to  be  described.  Such  a  condition  may  arise  as  a 
complication  or  sequela  of  any  one  of  the  acute  infectious  diseases  of  child- 
hood. A  convulsion  may  be  said  to  be  the  cause  in  certain  cases,  but  it  is 
probable  that  the  lesion  in  the  brain  is  responsible  for  this  symptom  rather 
than  that  it  is  the  provoking  factor.  Finally,  there  are  certain  cases  in  which 
it  is  impossible  to  discover  any  cause  whatever. 

Pathology  and  Morbid  Anatomy. — When  spastic  paralysis  is  present  it  is 
due  to  a  lesion  which  involves  the  motor  portion  of  the  cerebral  cortex  and 
neighboring  convolutions.  The  lesion  itself  in  long-standing  cases  is  scle- 
rotic or  atrophic  in  character  and  is  associated  with  similar  changes  in  the 
motor  fibres,  which  pass  from  the  cortex,  and  in  the  basal  ganglia  as  well. 
In  some  cases  the  sclerotic  change  is  limited  to  these  ganglia.  When  there 
is  diplegia  both  sides  of  the  brain  are  involved.  In  that  type  of  case  in 
which  mental  impairment  is  present  the  atrophy  and  sclerosis  affect  the 
anterior  convolutions  of  the  brain,  and  when  disorders  of  special  sense  are 
present  it  is  because  the  perceptive  centres  of  the  senses  affected  are  involved 
in  the  damaged  area.  It  is  readily  seen,  therefore,  that  as  the  lesions  are 
distributed  so  are  the  manifestations  of  the  disease  varied. 

The  exact  nature  of  the  cerebral  lesions  has  been  found  to  be  of  several 
types:  (1)  A  localized  atrophy,  or  failure  of  development,  may  produce 
an  excavation  of  the  surface  of  the  brain,  usually  due  to  meningeal 
hemorrhage  at  birth,  with  formation  of  a  clot  which  indents  the  delicate 
cortex  permanently.  This  indentation  is  called  porencephaly  (poros,  the 
Greek  word  for  "hole").  (2)  A  sclerotic  process  with  overgrowth  of  con- 
nective tissue  and  atrophy  of  the  nervous  protoplasm  may  be  present.  (3) 
Imperfect  development  of  the  cerebral  cells  may  be  found.  (4)  Atrophy 
may  follow  cerebral  softening  produced  by  the  closure  of  a  vessel  by  an 
embolus  or  thrombus.  (5)  An  inflammatory  process  in  the  pia  mater 
may  cause  an  adhesion  to  the  cerebrum  and  so  cause  atrophy  (meningo- 
encephalitis).    (6)  A  cerebral  hemorrhage  may  not  only  destroy  the  cerebral 


INFANTILE   CEREBRAL  PARALYSIS  927 

tissue,  but  cause  a  cyst  to  develop.  (7)  A  cyst  may  cause  atrophy  from 
pressure.  (8)  Hydrocephalus,  in  which  state  the  cerebral  ventricles  may  be 
so  distended  that  the  brain  tissues  atrophy  from  pressure.  (9)  Rarely  an 
external  hydrocephalus  may  produce  the  same  results. 

Symptoms. — The  symptoms  in  a  child  affected  by  this  accident,  like 
those  of  ordinary  apoplexy,  vary  greatly  in  speed  of  onset,  in  severity,  and 
in  type.  When  the  lesion  occurs  at  birth  there  are  often  no  symptoms  for 
several  days  or  even  weeks,  except  it  may  be  an  unusual  limpness  of  the 
limbs  and  some  difficulty  in  swallowing.  In  other  cases  unilateral  spasvis 
or  general  convulsions  speedily  develop,  but  these  are  not  of  long  duration, 
and  it  is  noticed  that  the  child's  head  is  not  held  erect,  but  falls  from  side  to 
side,  backward  or  forward.  The  convulsions  may  affect  the  entire  body, 
or  be  confined  to  the  side  in  which  paralysis  is  about  to  develop.  Associated 
with  these  convulsions  there  is  a  marked  rise  in  temperature,  the  fever  some- 
times reaching  as  high  as  105°.  After  the  convulsion  there  may  be  post- 
convulsive coma,  which  may  last  several  days.  Gradual  improvement  now 
takes  place,  and  as  the  child  returns  to  consciousness  it  is  found  that  there 
is  loss  of  power  upon  one  side  of  the  body.  Shortly  afterward  it  is  also  noticed 
that  the  arm  upon  the  affected  side  is  not  only  paralyzed,  but  that  it  is  in  a 
somewhat  spastic  state.  The  leg  suffers  in  a  similar  manner.  Later  on, 
clubfoot  and  a  sharply  flexed  hand  develop  from  secondary  contractures. 
The  paralyzed  limbs  fail  to  develop  as  they  should,  become  atrophied,  and 
are  often  considerably  shorter  than  the  limbs  upon  the  healthy  side.  The 
reflexes  are  exaggerated.     Sensation  is  not  impaired. 

If  the  child  survives,  the  paralyzed  parts  gradually  become  markedly 
distorted  and  tenotomies  may  be  necessary  to  prevent  the  contracture  from 
causing  so  great  a  deformity  as  to  make  any  motion  impossible.  Even  these 
means  may  not  make  walking  possible.  If  the  intellectual  portions  of  the 
brain  are  not  involved,  and  if  the  patient  reaches  the  years  of  puberty,  it  not 
infrequently  happens  that  by  prolonged  training  a  very  remarkable  degree  of 
ability  is  developed  in  the  non-paralyzed  side  so  that  the  individual  can  follow 
some  pursuit  which  will  render  him  self-supporting.  In  other  instances,  how- 
ever, the  spastic  condition  of  the  affected  limbs  is  very  marked,  the  hand  is 
sharply  flexed  at  the  wrist,  and  athetoid  movements  of  the  fingers  may  be 
present  whenever  any  attempt  is  made  to  move  them.  These  athetoid  move- 
ments occur  very  soon  after  the  paralysis  is  noticed  in  certain  cases.  In 
others  they  do  not  develop  for  a  long  time.  The  state  of  the  legs  is  even  more 
noticeable,  if  such  a  thing  be  possible.  Here  we  find  that  the  parts  are  at 
once  placed  in  strong  extension  if  they  are  touched,  the  muscles  of  the  calf 
are  tightly  contracted  and  the  feet  are  inverted  and  turned  inward.  The 
thighs  are  abducted.  When  the  attack  comes  on  after  the  child  has  learned 
to  speak,  there  may  be  marked  aphasia  for  a  time,  but  this  symptom  often 
gradually  disappears. 

Spastic  diplegia  may  affect  either  the  arms  or  the  legs,  usually  both  arms 
and  legs,  and  is  characterized  not  only  by  loss  of  power  in  these  parts,  but 
by  rigidity,  which  is  particularly  marked  in  the  lower  extremities.  The 
symptoms  usually  develop  slowly,  not  acutely  as  they  do  in  spastic  hemi- 
plegia. 


928 


DISEASES  OF   THE  NERVOUS  SYSTEM 


Various  deformities  o£  the  lower  limbs  occur,  and  the  muscles  of  the 
trunk,  particularly  at  the  back,  are  so  rigid  that  the  child  is  as  if  fixed 
in  a  plaster  cast.     In  other  instances  where  the  condition  has  developed 

some  time  after  birth,  the  patient  can 
sometimes  walk  by  the  aid  of  a  cane 
or  crutches,  but  in  those  instances  in 
which  the  lesion  is  severe  the  contrac- 
tures and  athetoid  movements,  the  exag- 
geration of  the  reflexes,  and  the  imper- 
fectly developed  muscles  all  combine  to 
make  the  child  absolutely  helpless. 
There  is  no  loss  in  the  control  of  the 
sphincters  nor  any  trophic  disturbances 
in  the  way  of  bed-sores,  nor  are  there 
any  sensory  disturbances. 

Both  of  these  types  not  infrequently 
suffer  from  epileptic  convulsions,  which 
may  be  of  the  Jacksonian  type.  In 
those  cases  which  are  due  to  lesions  in 
the  intellectual  area  of  the  brain,  idiocy 
may  be  present.  In  those  instances  in 
which  the  defect  of  mental  power  is  not 
complete  the  patient  is  called  an  imbe- 
cile. Such  patients  are  often  subject  to 
violent  outbursts  of  anger,  to  attacks  of 
malicious  mischief,  and  are  often  exceed- 
ingly filthy  in  their  habits. 

In  the  cases  in  which  the  posterior 
portions  of  the  brain  are  affected,  the  dis- 
orders of  special  sense  do  not  usually 
make  themselves  manifest  until  the  child 
is  at  least  a  year  or  eighteen  months  old. 
Often  prior  to  the  discovery  of  any 
symptoms  of  disorder  of  special  sense, 
epileptic  convulsions  have  called  atten- 
tion to  the  fact  that  the  cerebral  de- 
velopment is  imperfect.  In  some  in- 
stances the  disorders  of  vision  may  amount  to  nothing  more  than  a  hemia- 
nopsia. In  others  there  may  be  total  blindness,  or  deafness,  or  loss  of 
smell  and  taste.  In  these  cases  also  ordinary  epilepsy  and  Jacksonian 
epilepsy  are  often  present.  In  some  instances  minor  epilepsy  takes  the 
place  of  major  epileptic  attacks. 

When  a  hemiplegia  develops  in  a  child  of  a  year  or  more  it  is  usually  due 
to  hemorrhage  or  embolism  or  to  the  polioencephalitis  of  Striimpel  rather 
than  to  meningeal  disease. 

Diagnosis. — ^The  diagnosis  in  a  well-developed  case  of  infantile  cerebral 
paralysis  is  not  difficult.  The  early  development  of  the  malady  (after  a  hard 
labor  it  may  be) ,  the  marked  arrest  of  normal  development,  and  the  epileptic 


Fig.  119 

1 

1 

n 

Mt  ii 

1 

^^E 

Bh'    A] 

^H 

^^^^^^Ki' 

I 

H^B 

mi 

1 

1 

IB 

1 

'hm. 

'  '^Vm 

•        -J 

Hemitilogia,  "\\  Itli  conlraci  iire« 
had  suffered  since  the  age  of 
(Curschmann.) 


The  I 
two 


lalient 
years. 


INFANTILE   CEREBRAL  PARALYSIS  929 

convulsions,  with  the  spastic  state  of  the  muscles,  all  separate  this  form  of 
infantile  paralysis  from  those  forms  which  depend  for  their  existence  upon 
lesions  in  the  spinal  cord,  for  in  the  latter  the  paralyzed  parts  are  flaccid. 
There  are,  however,  two  forms  of  spinal  spastic  palsy  of  childhood  with 
which  this  condition  can  be  confused,  one  of  which  is  the  so-called  "  hered- 
itary spastic  spinal  paralysis,"  but  in  this  disease  the  mental  symptoms 
are  lacking  and  the  condition  is  progressive.  The  second  state  which 
resembles  this  disease  is  "  amaurotic  family  idiocy,"  but  in  this  malady  the 
paralysis  may  be  flaccid  or  spastic  and  blindness  is  an  early  symptom. 

Prognosis. — It  must  be  evident  that  the  prognosis  as  to  complete  recovery 
in  severe  cases  is  anything  but  good.  In  those  cases  in  which  the  mental 
powers  are  feeble  and  convulsions  frequently  recur,  the  outlook  is  bad  both 
as  to  recovery  and  a  long  duration  of  life.  If  they  live  they  are  hopeless  imbe- 
ciles or  idiots.  When  the  affection  is  confined  chiefly  to  one  side  of  the  brain 
— that  is,  when  there  is  hemiplegia — adult  years  may  be  reached  and  ordinary 
mental  pursuits  followed  in  many  cases. 

Some  of  these  patients,  moreover,  can  be  materially  improved  by  proper 
training,  in  which  instance  special  senses  which  are  not  impaired,  or  intel- 
lectual centres  which  have  escaped  the  wreck,  may  be  developed  to  such  an 
extent  that  a  fair  degree  of  comfort  and  intelligence  may  be  attainable. 
The  convulsions  cannot  be  cured,  as  they  depend  upon  faulty  development, 
but  they  may  be  modified  by  skilful  treatment,  consisting  in  the  administra- 
tion of  nervous  sedatives,  the  avoidance  of  all  causes  of  nervous  excitement 
and  irritation,  and  the  moderate  employment  of  the  bromides.  As  a  rule, 
better  results  can  be  obtained  from  hygienic  methods  and  from  mental  train- 
ing in  an  institution  devoted  to  this  purpose  than  can  be  obtained  at  home. 
At  one  time  it  was  considered  that  operative  interference  might  be  of  very 
great  value  in  these  cases,  but  we  now  know  that  little  can  be  expected  from 
such  a  plan  of  treatment.  In  those  cases  in  which  the  skull  has  seemed  to 
be  abnormally  small  it  was  proposed  that  the  skull  should  be  cut,  or  bone 
should  be  removed,  in  such  a  way  as  to  permit  expansion  of  the  brain.  But 
the  smallness  of  the  skull  is  probably  more  dependent  upon  the  size  of  the 
brain  than  is  the  size  of  the  brain  upon  the  condition  of  the  skull.  In  some 
instances  the  parents  prefer  running  the  risk  of  the  child's  death  as  the 
result  of  such  a  grave  operation  rather  than  to  have  it  continue  a  hopeless 
invalid,  and  in  such  cases,  if  there  are  distinct  localizing  symptoms,  epileptic 
or  otherwise,  the  question  of  cerebral  localization  and  operation  must  be 
carefully  considered. 

Little's  Disease. — The  name  "  Little's  disease"  has  been  apphed  by  some 
writers  to  the  cerebral  palsies  of  childhood;  but  is  probably  best  restricted 
to  cases  in  which  there  is  congenital  spastic  rigidity  of  the  limbs,  particu- 
larly of  the  legs,  tending  to  improvement.  In  Little's  disease,  thus  defined, 
there  is  normal  mental  capacity  and  no  epilepsy  or  athetosis.  The  condi- 
tion is  purely  motor  from  defective  development  of  the  pyramidal  system 
in  the  brain  or,  according  to  Dejerine,  in  the  spinal  cord. 


59 


930  DISEASES  OF   THE  NERVOUS  SYSTEM 


APHASIA. 

Definition  and  Symptoms. — Aphasia  is  a  condition  in  which  the  function 
of  speech  becomes  impaired  or  arrested  as  the  result  of  disease  involving 
those  parts  of  the  brain  which  are  concerned  with  the  expression  of  ideas 
in  words.  For  the  power  of  speech  it  is  necessary  that  the  individual  shall 
have  not  alone  the  motor  centres  which  will  cause  the  proper  muscular 
movements  which  give  rise  to  certain  sounds,  but  in  addition  there  must 
be,  in  close  association  with  these  centres,  others  in  which  the  conception  of 
an  idea  must  originate,  and  still  others  in  which  a  sense  of  the  appearance 
of  words,  or  sounds  of  words,  is  stored.  When  a  child  is  learning  to  talk, 
an  object,  such  as  a  horse,  is  pointed  out  to  him,  and  the  word  "horse"  is 
frequently  repeated  at  the  same  moment.  He  therefore  learns  to  associate 
a  certain  shape  and  form  with  the  word  "horse."  For  him  to  do  this  it  is 
necessary  that  his  visual  apparatus  shall  carry  to  his  brain  a  certain  form, 
and  that  his  brain  should  store  up  that  form  as  typifying  a  certain  object. 
It  is  also  necessary  that  his  auditory  apparatus  shall  carry  to  his  brain  a 
certain  sound  or  sounds,  and  that  his  brain  shall  associate  this  sound  with 
the  form  that  he  has  seen.  In  addition  it  may  be  that  he  has  touched  or 
stroked  the  horse,  and  so  his  sense  of  touch  has  conveyed  to  his  brain  a  cer- 
tain model,  or  form,  which  is  associated  with  those  received  by  means  of 
his  eyes  and  ears.  When,  therefore,  he  sees  a  horse  a  second  time  the  mem- 
ories or  imprints  derived  from  these  various  sources  are  utilized,  and  he 
attempts  to  reproduce  the  word  "horse"  by  a  process  which  calls  into  play 
certain  muscles  which  are  necessary  for  making  this  sound.  Speech  is  there- 
fore in  one  sense  a  complicated  function,  closely  connected  with  the  organs 
of  special  sense,  of  intellection,  and  with  the  motor  neurones  as  well.  This  is 
perhaps  made  more  clear  by  the  following  diagram: 


A 

o 

A,  pathways  for  receiving  imprints  or  models ;  B,  centre  for  storage  of  models;  C,  centre  for  storage  of 
motor  memories ;  D,  concept  centre  ;  £,  motor  centres  for  controlling  muscles  of  speecti  at  F. 

A  visual  impulse,  an  auditory  impulse,  a  touch  impulse,  an  olfactory 
impulse,  or  a  taste  impulse,  or  all  of  them  together,  pass  to  the  centre  B, 
where  they  are  received  and  stored.  From  B  these  memories  or  imprints 
are  transmitted,  whenever  they  are  needed,  to  those  centres  in  the  brain 
which  are  concerned  with  the  power  of  the  conception  of  an  idea,  or  they 
may  be  transferred  directly  to  C,  which  may  transform  them  into  speech 
by  mimicry,  without  any  idea  or  higher  intellectual  process  than  that  con- 
cerned with  imitation.     If  the  child  thinks  of   a  horse  at  D,  he  receives 


APHASIA  931 

memories  of  the  character  of  a  horse  from  B  and  sends  from  D  an  impulse 
which  cause  C  to  send  impulses  to  the  organs  of  speech.  It  is  evident, 
therefore,  that  if  the  sensory  tracts  are  diseased  before  the  centres  for  storing 
the  character  of  external  objects  have  received  and  retained  models  or 
impressions  speech  will  be  impossible,  or  if  any  part  of  the  mechanism 
described  in  the  diagram  is  undeveloped  or  damaged,  the  entire  chain 
fails  because  one  of  its  links  is  broken. 

This  process  may,  however,  be  even  more  complicated  than  that  described. 
Thus,  there  may  be  stored  in  the  storage  centre  not  only  the  model  or  imprint 
of  a  horse  but  also  the  additional  memory  of  the  appearance  of  the  word 
"horse"  when  in  type,  and  in  addition  there  may  be  stored  the  memory  of 
certain  movements  which  are  characteristic  of  a  horse,  so  that  the  child  can 
imitate  its  movements  or  perhaps  draw  an  outhne  of  its  appearance.  While 
pantomime  and  drawing  are  not  speech,  they  are  so  nearly  related  to  it  as  to 
really  form  part  of  it.  Again,  it  is  necessary  that  there  should  be  stored  at 
C  the  models  or  memories  of  those  muscular  movements  which  will  give  rise 
to  the  sound  of  the  word  horse,  for  this  is  part  of  learning  how  to  talk. 

In  certain  cases  in  which  the  brain  is  diseased  the  patient  may  see  and 
feel  and  hear  a  horse,  and  his  concept  centres  may  know  perfectly  that  a 
horse  is  before  him,  or  that  the  word  "  horse  "  is  in  print,  but  he  cannot  say 
the  word  "horse"  because  the  centres  concerned  with  the  storage  of  mem- 
ories of  the  muscular  movements  necessary  to  speak  the  word  "horse"  are 
destroyed.  He  may  write  the  word  "  horse  "  or  draw  a  horse,  but  he  cannot 
•say  "horse."^  To  this  form  of  motor  aphasia  the  word  wphemia  is  applied. 
If  the  centre  in  which  the  memories  of  how  to  write  the  word  "horse"  are 
destroyed  the  condition  is  called  agraphia,  and  if  those  in  which  the  muscular 
movements  required  to  describe  a  horse  by  gesture  are  diseased  it  is  said 
to  be  amimia.  When  the  tracts  that  associate  the  storage  centres  for  mem- 
ories of  words  are  interfered  with,  the  patient  skips,  or  jumbles,  or  repeats 
his  words,  and  this  is  called  conduction  aphasia;  and  if  he  speaks  one  word 
when  he  means  another,  it  is  called  paraphasia. 

On  the  other  hand,  when  the  sensory  portion  of  the  speech  mechanism 
is  diseased  the  patient  may  be  able  to  say  the  word  "horse,"  but  if  he  sees 
a  horse  he  cannot  say  that  he  has  seen  it  because  he  has  lost  the  memories 
of  the  horse;  or  if  he  sees  the  word  "horse  "  in  print,  he  may  be  able  to  repro- 
duce the  letters  in  writing,  in  their  order,  but  he  is  entirely  unable  to  read, 
for  he  has  lost  the  memory  of  the  significance  of  these  letters  when  so  joined. 
This  is  called  alexia,  or  word  blindness,  an  unfortunate  term,  as  blindness 
would  indicate  failure  of  visual  power,  which  does  not  exist.  Again,  in  cer- 
tain cases  there  is  loss  of  memory  of  sounds.  The  voice  of  a  speaker  may 
be  heard  and  even  imitated,  but  the  patient  understands  nothing  more  than 
if  an  unknown  language  was  spoken.  It  conveys  no  idea  to  his  mind.  This 
is  called  word  deafness — another  unfortunate  term,  because  hearing  in  the 
ordinary  sense  of  that  word  is  perfect.  Apraxia  is  still  another  nearly 
related  state  in  which  the  patient  fails  to  appreciate  the  purposes  or  uses 
of  an  object.  ^  He  may  see,  hear,  and  touch  a  knife  or  a  coin,  but  his  mind 
cannot  grasp  its  uses. 

'  As  a  matter  of  fact,  these  powers  are  usually  lost. 


932  DISEASES  OF   THE  NERVOUS  SYSTEM 

When  we  come  to  study  the  lesions  which  produce  these  disturbances 
in  the  abiUty  to  express  an  idea,  we  find  that  when  the  patient  has  aphemia 
or  motor  aphasia  the  damage  has  been  done  to  the  third  left  frontal  con- 
volution (Broca's  convolution).  In  such  a  case  he  also  cannot  write  either 
his  own  ideas  or  the  words  that  he  hears  spoken,  but  he  can  copy.  If  the 
lesion  is  a  severe  one,  his  power  of  understanding  words  he  sees  written  or 
hears  spoken  is  usually  impaired.  In  other  words,  he  also  suffers  from 
word-blindness  and  word-deafness.  When  he  has  word-blindness  or  alexia, 
the  lesion  is  at  the  angular  gyrus.  If  there  is  a  pure  alexia  the  lesion  is  in 
the  subcortical  substance  of  the  angular  gyrus.  Aphasia  also  develops 
when  a  lesion  takes  place  from  hemorrhage,  embolism,  or  thrombosis  in  the 
knee  of  the  internal  capsule,  for  at  this  point  the  fibres  which  convey 
speech  impulses  are  destroyed. 


TUMORS  OF  THE  BRAIN  AND  ITS  MEMBRANES. 

Intracranial  tumors  arise  from  the  substance  of  the  brain  itself  or  from 
the  membranes  which  surround  it.  A  great  variety  of  these  growths  have 
been  recorded,  but  by  far  the  most  common  are  tubercle,  gumma,  glioma, 
and  sarcoma.  Cancer,  fibroma,  osteoma,  neuroma,  and  vascular  tumors 
also  rarely  occur.    Echinococcus  cysts  may  develop. 

Etiology  and  Frequency. — The  causes  of  these  morbid  growths  are  not 
understood  except  in  the  case  of  tubercle  and  gumma.  Sex  seems  to  exercise 
a  very  distinct  influence,  for  we  find  that  males  suffer  very  much  more  fre- 
quently than  females.  Gowers  states  that  out  of  650  cases  of  brain  tumor 
440  occurred  in  males  to  210  in  females.  Dana  gives  the  figures  at  644  to 
320,  and  Starr's  figures  are  nearly  identical  in  their  proportions.  This  great 
preponderance  in  males  is  not  explained  by  either  syphilis  or  injury,  for 
there  is  no  greater  frequency  of  gumma  in  men  than  in  women.  On  the 
contrary,  tubercle  and  glioma  are  the  growths  that  are  particularly  fre- 
quent in  men.  Gowers  has  shown  that  after  the  first  six  months  of  life  till 
old  age  all  ages  suffer  about  equally.  Thus,  the  percentage  in  the  first 
decade  is  18.5,  in  the  second  14,  in  the  third  20,  in  the  fourth  decade  18.5, 
and  in  the  fifth  14.  Most  of  the  growths  in  childhood  are  tuberculous, 
and  indeed  they  form  53  per  cent,  of  all  growths  at  all  ages,  if  gumma  be 
excluded. 

Pathology  and  Morbid  Anatomy. — Tumors  of  the  brain  affect  its  tissues 
in  its  different  areas  as  follows,  according  to  Gowers:  In  the  hemispheres 
297,  in  the  cerebellum  179,  in  the  base  of  the  brain  76,  in  the  pons  59,  in  the 
central  ganglia  48,  in  the  medulla  31,  in  the  corpora  quadrigemina  13,  and 
in  the  crus  10. 

Tuberculous  tumors  occur  as  solid,  firm,  round  masses  which  are  not 
rarely  multiple.  Their  size  varies  from  that  of  a  pea  to  a  hen's  egg  or  even 
larger.  The  growth  starts  from  the  lymphoid  sheaths  of  the  vessels,  and 
rapidly  obliterates  them.  For  this  reason  it  is  devoid  of  vessels  and  its  tissue 
soon  undergoes  necrosis,  so  that  on  section  it  is  cheesy  and  shows  spots 
of  softenin:^.     As  the  surface  is  soft,  and  the  surrounding  brain  substance 


TUMORS  OF   THE  BRAIN  AND  ITS  MEMBRANES  933 

is  also  softened,  the  mass  is  clearly  outlined,  hence  the  name  tuberculoma. 
Finally,  the  growth  may  become  calcified  or  undergo  suppuration.  Tuber- 
culous growths  are  often  found  in  the  cerebellum,  and  they  also  occur  in  the 
pons  and  cerebrum.  When  in  the  cerebrum  they  are  usually  found  along 
the  great  vessels  in  the  interpeduncular  space  or  in  the  fissure  of  Sylvius; 
not  rarely  the  growth  is  near  a  Pacchionian  body,  but  it  may  be  found  in 
the  depths  of  the  centrum  ovale. 

Gummata  of  the  brain  rarely  reach  a  size  greater  than  that  of  a 
hickory-nut.  They  are  also  somewhat  cheesy  in  appearance  and  have 
an  irregular  surface,  which  may  be  gelatinous,  or  indurated  and  hard, 
and  enclosed  in  a  fibrous  capsule.  These  growths  are  thought  to  spring 
from  the  bloodvessels  of  the  dura  mater. 

Sarcoma  occurs  as  round,  oval,  or  spindle-cell  tumors  which  destroy  the 
tissues  of  the  brain  as  they  grow.  When  they  are  of  the  gliomatous  type 
they  differ  greatly  from  all  the  growths  so  far  described,  for  they  are  not 
round,  but  extend  by  a  process  of  infiltration  between  the  nerve  cells.  They 
may  be  soft  and  mucoid  (myxoglioma),  or  firm  and  fibrous  (fibroglioma). 
Gliomas  of  the  soft  variety  are  liable  to  hemorrhage.  A  cystic  form  of 
glioma  due  to  softening  is  not  rare.    Gliomata  are  usually  single. 

The  secondary  changes  produced  by  these  growths  are  of  importance 
and  depend  chiefly  upon  the  pressure  of  the  tumor  upon  healthy  tissues 
which  in  this  way  are  destroyed.  The  very  growth  of  the  tumor  inside  the 
skull  also  increases  intracranial  pressure,  and  if  it  be  so  situated  that  it 
prevents  the  free  passage  of  cerebrospinal  fluid  from  the  choroid  plexus 
in  the  lateral  ventricle  through  the  third  ventricle  and  the  iter  a  iertio  ad 
quartum  ventriculwn,  then  distention  of  the  lateral  ventricles  or  internal 
hydrocephalus  develops.  A  tumor  of  the  pons,  of  the  corpora  quadrigemina 
of  the  middle  lobe  of  the  cerebellum,  or  in  the  third  ventricle  may  cause  such 
obstruction.  A  third  result  of  the  intracranial  tumor  is  irritation  of  the 
nerve  cells  of  the  brain  and  inflammation  in  them  or  in  the  meningeal 
membranes,  and  lastly  it  may  cause  actual  thinning  of  the  skull  by  the 
pressure  induced. 

Symptoms. — By  far  the  most  common  symptom  of  brain  tumor  is  head- 
ache. This  headache  is  usually  severe  and  is  characterized  by  sharp  exacer- 
bations. In  some  instances  it  is  dull  and  boring  in  character.  In  others 
it  is  sharp,  stabbing,  and  tearing.  By  reason  of  its  constancy  it  prevents 
sleep,  and  in  its  most  severe  paroxysms  may  produce  temporary  aberration  of 
mind.  The  pain  is  widely  diffused,  and  is  particularly  severe  if  it  encroaches 
on  the  dura  which  is  supplied  with  sensation  by  the  fifth  nerve.  If  the  pain 
is  localized  it  does  not  necessarily  indicate  that  the  growth  is  in  that  neigh- 
borhood, although  in  those  cases  in  which  the  tumor  is  superficial  the  locality 
of  the  growth  and  of  the  pain  is  often  identical. 

Next  to  headache  in  constancy  as  a  symptom  is  vomiting.  The  expulsion 
of  the  stomach  contents  is  usually  spoken  of  as  "projectile,"  and  in  this 
respect  it  resembles  the  vomiting  of  certain  forms  of  intestinal  obstruction. 
Although  the  vomiting  is  severe,  nausea  is  often  absent.  This  symptom  is 
supposed  to  be  most  frequent  and  severe  when  the  growth  is  rapidly  pro- 
gressing.    Vertigo  also  occurs  and  varies  in  severity  from  slight  dizziness  to 


934  DISEASES  OF   THE  NERVOUS  SYSTEM 

a  degree  which  causes  the  patient  to  fall.  Not  infrequently  this  vertigo 
causes  the  patient  to  walk  in  the  direction  in  which  it  is  not  his  intention  to 
go.  Vertiginous  symptoms  are  more  common  in  tumor  of  the  cerebellum 
than  in  lesions  elsewhere,  and  often  the  patient  falls  to  one  side.  Another 
very  important  symptom  of  brain  tumor  is  optic  neuritis,  which  occurs  in  a 
large  proportion  of  cases  and  which  often  enables  us  to  make  a  diagnosis  of 
brain  tumor  with  the  aid  of  the  ophthalmoscope  when  the  other  symp- 
toms are  so  obscure  that  it  is  difficult  to  determine  the  nature  of  the 
patient's  disease. 

Optic  neuritis  is  usually  most  marked  in  cases  of  tumor  of  the  cerebellum, 
of  the  midbrain,  and  of  the  great  ganglia  near  the  base.  It  occurs  less  fre- 
quently when  the  tumor  is  in  the  cortex  or  springs  from  one  of  these  mem- 
branes, but  the  localizing  value  of  neuritis  is  really  not  great.  Nearly  always 
both  optic  nerves  are  involved,  although  sometimes  the  lesion  develops  in 
one  before  it  attacks  the  other.  Gowers  gives  three  reasons  for  this  optic 
neuritis :  First,  irritation  of  the  nerve  fibres  produced  by  the  pressure  which 
finally  causes  inflammation.  Second,  distention  of  the  nerve  sheaths  and 
the  lymphatic  spaces  of  the  papilla  by  subarachnoid  fluid,  which,  perhaps, 
contains  irritating  poisons.  The  third  cause  is  thought  to  be  inflammation 
of  the  meninges,  which  is  so  frequently  present,  and  which  may  extend  to 
the  optic  nerve. 

Slowness  of  thought  and  gradual  mental  failure  are  not  infrequently 
present.  Sometimes  aphasia  develops.  All  these  three  symptoms  are 
prone  to  occur  when  the  tumor  affects  the  frontal  lobe,  and  the  symp- 
tom of  aphasia  is,  of  course,  most  frequently  developed  when  the  left 
frontal  lobe  is  involved.  Epileptiform  convulsions  occur  in  about  one- 
quarter  of  the  cases  of  brain  tumor,  and  are  especially  marked  in  those 
instances  in  which  the  growth  directly  or  indirectly  produces  irritation  of 
the  cortex.  So,  too,  there  may  be  symptoms  which  for  a  time  resemble  the 
early  stages  of  an  apoplexy.  Quite  rarely  actual  rupture  of  a  bloodvessel 
occurs,  and  so  the  symptoms  are  really  apoplectic. 

Paralysis  due  to  brain  tumor  may  be  unilateral  or  bilateral.  When  uni- 
lateral it  may  manifest  itself  as  a  monoplegia  or  as  a  hemiplegia.  It  is 
usually  gradual  in  onset,  and  when  hemiplegic  in  type  is  due  to  the  presence 
of  a  growth  in  the  upper  part  of  the  pons,  in  the  crus,  or  in  the  internal  cap- 
sule, or  over  a  wide  area  in  the  cortex.  Localized  paralysis,  such  as  mono- 
plegia, may  be  due  to  a  growth  involving  the  cortex  or  the  subcortex  before 
the  fibres  have  come  together  so  closely  that  even  a  small  tumor  must 
affect  the  whole  bundle  and  produce  widespread  paralysis.  Such  a  mono- 
plegia involving  the  arm  or  leg  is  not  infrequently  associated  with  epilepti- 
form attacks,  limited  to  the  paralyzed  part.  If  the  growth  is  in  the  lower 
third  of  the  pons  the  ordinary  form  of  crossed  paralysis  may  be  present,  the 
face  being  paralyzed  on  the  side  of  the  lesion,  while  the  arm  and  leg  are 
paralyzed  on  the  opposite  side. 

A  rarer  form  of  crossed  paralysis  (Weber's  syndrome)  may  result  from 
tumor  of  one  crus  involving  the  third  nerve.  The  eyes  are  deviated  to  the 
side  opposite  the  lesion  and  the  pupil  dilated  on  the  side  of  the  lesion,  while  the 
arm  and  leg,  as  in  ordinary  hemiplegia,  are  paralyzed  upon  the  opposite  side. 


TUMORS  OF  THE  BRAIN  AND  ITS  MEMBRANES  935 

Bilateral  paralysis  due  to  brain  tumor  can  only  occur  when  the  growth 
is  multiple  and  presses  upon  both  sides  of  the  brain,  or  when  it  is  so  situated 
that  it  can  at  once  cut  off  fibres  from  both  sides  as  they  approach  the  middle 
area,  as  in  the  pons  or  in  the  medulla.  Under  these  circumstances  the  legs 
are  usually  more  affected  than  the  arms,  even  though  the  face  as  well  as 
the  arms  be  included  in  the  paralysis.  Contractures,  tonic  spasms,  or  con- 
vulsions, either  generalized  or  Jacksonian,  may  also  occur.  They  usually 
indicate  that  the  growth  is  situated  somewhere  near  the  cortex,  where 
it  produces  other  irritations. 

If  the  tumor  is  in  the  frontal  area  and  grows  forward  it  may  cause 
protrusion  of  the  eyeballs  and  paralysis  of  the  extrinsic  muscles  of  the 
eye,  while  if  it  grows  backward  it  may  cause  spasms  and  epileptiform 
convulsions  by  the  irritation  of  the  motor  area  of  the  cortex. 

The  development  of  a  growth  in  the  central  region  produces  symptoms 
which  are  more  definite  than  those  which  are  found  in  association  with 
growths  elsewhere,  because  it  is  the  motor  area  of  the  brain.  Not  infre- 
quently localized  convulsions,  or  Jacksonian  epilepsy,  occur  in  such  cases 
and  paralysis  limited  to  the  same  muscles  may  follow  such  an  attack.  The 
part  in  which  the  convulsion  begins  and  the  subsequent  paralysis  indicate 
the  presence  of  the  tumor  in  or  beneath  the  centre  supplying  the  centres 
controlling  these  muscles.  Disorders  of  sensation  in  the  affected  limb  may 
be  present,  consisting  of  numbness,  tingling,  and  even  hemiansesthesia. 

When  a  tumor  involves  the  parietal  region  the  symptoms  are  not  definite, 
but  pertain  chiefly  to  common  sensation  and  "muscle  sense." 

If  the  superior  parietal  lobule  be  invaded  there  is  more  or  less  loss  of 
"muscle  sense,"  and  often  the  symptom  astereognosis  is  present.  When 
the  angular  gyrus  are  involved,  word  blindness  may  be  present. 

When  that  portion  of  the  parietal  area  near  the  longitudinal  fissure  is 
invaded  we  not  infrequently  have  spasms  or  convulsions  in  the  lower 
extremities  on  the  side  opposite  the  lesion,  because  the  growth  begins  to 
invade  the  part  of  the  leg  centre  which  is  on  the  inner  surface  of  the  hemi- 
sphere. 

Tumors  of  the  occipital  lobe,  if  in  the  cuneus  or  otherwise  near  the  cal- 
carine  fissure,  produce  lateral  homonymous  hemianopsia.  If  the  growth  in  the 
occipital  lobe  is  sufficiently  far  forward  to  involve  some  of  the  parietal  area, 
and  so  do  damage  to  the  angular  gyrus,  word-blindness  and  hemianopsia 
may  develop,  and  if  the  invasion  extends  still  farther,  hemiataxia,  hemi- 
ansesthesia, and  even  some  hemiplegia  due  to  involvement  of  some  of  the 
fibres  of  the  internal  capsule  may  be  present. 

In  the  first  left  temporal  convolution  brain  tumor  produces  word-deafness, 
a  form  of  sensory  aphasia.  Occasionally  large  tumors  in  the  temporal 
area  produce  vertigo. 

Tumors  of  the  corpus  callosum  are  not  only  very  unusual,  but  produce 
symptoms  which  are  not  very  definite,  being  primarily  those  of  mental 
failure  and  secondarily  those  due  to  encroachment  upon  neighboring  parts. 
In  addition  to  the  general  symptoms  of  brain  tumor,  the  growth  in  this 
region  produces  hemiplegia,  ultimately  developing  into  paraplegia,  great 
mental  dulness,  and  finally  coma. 


936 


DISEASES  OF   THE  NERVOUS  SYSTEM 


'^O      SPHB^ 


Showing  the  areas  of  the  brain  concerned  with  special  functions.      1.   Prefrontal    area.     2.  Central 
area.     3.   Parietal  area.     4.  Occipital  area.     5.   Temporal  area.      (Modified  from  Fuller.) 


Fig.  122 


6.  Corpus  callosum.     7.  Thalamus  opticus.      10.  Corpora  quadrigemina.      11.   Crus.       12.  Pons. 
13.  Medulla  oblongata.       14.  Cerebellum.      15.   Fourth  ventricle.      (Modified  from  Reichert.) 


TUMORS  OF   THE   BRAIN   AND   ITS  MEMBRANES 


937 


When  a  tumor  involves  the  great  basal  gangUa  or  the  fibres  of  the  internal 
capsule,  hemiplegia  is  the  most  prominent  symptom,  and  hemiansesthesia 
and  choreic  movements  may  be  present. 

If  the  posterior  part  (pulvinar)  of  the  optic  thalamus  and  nearby  tissues, 
particularly  one  of  the  optic  tracts,  are  involved  by  the  growth,  hemianopsia 
may  be  present,  but  this  hemianopsia  may  be  separated  from  that  which 
is  due  to  a  lesion  in  the  occipital  lobe  by  the  presence  of  Wernicke's  sign 
(hemianopic  pupillary  inaction). 


Fig.  123 


10.  Corpora  quadrigemina. 


11.  Crus.     12.  Pons.      13.  Medulla  oblongata.      14.   Cerebellum. 
(Modified  from  Reichert.) 


Having  from  these  several  symptoms  determined  that  a  brain  tumor 
is  present,  it  still  remains  for  the  physician  to  determine  its  locality,  and 
this  can  only  be  done  by  his  knowledge  of  cerebral  localization.  For  this 
study  the  brain  can  best  be  divided  into  fifteen  parts,  most  of  which  can  be 
seen  on  the  accompanying  diagrams  (Figs.  121,  122;  and  123). 

The  numbers  in  the  text  refer  to  the  numbers  in  the  figures  and  show 
where  the  growth  would  be  situated. 


938 


DISEASES  OF   THE  NERVOUS  SYSTEM 


Tamois  of  the  prefrontal  area 
(See  Fig.  121). 


Table  of  Cerebral  Localizing  Symptoms.^ 

No  symptoms,  or 

Stupidity. 

Silliness. 

Emotionalism. 

Loss  of  smell  on  one  side  or  both  sides. 

Hemianopsia  and  optic  neuritis. 

Protrusion  of  the  eyeball. 

Paralysis  of  the  extrinsic  ocular  muscles. 


Tumors  of  the  central  area . 
(See  Fig.  121.) 


Tumors  of  the  parietal  area 
(See  Fig.  121.) 


Tumors  of  the  occipital  lobe 
(See  Fig.  121.) 


Tumors  of  temporal  area 
(See  Fig.  121.) 


Tumors  of  corpus  eallosum 
(Very  rare.) 
(See  Fig.  122.) 


7,8,9. 
Tumors  of  the  great  basal  ganglia 

and  capsule. 
(See  Fig.  122,  for  7  and  Fig.  118 

for  8  and  9.) 


10. 

Tumor  of  the  corpora   quadri- 
gemina  (vermis  of  the  cerebel- 
lum) and  pineal  gland. 
Additional  information  as  to 
these  lesions  can  be  had  by  study- 
ing Figs.  118  and  123. 


Jacksonian  epilepsy. 

Sensory  disorders,  tingling  or  hemiansesthesia. 

Impaired  muscle  sense. 

Motor  aphasia  and  agraphia. 

Local  palsy  after  spasm. 

No  symptoms,  or 

Loss  of  muscle  sense  if  supramarginal  gyrus  is  affected. 

Word-blindness  if  angular  gyrus  and  inferior  lobule  are  affected. 

Paralysis  or  spasm  of  the  lower  limbs  if  the  upper  margin  of  the 
cerebral  area  is  invaded. 

Perhaps  slight  paralysis  of  the  sixth  nerve  if  the  angular  gyrus  is 
affected. 

Homonymous  hemianopsia  if  the  cuneus  or  the  neighborhood  of  the 
calcarine  fissure  and  first  occipital  convolution  are  involved. 

Failure  to  grasp  meaning  of  surrounding  objects  (mind-blindness)  if 
cuneus  escapes. 

Word-blindness  and  some  hemianopsia  if  the  angular  gyrus  is  affected. 

Hemiataxia,  hemiansesthesia,  and  partial  hemiplegia  if  the  internal 
capsule  is  slightly  involved  in  the  posterior  part,  and  also  homony- 
mous hemianopsia  from  involvement  of  the  optic  radiations. 

No  symptoms  if  on  right  side. 

Word-deafness  if  the  posterior  part  of  the  first  and  second  temporal 

convolution  is  involved. 
Vertigo  and  forced  movements,  if  the  growth  is  low  down,  due  to 

irritation  of  internal  ear. 

Gradually  developing  hemiplegia  followed  by  paraplegia. 

Dulness  and  other  mental  symptoms  suggesting  paresis. 

Stupor   \   and  various  symptoms  due  to  pressure  upon  neighboring 

Coma     i       structures. 

Death. 

Progressive  hemiplegia. 

An£esthesia(?). 

Choreic  movements  if  tumor  involves  optic  thalamus  (7)  and  nearby 
part  of  capsule  (8).    Starr  thinks  that  these  movements  are  cortical. 

No  localizing  symptoms  if  the  tumor  involves  the  caudate  or  lenticular 
nucleus  (9). 

Hemianopsia  and  the  hemiopic  pupillary  inaction  of  Wernicke,^ 
if  the  optic  tract  or  its  endings  near  the  posterior  part  of  the  optic 
thalamus  and  adjacent  tissues  are  involved.  If  this  pupillary  in- 
action of  Wernicke  is  absent  hemianopsia  indicates  a  lesion  in  the 
occipital  lobe  involving  the  cortex  or  the  optic  radiations. 

Cerebellar  inco-ordination. 

Forced  movements. 

Ocular  palsies,  often  symmetrical. 

Hemianopsia  if  primary  optic  centres  of  one  side  are  destroyed; 
blindness  if  destroyed  on  both  sides. 

Deafness  or  partial  deafness  if  posterior  tubercles  of  corpora  quadri- 
gemina  are  affected. 


1  In  the  preparation  of  this  table  much  use  has  been  made  of  the  facts  stated  by  Dana  in  his  work 
on  Nervous  Diseases. 

2  A  ray  of  light  thrown  on  the  blind  half  of  the  retina  will  not  produce  reflex  pupillary  contraction, 
though  the  pupils  react  normally  if  the  light  strikes  the  other  half  of  the  retina. 


TUMORS  OF   THE  BRAIN  AND  ITS  MEMBRANES 


939 


11. 


Tumors  of  crus    .    .    . 
(Very  rare.) 


12. 
Tumors  in  the  pons 


Tumors  in  medulla     .....  j 
L 


14. 
Cerebellar  tumor 


15. 
Tumor  in  anterior  fossa 


Hemiplegia. 
Hemiansesthesia  (?). 

Paralysis  of  oculomotor  nerve  upon  same  side  as  tumor  (crossed 
paralysis). 

Facial  palsy  on  same  side  as  tumor;   hemiplegia  on  opposite  side 

(crossed  paralysis). 
Trifacial  paralysis  on  same  side  as  tumor  if  below  middle  of  pons  ; 

hemiansesthesia  on  opposite  side  (crossed  sensory  paralysis). 
Hemiansesthesia  and  hemiplegia  if  tumor  is  large  and  above  middle 

of  the  pons. 
Conjugate  deviation  of  eyes  away  from  the  lesion. 
Hemiplegia  and  hemiansesthesia  with  hypoglossal  paralysis  or  other 

cranial  nerve  palsy  on  side  of  lesion.    Glycosuria  and  vasomotor 

disturbance. 
Sjrmptoms  of  bulbar  paralysis  if  growth  is  large. 
Headache  ~| 

Vomiting 
Vertigo 
Optic  neuritis     J 
Reeling  gait  if  in  middle  lobe. 
Glycosuria  and  cranial  nerve  palsies  if  pressing  upon  or  in  middle 

lobe. 
Bulbar  symptoms  {i.  e.,  cranial  nerve  palsies). 
Hydrocephalus  if  tumor  presses  on  aqueduct  of  Sylvius. 
Same  symptoms  as  prefrontal  tumors. 
Loss  of  smell,  sight,  and  oculomotor  paralysis.    Acromegaly,  optic 

neuritis,  and  temporal  hemianopsia  if  the  tumor  is  in  middle  fossa 

and  involves  optic  chiasm. 


j-  unusually  severe. 


Diagnosis. — As  already  stated,  the  important  symptoms  in  the  diagnosis 
of  brain  tumor  are  headache,  vertigo,  optic  neuritis,  convulsions,  and  par- 
alysis. It  must  be  remembered,  however,  that  these  symptoms  are  none  of 
them  pathognomonic  of  brain  tumor,  and  that  each  of  them  is  often  present 
in  other  maladies.  It  is  the  combination  of  symptoms  rather  than  any  one 
of  them  alone  that  indicates  or  establishes  the  diagnosis.  Headache  and 
vertigo  are  due  to  a  host  of  causes,  as  convulsions  and  paralysis  are 
common  conditions;  it  is  the  localization  of  the  convulsions  and  of  the 
paralysis,  pointing  to  a  distinct  focus,  that  is  significant.  Hysteria  may, 
however,  cause  localized  palsies  and  localized  anaesthesia.  Sometimes,  too, 
localized  convulsions  are  not  only  due  to  tumor,  but  are  symptomatic  of  a 
general  condition  such  as  poisoning,  or  of  a  widespread  nervous  disease 
such  as  paresis.  The  most  valuable  sign  of  brain  tumor,  optic  neuritis,  may 
be  present  in  chronic  contracted  kidney,  chronic  lead  poisoning,  and  severe 
anaemia,  etc.,  but  these  conditions  can  be  eliminated  from  the  case  by  the 
absence  of  the  other  signs  and  symptoms  of  these  maladies. 

Among  the  pathological  states  that  may  produce  symptoms  of  brain 
tumor  is  to  be  mentioned  localized  meningitis  due  to  tuberculosis  or  syphilis. 
(See  Meningitis.)  In  tuberculosis  the  degree  of  optic  neuritis  is  usually 
slight;  there  is  a  primary  tuberculous  focus  existing  elsewhere,  and,  as  the  case 
progresses,  evidences  of  a  general  meningeal  inflammation  may  develop. 
Syphilitic  meningitis  is  usually  diffuse,  not  localized,  and  when  localized 
is  to  be  considered  as  a  gumma  or  tumor.  Another  cause  of  such  symptoms 
is  abscess.  This  may  be  differentiated  by  its  rapid  development  and  by  the 
presence  of  a  septic  focus  elsewhere,  as  in  the  ear  or  in  other  parts  of  the 
body.     (See  Brain  Abscess.) 


940  DISEASES  OF   THE  NERVOUS  SYSTEM 

The  question  as  to  the  character  of  the  growth  is  determined  by  the  fol- 
lowing facts  in  many  cases.  Tuberculous  growths  are  frequently  met  with, 
particularly  in  children.  The  presence  of  tuberculous  infection  elsewhere 
also  points  to  this  form  of  tumor.  So,  too,  the  presence  of  a  malignant 
growth  in  some  other  part  of  the  body  suggests  that  the  lesion  in  the  brain 
is  of  the  same  character.  A  history  or  the  presence  of  the  scars  of  syphilis 
will  indicate  the  existence  of  a  gumma.  Cowers  states  that  if  the  tumor 
be  in  the  cerebellum  or  pons,  there  is  some  probability  "  of  its  being  tubercle 
or  glioma,  and  if  it  is  in  the  cortex  the  probability  that  it  is  syphilitic  is  con- 
siderable." "A  tumor  outside  the  brain  tissue  is  probably  sarcoma."  So, 
too,  the  disappearance  of  the  symptoms  under  active  antisyphilitic  treatment 
point  to  syphilis  as  the  cause.  "A  tumor  which  grows  rapidly  at  the  onset 
and  then  becomes  stationary  is  probably  tuberculous." 

Prognosis. — ^The  prognosis  in  all  forms  of  brain  tumor  is  grave.  It  is 
least  so  in  gumma  and  next  best  in  tubercle,  for  in  the  former  active  treat- 
ment may  cure,  and  in  the  second  a  long  period  of  arrest  may  ensue.  A 
growth  in  the  pons  or  medulla  is  more  dangerous  as  to  life  than  one  in  the 
cortex,  but  the  presence  of  severe  symptoms  of  brain  tumor,  be  the  seat  of 
the  growth  what  it  may,  is  always  of  grave  omen. 

Treatment. — From  what  has  been  said  of  the  etiology  and  pathology 
of  brain  tumor  it  must  be  evident  that  medicinal  treatment  can  do  nothing 
more  than  palliate  the  patient's  suffering,  unless  the  growth  be  syphilitic. 
For  the  relief  of  the  headache  the  various  coal-tar  products,  such  as  ace- 
tanilid,  phenacetin,  or  antipyrin,  may  be  employed,  and  their  efficiency  is 
usually  much  increased  by  giving  simultaneously  1  or  2  grains  of  caffeine 
and  10  or  20  grains  of  one  of  the  bromides,  preferably  the  bromide  of  stron- 
tium or  bromide  of  sodium.  In  those  cases  in  which  the  headache  becomes 
so  severe  as  to  be  insupportable,  hypodermic  injections  of  morphine  may  be 
employed,  but  it  is  an  interesting  therapeutic  fact  that  this  drug  gives  less 
relief  in  the  pain  of  brain  tumor  than  in  almost  any  other  affection  charac- 
terized by  pain.  Excessive  vomiting  is  to  be  checked  by  administrations 
per  rectum  of  10  or  20  grains  of  chloral  with  60  grains  of  bromide  of  sodium, 
to  which  may  be  added  30  to  60  minims  of  deodorized  tincture  of  opium. 
So,  too,  epileptiform  convulsions,  if  they  are  severe,  may  be  prevented,  at 
least  in  part,  by  the  use  of  the  bromides,  or,  if  an  aura  is  present,  by 
inhalations  of  nitrite  of  amyl. 

In  those  cases  in  which  there  is  the  history  of  syphilis,  the  administration 
of  mercury  and  the  iodide  of  potassium  is,  of  course,  strongly  indicated, 
and  if  a  gumma  is  producing  symptoms  such  as  convulsions,  which  may 
in  themselves  endanger  the  patient's  life,  the  mercury  should  be  pushed  as 
actively  as  possible,  being  given  by  the  mouth,  by  inunction,  by  hypo- 
dermic injection — that  is,  by  every  avenue  of  entrance — in  the  hope  that  it 
may  exercise  its  influence  upon  the  syphilitic  growth  before  a  convulsion 
sufficiently  violent  to  cause  death  ensues.  In  other  instances,  when  there 
are  no  acute  symptoms  which  demand  immediate  interference,  protiodide 
of  mercury  may  be  alternated  with  iodide  of  potassium,  iodide  of  sodium, 
or  iodide  of  strontium. 

When  the  growth  is  due  to  tuberculosis  the  administration  of  cod-liver 


ABSCESS  OF   THE  BRAIN  941 

oil,  iron,  and  arsenic,  and  residence  in  a  climate  in  which  plenty  of  fresh 
air  and  sunshine  can  be  constantly  obtained,  is  essential.  In  such  cases 
great  improvement  in  the  general  health  may  do  something  toward  arresting 
the  local  process. 

In  those  forms  of  brain  tumor  which  are  not  tuberculous  or  syphilitic, 
the  use  of  drugs,  except  to  relieve  pain,  is  practically  useless,  and  opera- 
tive interference  offers  the  patient  the  best  chance  of  recovery.  Surgical 
procedures  can,  however,  only  be  resorted  to  in  those  cases  in  which  a 
definite  localization  of  the  tumor  can  be  made,  and  where  that  locality  is 
so  situated  that  the  surgeon  can  reach  it  without  doing  damage  to  vital 
parts.  The  earlier  the  operation  is  performed  the  better  is  the  outlook. 
M.  Allen  Starr  has  collected  400  cases  of  brain  tumor  which  were  operated 
upon.  In  154  instances  tumor  of  the  cerebrum  was  successfully  removed, 
and  the  patients  recovered.  In  52  cases  the  patients  died.  In  16  instances 
in  which  the  tumor  was  in  the  cerebellum  it  was  removed  and  the  patients 
recovered.  In  8  instances  death  followed  removal.  It  is  interesting  to  note 
that  in  91  instances  of  supposed  cerebral  tumor  the  growth  could  not  be 
found  on  operation.  The  same  failure  to  discover  a  growth  was  met  with 
in  22  instances  of  supposed  cerebellar  tumor. 

Of  the  cases  which  recovered  52  were  sarcoma,  29  were  cysts,  8  were 
gummata,  19  were  tuberculous,  and  15  were  gliomas. 

For  the  measures  which  are  to  be  pursued  in  the  removal  of  brain  tumor, 
the  reader  is  referred  to  the  modern  works  on  surgery. 


ABSCESS  OF  THE  BRAIN. 

Definition. — Abscess  of  the  brain  is  a  condition  in  which  an  accumulation 
of  pus  takes  place  in  the  cerebrum,  or  the  cerebellum,  or  between  these 
parts  and  their  covering  membranes.  In  the  latter  case  the  brain  substance 
forms  one  wall  of  the  abscess  and  the  membranes  the  other  wall.  The 
latter  type  of  abscess  differs  from  purulent  meningitis  in  that  the  inflam- 
matory process  is  primarily  in  the  nervous  tissues,  and  that  it  is  limited  to  a 
comparatively  small  area.  Abscess  of  the  brain  without  involvement  of 
the  membranes  is  much  the  more  common  form,  and  the  white  matter  suffers 
very  much  more  frequently  than  the  gray  substance.  Abscess  rarely  occurs 
in  the  central  ganglia,  the  pons,  the  medulla,  or  the  middle  lobe  of  the  cere- 
bellum. 

Etiology. — Abscess  of  the  brain  is  always  due  to  an  infection  by  some 
pathogenic  organism.  In  some  instances  the  process  is  excited  by  an  injury 
which  affords  a  nidus  in  which  the  organism  may  develop;  in  other  cases 
a  septic  embolus  is  carried  from  another  part  of  the  body  in  which  there  is 
an  infected  area;  instill  others  the  infection  takes  place  more  directly,  as  in 
those  instances  in  which  by  fracture  of  the  skull  injury  and  infection  both 
occur,  or,  as  in  the  case  of  abscess  of  the  middle  ear  and  mastoid  disease, 
the  infection  spreads  by  way  of  the  sinus. 

Middle-ear  disease  is  the  cause  in  a  great  proportion  of  cases,  about  45 
per  cent,  arising  from  this  primary  focus  of    infection  and  25  per  cent. 


942  DISEASES  OF   THE  NERVOUS  SYSTEM 

from  injury.  The  remaining  causes  are  infection  of  the  other  cranial  bones 
than  the  mastoid  or  septic  foci  elsewhere. 

Males  are  affected  far  more  frequently  than  females,  in  the  proportion  of 
3  to  1.  This  is  largely  due  to  the  fact  that  males  are  so  much  more  exposed 
to  injury  than  females.  If  the  cases  of  abscess  due  to  middle-ear  disease 
are  studied  by  themselves,  the  proportion  is  almost  equal;  but  if  those  due 
to  trauma  are  considered  by  themselves,  the  proportion  is  5  of  men  to  1  of 
women. 

The  disease  is  most  frequent  between  the  tenth  and  twentieth  years  of 
life.  In  the  second  decade  ear  disease  is  the  common  cause,  and  in  the 
third  decade  ear  disease  and  injury,  or  a  distant  focus  of  infection,  are  about 
equal  in  frequency  as  causes. 

Pathology  and  Morbid  Anatomy. — A  majority  of  cases  of  brain  abscess 
affect  the  right  side  of  the  brain.  Out  of  71  cases  collected  by  Oppenheim 
55  were  in  the  temporal  lobe,  13  in  the  cerebellum,  2  in  the  pons,  and  1  in 
the  crus. 

The  pathological  process  which  results  in  abscess  consists  primarily  of 
an  encephalitis  which  speedily  goes  on  to  the  stage  of  suppuration.  This 
encephalitis  may  be  due  to  any  organism  capable  of  causing  an  active 
inflammatory  process.  Thus,  the  Streptococcus  pyogenes,  the  Staphylo- 
coccus pyogenes  aureus,  and  the  pneumococcus  may  be  the  provoking 
factors.  In  other  cases  the  typhoid  bacillus  may  be  the  cause,  and  even  the 
streptothrix  may  produce  such  a  lesion,  as  in  a  case  seen  by  me  in  consulta- 
tion with  Dr.  J.  H.  Musser.  The  abscess  is  nearly  always  single,  but  two 
or  more  pockets  of  pus  may  be  present.  The  size  of  the  abscess  varies 
greatly.  In  some  cases  it  is  so  small  as  scarcely  to  be  recognized,  a  small 
collection  of  pus  being  found  in  the  centre  of  an  area  of  softening;  whereas 
in  other  cases  the  quantity  of  pus  may  be  very  large,  varying  in  quantity 
from  a  drachm  to  several  ounces. 

The  abscess  may  be  surrounded  by  an  inflammatory  fibrous  wall  which 
serves  to  separate  it  from  the  neighboring  white  matter,  or  it  may  be  con- 
tained in  a  cavity  without  any  such  well-defined  margin,  the  walls  of  the 
abscess  being  composed  of  softened  brain  tissue.  The  latter  form  is  prone 
to  spread  more  rapidly  than  the  abscess  which  has  been  v\^alled  off.  On 
the  other  hand,  the  wall  of  the  abscess  may  rupture  and  produce  sudden 
death.  Not  rarely  the  extension  of  the  inflammatory  process  produces  a 
meningitis  if  the  abscess  is  situated  near  the  surface  of  the  brain,  and  a 
septic  thrombosis  of  the  nearby  vessels  may  occur. 

Symptoms. — It  is  of  interest  to  note  that  cerebral  abscess  may  occur 
without  producing  symptoms  sufficiently  typical  to  lead  to  an  antemortem 
diagnosis.  In  the  great  proportion  of  cases,  however,  the  s^noaptoms  of  its 
existence  are  well  developed.  The  most  constant  of  these  is  headache, 
general  or  localized;  it  is  excruciating  when  associated  with  middle- 
ear  disease;  next  in  constancy  is  mental  disturbance,  the  patient  being 
alternately  irritable  and  dull,  and  often  seeming  to  be  exceedingly 
ill.  The  temperature,  unlike  that  of  septic  processes  elsewhere,  is  usually 
normal  or  subnormal,  unless  the  abscess  ruptures,  when  it  may  be  hyper- 
pyretic.    The  surface  of  the  skull  is  often  hypersensitive,  and  in  some  cases 


ABSCESS  OF   THE  BRAIN  943 

it  has  been  possible  to  localize  the  abscess  by  the  dulness  on  percussion 
produced  by  its  presence.  Optic  neuritis  is  often  present.  None  of  these 
symptoms  is  in  any  sense  pathognomonic,  since  all  may  occur  in  other 
states  of  disease;  but  when  they  are  taken  into  consideration  in  connection 
with  a  history  of  middle-ear  disease,  injury,  or  the  presence  of  a  septic 
focus  elsewhere,  they  possess  great  diagnostic  value.  The  deafness  due 
to  destruction  of  the  auditory  centre  is  masked  by  the  deafness  due 
to  the  disease  in  the  ear.  Paralysis  of  one  side  of  the  face  is  not  of 
much  diagnostic  value,  since  this  symptom  is  often  due  to  the  inflam- 
mation about  the  facial  nerve  as  it  passes  through  the  stylomastoid 
foramen. 

The  value  of  localizing  symptoms  depends,  of  course,  upon  the  part 
of  the  brain  which  happens  to  be  affected.  When  the  infection  spreads 
from  the  mastoid  bone  after  or  during  otitis  media,  and  infects  the  temporal 
lobe,  there  are  no  localizing  nervous  symptoms  because  we  are  in  the  dark 
as  to  the  function  of  the  temporosphenoidal  lobe.  In  a  few  cases  a  lesion 
in  the  left  temporosphenoidal  lobe  has  caused  aphasia.  When  the  occipital 
lobe  is  involved  the  patient  may  present  the  symptom  called  optical  aphasia, 
for  in  this  lobe  is  situated  the  memories  of  objects  and  of  words  seen.  Starr 
has  observed  a  case  of  this  character.  The  patient  knows  an  object  when  it 
is  placed  before  him,  but  cannot  name  it.  A  lesion  of  the  temporal  lobe 
may  also  produce  this  symptom  by  pressure,  and  it  may  likewise  cause 
hemiplegia  or  hemiansesthesia  by  pressure  upon  the  internal  capsule.  Hemi- 
anopsia may  also  be  caused  in  this  manner. 

When  the  abscess  is  in  the  cerebellum  the  symptoms  are  those  charac- 
teristic of  cerebellar  tumor,  viz.,  a  staggering  gait,  vertigo,  and,  it  may  be, 
vomiting,  diplopia,  and  nystagmus.  In  some  instances  the  patient  staggers 
toward  the  diseased  side.  If  pressure  is  brought  to  bear  by  the  abscess 
upon  the  crus  or  pons  there  may  be  paralysis  of  the  oculomotor  or  facial 
nerves  on  the  side  of  the  lesion,  with  increase  in  the  knee-jerks  on  the  opposite 
side. 

Diagnosis. — ^The  diagnosis  of  brain  abscess  is  not  difficult  if  the  symp- 
toms just  described  have  been  preceded  by  a  history  of  injury  or  of  a  septic 
process  elsewhere,  near  or  remote.  There  are  two  other  states  with  which 
it  may  be  confused,  namely,  meningitis  and  thrombosis  of  the  lateral  sinus. 
In  the  former  condition  the  onset  is  usually  more  abrupt,  the  headache  is 
prone  to  be  more  severe  in  the  early  stages,  and  a  sharp  febrile  movement 
is  usually  present;  whereas,  as  has  already  been  pointed  out,  in  cerebral 
abscess  fever  is  often  absent  unless  the  abscess  ruptures.  The  pressure  of 
abscess  produces  a  slow  pulse  like  that  of  cerebral  compression,  but  in 
meningitis  the  pulse  is  usually  very  rapid.  Additional  symptoms  of  menin- 
gitis, which  are  of  great  value,  are  the  stiffness  of  the  muscles  of  the  neck, 
the  muscular  twitchings,  the  early  development  of  squint,  and,  last  of  all, 
the  presence  of  a  pathological  state  of  the  cerebrospinal  fluid  obtained  by 
lumbar  puncture.     (See  Cerebrospinal  Fever.) 

When  thrombosis  of  a  lateral  sinus  is  present  the  febrile  movement  is  sharp 
and  severe,  with  marked  remissions  and  exacerbations  as  in  sepsis.  There 
is  sweUing  of  the  jugular  vein  on  the  affected  side  and  of  the  conjunctiva 


944  DISEASES  OF   THE  NERVOUS  SYSTEM 

as  well,  associated,  it  may  be,  with  exophthalmos.  Swelling,  oedema, 
and  pain  on  pressure  over  the  mastoid  may  also  be  present.  The  use  of  the 
ophthalmoscope  also  reveals  choked  disk  in  many  cases  as  an  early  symptom. 

Prognosis. — This  depends  very  largely  upon  the  site  of  the  abscess  and 
the  ability  of  the  surgeon  to  evacuate  and  drain  it.  In  all  cases  the  prognosis 
is  necessarily  grave.  That  many  patients  may  recover  if  promptly  relieved 
is  shown  by  recent  statistics,  which  show  that  60  per  cent,  of  traumatic 
abscess  recover  after  operation,  and  about  50  per  cent,  of  abscess  due  to  ear 
disease  do  likewise. 

Treatment. — The  treatment  is  purely  surgical,  and  for  the  necessary 
procedures  reference  must  be  had  to  surgical  treatises. 


ACUTE  CEREBRITIS  OR  ENCEPHALITIS. 

Definition. — Acute  cerebritis,  sometimes  called  "  acute  encephalitis,"  is  a 
condition  in  which  there  is  an  acute  inflammation  of  the  brain  arising  as  a 
primary  disease  not  secondary  to  meningitis. 

Etiology. — The  cause  of  acute  cerebritis  is  always  an  infection  due  to 
the  entrance  of  a  micro-organism  into  the  body,  and  in  most  instances  the 
condition  arises  as  a  complication  of  measles,  scarlet  fever,  smallpox,  or 
ulcerative  endocarditis,  or  in  the  convalescence  from  influenza.  Acute 
alcoholism  and  other  forms  of  poisoning  may,  by  diminishing  vital  resist- 
ance in  the  brain,  predispose  to  this  condition.  Possibly  trauma  may  have 
a  like  result.  Whatever  may  be  the  cause,  this  condition  as  a  primary  acute 
disease  is  very  rare. 

Pathology  and  Morbid  Anatomy. — The  inflammatory  process  is  not  widely 
diffused,  as  a  rule,  but  is  found  to  exist  chiefly  in  the  distribution  of  one  or 
more  nearly  related  bloodvessels.  At  times  it  affects  the  same  areas  on  both 
sides  of  the  brain.  In  some  instances  only  the  cortex  is  involved,  while  in 
others  the  process  chiefly  affects  the  white  matter.  A  limited  form  of  this 
condition  is  the  acute  inflammation  of  the  medulla,  pons,  or  midbrain  (polio- 
encephalitis inferior  of  Wernicke  or  acute  bulbar  paralysis). 

The  changes  found  in  the  affected  parts  are  those  characteristic  of  acute 
inflammation  in  all  the  nervous  tissues,  and  indeed  in  any  acute  inflamma- 
tion, namely,  hypera3mia,  out-wandering  of  blood  cells,  and  minute  hemor- 
rhagic extravasations,  followed  by  the  ordinary  degenerative  changes  in  the 
nerve  cells  produced  by  an  interference  with  their  normal  blood  supply  and 
the  effects  of  toxaemia.  The  nerve-cell  body  or  ganglion  cell  itself  suffers  from 
cloudy  swelling,  loses  its  sharp  outlines,  and  its  nucleus  becomes  indistinct 
or  disappears .  The  axones  and  dendrites  also  undergo  a  similar  change. 
The  interstitial  tissues  are  at  first  filled  with  small  cells,  and  ultimately  there 
is  an  overgrowth  of  the  neuroglia  cells,  so  that  patches  of  sclerosis  are  pro- 
duced. This  last  result  is,  of  course,  permanent,  and  if  it  takes  place  to 
any  great  extent  may  seriously  impair  the  function  of  the  brain.  If  the  inflam- 
matory process  is  in  the  cortex,  adhesions  to  the  meninges  may  take  place. 

Symptoms. — The  symptoms  of  acute  cerebritis  depend  to  a  large  extent 
upon  the  portion  of  the  brain  which  is  chiefly  affected,  although  the  general 


ACUTE   CEREBRI TIS  945 

manifestations  of  an  acute  inflammatory  process  in  the  brain  are  present 
in  all  cases.  The  patient  is  seized,  after  a  few  hours  of  general  distress,  with 
headache  and  dizziness,  followed  by  a  chill  and,  it  may  be,  vomiting.  These 
symptoms  are  in  turn  speedily  followed  by  fever  and  rapidity  of  the  pulse 
and  respirations,  and  these  in  turn  in  some  instances  by  delirium  of  a  violent 
type.  If  the  case  is  severe  the  patient  may  now  pass  into  coma,  and  then 
gradually  pass  to  death,  or,  after  several  days,  or  even  weeks,  of  these  symp- 
toms, consciousness  gradually  returns,  the  temperature  falls,  and  recovery 
takes  place,  although,  as  already  stated,  permanent  impairment  of  some 
of  the  cerebral  functions  may  persist. 

The  special  symptoms  which  depend  upon  the  areas  of  the  brain  which 
are  affected  consist  in  hemiplegia,  monoplegia,  aphasia,  or  in  word-blind- 
ness and  word-deafness,  hemianopsia,  or  mutism.  Any  of  these  may  become 
permanent.  In  still  other  cases  the  patient  suffers  from  impairment  of  the 
intellectual  powers  or  the  changes  in  the  motor  cortex  produce  epileptic 
attacks,  and  in  other  instances  the  development  of  the  sclerotic  patches 
already  named  results  in  the  production  of  a  condition  identical  with 
disseminated  sclerosis  with  nystagmus,  tremor,  and  peculiar  speech.  The 
very  rare  condition  called  "  polioencephalitis  superior  of  Wernicke "  is 
manifested  by  the  presence  of  ptosis,  strabismus,  nystagmus,  and  even  optic 
neuritis  with  vertigo  and  a  staggering  gait.  In  addition  there  may  be  difficult 
speech  and  facial  paralysis. 

Diagnosis. — Acute  encephalitis  may  be  confused  with  brain  tumor  when 
epileptiform  convulsions  and  paralyses  are  prominent,  but  the  absence  of 
choked  disk  and  the  rapid  onset  will  distinguish  the  former.  In  its  "coma- 
tose" and  "epileptic"  forms  it  may  resemble  apoplexy  or  epilepsy,  and  a 
close  study  of  the  entire  clinical  picture  is  necessary,  with  the  history,  to 
differentiate  such  cases. 

Prognosis. — That  the  prognosis  in  acute  encephalitis  in  the  early  course 
of  the  malady  must  be  uncertain  is  manifest  when  we  consider  the  character 
of  the  lesions  which  are  present.  Even  after  the  active  stage  of  the  disease 
is  passed  the  outlook  as  to  complete  restoration  to  health  is  still  clouded 
because  it  is  not  possible  to  tell  what  secondary  changes  may  develop  in  the 
brain  or  its  membranes.  All  cases  of  acute  encephalitis  are  to  be  regarded 
as  of  much  gravity.  A  high  temperature,  convulsions,  profound  and  pro- 
longed coma  are  all  very  unfavorable  symptoms.  Even  in  the  very  grave 
cases  a  remarkable  degree  of  recovery  may  occur. 

Treatment. — This  consists  in  the  application  of  an  ice-bag  to  the  head, 
and  in  the  use  of  moderate  doses  of  tincture  of  aconite  if  there  is  circulatory 
excitement.  If  the  bowels  are  confined,  an  active  saline  purgative  is  useful 
to  move  them  and  to  deplete  the  bloodvessels.  A  hot  foot-bath  may  also  be 
used.  Phenacetin  and  acetanilid  may  be  employed  for  the  relief  of  pain, 
but  they  usually  fail.  On  the  other  hand,  the  use  of  opium  or  morphine 
often  makes  the  pain  worse.  Absolute  rest  in  a  darkened  room  is  essential. 
After  the  acute  process  is  over  iodide  of  potassium  may  be  given  in  the  dose 
of  10  grains  three  times  a  day,  with  the  hope  that  in  this  manner  inflammatory 
exudates  and  adhesions  may  be  absorbed. 

60 


9i6  DISEASES  OF   THE  NERVOUS  SYSTEM 


THROMBOSIS  OF  THE  VENOUS  SINUSES. 

Etiology. — Thrombosis  of  the  venous  sinuses  is  due,  as  are  cases  of  throm- 
bosis elsewhere,  to  an  inflammation  of  the  endothehum  which  hues  these 
vessels.  This  inflammation  may  be  the  result  of  a  septic  infection  in  remote 
or  in  neighboring  tissues,  as,  for  example,  in  suppurative  otitis  media. 
Where  the  cause  is  sepsis  the  thrombus  usually  contains  micro-organisms. 
The  vast  majority  of  instances  depend  upon  suppuration  in  the  ear. 

Pathology  and  Morbid  Anatomy. — The  size  of  the  thrombus  varies  very 
greatly.  Beginning  as  a  small  clot  in  one  sinus,  it  may  gradually  increase 
in  size  until  the  sinus  is  filled,  and  may  even  extend  to  adjacent  sinuses  and 
into  neighboring  veins.  If  septic  in  origin  it  may  be  purulent  in  character. 
The  longitudinal  sinus  is  very  rarely  affected.  The  lateral  sinus  is  the  one 
most  commonly  involved,  and  after  it  the  cavernous  sinus. 

Symptoms. — The  symptoms  of  thrombosis  of  the  lateral  sinus  are  con- 
gestion of  the  veins  in  the  neighborhood  of  the  mastoid,  with  swelling  of  the 
tissues  covering  it.  There  is  often  pain  and  tenderness  on  pressure.  Not 
rarely  the  cervical  glands  are  enlarged  from  infection,  and  wryneck  may 
be  present.  Choked  disk  is  frequently  present  upon  both  sides.  With  the 
infection  of  the  sinus  there  is  usually  a  history  of  a  rigor  followed  by  high 
fever,  with  headache,  vomiting,  delirium,  and  finally  coma.  The  fever  not 
rarely  follows  a  septic  course,  rising  and  falling  sharply.  Other  evidences 
of  septicoBmia  may  also  be  present,  such  as  sweating,  diarrhoea,  and  the 
occurrence  of  infarctions  in  such  organs  as  the  lungs,  spleen,  and 
kidneys. 

In  thrombosis  of  the  cavernous  sinus  there  is  local  swelling,  congestion 
of  the  face  about  the  eyes,  epistaxis,  and  undue  fulness  of  the  retinal  veins. 
Occasionally  squint  develops  as  a  result  of  interference  with  the  function 
of  the  oculomotor  and  abducens  nerve. 

Thrombosis  of  the  longitudinal  sinus  is  manifested  by  intense  venous 
congestion  in  the  scalp,  and  indeed  of  the  entire  head.  Choked  disk  may 
be  present  and  epistaxis  may  occur. 

Prognosis. — This  is  unfavorable  unless  surgical  interference  gives  relief, 
and  surgical  interference  is  practically  limited  to  cases  of  disease  of  the  lateral 
sinus. 

Treatment. — This  is  purely  surgical,  and  consists  in  trephining  or  other- 
wise opening  both  the  source  of  infection  and  the  sinus  and  thus  removing 
the  focus  and  the  clot.  For  details  as  to  the  method  of  operation,  and  as  to 
the  statistics  of  recovery  following  such  operations,  the  reader  is  referred 
to  books  on  surgery. 

CEREBRAL  MENINGITIS. 

Definition  and  Etiology. — By  meningitis  is  meant  an  inflammation  of  the 
membranes  covering  the  brain  or  spinal  cord.  From  an  anatomical  stand- 
point there  are  three  of  these — the  dura  mater,  the  arachnoid,  and  the  pia 
mater — ^but  from  the  standpoint  of  the  clinician  and  pathologist  these  mem- 


CEREBRAL  MENINGITIS  947 

branes  may  be  divided  into  two  parts,  the  dura  mater  on  the  one  hand  and 
the  arachnoid  and  pia  mater  (pia-arachnoid)  on  the  other,  for  the  dura  is 
often  inflamed  by  itself,  but  the  pia  and  arachnoid  are  always  affected 
together.  When  the  dura  is  alone  involved  it  is  called  pachymeningitis,  and 
when  the  other  membranes  are  affected  it  is  called  leptomeningitis. 

Pachymeningitis. — Pachymeningitis  may  occur  in  an  internal  form,  when 
the  smooth  inner  layer  of  this  membrane  is  inflamed  (pachymeningitis 
interna),  and  in  an  external  form,  in  which  the  outer  layer  is  chiefly  affected 
where  it  is  in  contact  with  the  bone  (pachymeningitis  externa).  The  latter 
is  the  most  common  type  by  far. 

Pachymeningitis  externa  is,  in  the  greater  proportion  of  cases,  secondary 
to  some  traumatism  or  to  disease  of  the  bone.  Thus,  a  blow  on  the  head 
which  fractures  the  skull,  or  necrosis  of  the  skull,  may  so  result.  Very  much 
more  rarely  an  acute  infection  arises,  as  in  an  infectious  and  septic  malady 
such  as  erysipelas. 

Pathology  and  Morbid  Anatomy. — The  inflammatory  process  resembles  that 
seen  in  any  inflammation,  namely,  hyperemia  followed  by  swelling  and 
cellular  infiltration,  and  this  in  turn  by  the  formation  of  pus  which  is  found 
between  the  skull  and  the  dura  mater,  or,  in  extraordinary  cases,  between 
the  layers  of  this  membrane.  When  the  inflammatory  process  does  not  go 
on  to  suppuration,  the  external  layer  of  the  dura  becomes  thickened  and 
adherent  to  the  skull.  If  the  inflammation  is  very  severe  the  inner  layer  of 
the  dura  is  affected,  and  the  pia  mater  may  become  involved  and  adherent 
to  it. 

Symptoms. — These  consist  in  those  characteristic  of  the  cause,  as  the 
primary  unconsciousness  from  a  blow,  or  the  pain  of  bone  disease,  and  in 
the  development,  as  direct  symptoms,  of  headache,  confusion  of  mind, 
delirium,  and  in  severe  cases  convulsive  seizures.  Fever  may  or  may  not  be 
present.  If  pus  collects,  symptoms  of  pressure  on  the  brain  may  develop, 
and  paralysis  of  the  opposite  side  of  the  body  may  ensue  (hemiplegia). 

Diagnosis. — ^The  history  of  injury,  of  bone  disease,  or  of  some  focus  of 
infection  makes  the  diagnosis  possible. 

Prognosis. — This  is  bad  in  direct  proportion  to  the  severity  of  the  inflam- 
matory process  and  the  degree  to  which  the  pia  mater  is  involved.  External 
pachymeningitis  is  less  grave  than  leptomeningitis. 

Treatment. — This  consists  in  the  use  of  saline  purgatives  to  relieve  cranial 
congestion,  in  applying  an  ice-cap  to  the  head,  rest  in  bed  in  a  darkened 
room  to  secure  perfect  quiet,  and  in  the  employment  of  aconite  as  a  cardio- 
vascular sedative  if  the  pulse  is  excited.  If  symptoms  of  cerebral  com- 
pression develop,  as  coma  or  paralysis,  the  fluid  or  pus  must  be  evacuated 
by  operation. 

Pachymeningitis  Interna. — Pachymeningitis  interna  occurs  in  a  purulent 
and  in  a  hemorrhagic  form,  the  purulent  being  very  rare.  To  the  hemor- 
rhagic type  the  terms"  hemorrhagic  internal  pachymeningitis " or" hematoma 
of  the  dura  mater  "  are  sometimes  applied.  Even  this  type  is  rarely  met  with, 
and  its  existence  is  rarely  recognizable  before  autopsy.  It  aft'ects  males  far 
more  commonly  than  females  (4  to  1,  Gowers),  and  is  generally  met  with 
after  the  fiftieth  year.    It  is  also  met  with  more  commonly  in  the  first  twelve 


948  DISEASES  OF   THE  NERVOUS  SYSTEM 

months  of  life  than  in  childhood  or  early  manhood.  As  a  rule,  in  adults  it 
develops  in  the  course  of  some  form  of  chronic  insanity,  particularly  in  the 
course  of  general  paralysis  of  the  insane,  or  in  cases  of  chronic  inebriety. 
Very  rarely  it  has  complicated  the  course  of  one  of  the  acute  infectious  dis- 
eases, such  as  typhoid  fever  or  smallpox.  In  children  it  may  complicate 
scurvy. 

Pathology  and  Morbid  Anatomy. — The  exact  method  or  process  by  which 
the  hemorrhagic  extravasation  takes  place  is  not  known.  The  autopsy 
reveals  a  bilateral,  and  rarely  a  unilateral,  extravasation  between  the  layers 
of  the  dura  and  between  the  dura  and  the  arachnoid.  Not  only  is  a  bloody 
fluid  formed  in  these  spaces,  but  a  pseudomembrane  is  also  present;  it  may 
be  in  several  layers.  These  layers  are  at  first  red  and  later  may  be  pallid, 
and,  by  adhering  together  at  spots,  form  pockets  in  which  the  bloody  fluid  is 
found.  When  the  condition  has  existed  a  long  time  this  fluid  may  be  decolor- 
ized and  contain  crystals  of  cholesterin.  Very  rarely  suppuration  takes 
place. 

Symptoms. — ^The  symptoms  are  in  many  cases,  if  the  disease  complicates 
chronic  insanity,  so  suppressed,  or  absent,  that  no  suspicion  of  the  state  just 
described  is  harbored.  In  some  cases  the  patient  develops  attacks  which 
resemble  those  of  apoplexy,  which  are  supposed  to  be  due  to  fresh  extrav- 
asations of  blood.  In  other  instances  there  are  signs  of  cerebral  com- 
pression, as  shown  by  stupor,  or  coma,  or  optic  neuritis.  Headache  and 
vomiting  may  be  present.     Partial  hemiplegia  may  develop. 

The  prognosis  is  very  unfavorable.  Treatment  is  almost  useless.  Quiet 
and  rest,  with  cold  to  the  head,  is  all  that  can  be  done.  In  cases  with 
strictly  localized  symptoms  surgical  intervention  is  justifiable. 

Leptomeningitis. — -Leptomeningitis  is  the  form  of  meningitis  which  com- 
plicates the  course  of  all  of  the  acute  infections,  notably  pneumonia,  erysip- 
elas, septicaemia,  and  less  frequently  variola,  scarlet  fever,  typhoid  fever, 
and  measles.  Measles  produces  it  very  commonly  because  this  malady  is 
often  followed  by  otitis  media,  and  because  otitis  media  not  rarely  causes 
mastoid  abscess,  and,  from  this  focus,  infection  involves  the  meninges  or 
the  lateral  sinus.  It  is  probable,  too,  that  a  very  considerable  proportion  of 
cases  of  leptomeningitis  are  caused  by  infection  which  takes  place  through  the 
nose.  It  can  be  readily  understood  that  any  infectious  micro-organism  which 
can  gain  access  to  the  meninges  through  the  openings  in  the  skull  or  in  the 
blood  may  cause  such  an  inflammation,  and,  in  addition,  that  the  possibility, 
or  probability,  of  infection  is  greatly  increased  by  any  disease  which  lowers 
vital  resistance,  such  as  nephritis.  It  must  not  be  thought,  however,  that 
all  cases  of  leptomeningitis  due  to  the  pneumococcus  are  complications  of 
croupous  pneumonia,  for  this  micro-organism  may  produce  a  meningitis 
by  direct  infection,  without  the  lung  being  affected  in  the  least.  It  is  prob- 
able, too,  that  the  typhoid  bacillus  may,  in  a  case  which  has  long  since  con- 
valesced from  the  fever,  act  in  a  similar  manner.  (For  the  relationship  of 
leptomeningitis  to  pneumonia  and  typhoid  fever  the  reader  is  referred  to 
the  articles  on  those  diseases.    Also  to  that  on  cerebrospinal  meningitis.) 

Meningitis  is  more  common  in  children  during  the  first  decade  of  life 
than  at  any  other  period,  but  in  these  cases  the  inflammation  usually  involves 


CEREBRAL  MENINGITIS  949 

the  meninges  at  the  base,  whereas  in  adults  that  part  of  the  meninges  which 
covers  the  convexity  is  chiefly  affected. 

Morbid  Anatomy  and  Pathology. — The  inflammatory  process  may  involve 
the  whole  membrane  or  be  quite  limited.  The  limited  cases  are  those  which 
arise  from  direct  infection  from  a  nearby  focus  of  disease.  Thus,  in  cases 
which  are  secondary  to  middle-ear  disease  the  lesion  is  often  unilateral, 
whereas  in  those  cases  in  which  the  pneumococcus  is  the  infecting  agent 
the  entire  convexity  on  both  sides  is  usually  affected.  In  the  latter  type  of 
case  the  effusion  which  develops  is  often  large  in  quantity  and  purulent. 
If  the  cause  is  tuberculous  the  base  is  usually  affected.  (See  Tuberculous 
Meningitis.)  The  actual  lesions  found  in  the  meninges  in  these  cases  are 
noteworthy.  Beginning  with  hypersemia  and  congestion  they  pass  on  to 
cloudiness  of  the  membranes  affected,  which  is  particularly  well  marked 
along  the  course  of  the  bloodvessels  because  of  the  engorgement  of  the 
accompanying  lymph  vessels.  Small  spots  of  purulent  material  are  dotted 
along  these  vessels  which,  as  they  increase  in  size,  coalesce,  and  so  consider- 
able areas  are  covered  by  pus.  When  the  process  is  severe  the  dura  mater 
and  the  cerebral  cortex  may  be  involved  by  the  inflammatory  changes. 

Symptoms.— In  studying  the  symptoms  of  leptomeningitis  it  must  be 
recalled  that  the  manifestations  of  involvement  of  the  cortical  area  are  by 
no  means  pathognomonic.  Every  physician  of  experience  has  seen  cases 
of  typhoid  fever  or  croupous  pneumonia  present  evidences  of  meningitis, 
yet  the  autopsy  has  revealed  no  such  lesion  present.  In  other  words,  as 
pointed  out  when  these  diseases  were  discussed,  toxins  produced  by  the 
specific  organisms  may  cause  symptoms  identical  with  those  of  meningeal 
inflammation.    This  is  exceedingly  common  in  the  pneumonia  of  children. 

There  are,  however,  certain  symptoms  of  meningitis  which  are  certainly 
indicative  of  either  inflammation  or  irritation  of  the  meninges,  particularly 
if  they  are  associated  with  a  disease  or  an  injury  qualified  to  produce  menin- 
geal involvement.  These  consist  in  fever,  headache,  vomiting,  retraction  of 
the  head,  and  rarely  convulsions.  Grinding  of  the  teeth,  obstinate  constipa- 
tion, and  an  excessive  hypercBsthesia  of  the  skin  of  the  arms  and  legs  are  also 
common  symptoms.  When  the  inflammatory  process  is  basilar  the  symp- 
toms are  much  more  definite  and  reliable.  In  addition  to  those  just  named 
we  find  that  optic  neuritis  is  present,  and  strabismus  and  ptosis,  due  to  the 
pressure  exercised  upon  the  cranial  nerves,  develop.  The  pupils  may  be 
contracted  in  the  early  stages  because  of  irritation  of  the  oculomotor  nerves, 
and  later  widely  dilated  by  reason  of  paralysis  of  these  nerves.  Fever  may 
or  may  not  be  present,  and  the  pulse  is  usually  slow  even  if  the  temperature 
is  raised.  Kernig's  sign  may  be  present.  (See  Cerebrospinal  Meningitis.) 
A  rapid  loss  of  flesh  takes  place  in  nearly  all  cases. 

Diagnosis. — The  symptoms  of  basilar  leptomeningitis,  whatever  its  cause, 
are  usually  unmistakable.  A  very  useful  aid  to  diagnosis  is  lumbar  punc- 
ture, already  described  under  Cerebrospinal  Meningitis.  If  the  cerebro- 
spinal fluid  escapes  with  a  spurt  from  the  needle,  it  is  indicative  of  the 
presence  of  tuberculous  meningitis,  but  by  no  means  positive  of  this  condi- 
tion, for  it  sometimes  happens  that  a  similar  high  pressure  exists  in  cases  of 
purulent  meningitis  and  of  spinal  tumor.    If  disintegrated  blood  is  present 


950  DISEASES  OF   THE  NERVOUS  SYSTEM 

in  the  cerebrospinal  fluid  it  is  an  indication  of  the  presence  of  pachymenin- 
gitis or  injury.  Fresh  blood,  on  the  other  hand,  is  probably  due  to  the 
puncture.  If  the  fluid  is  perfectly  clear,  every  inflammatory  affection  of  the 
meninges  except  tuberculosis  may  be  excluded.  In  tuberculosis  it  may  be 
clear,  but  is  often  cloudy,  and  toward  the  end  of  the  case  even  purulent. 
The  normal  proportion  of  albumin  in  it  is  0.02  to  0.04,  and  if  more  than 
0.05  is  present  an  inflammatory  process  is  probably  going  on.  If  the  small 
quantity  of  sugar  which  is  normally  present  is  absent,  this  is  a  sign  that 
inflammation  is  present. 

Treatment. — Aside  from  the  emplo}Tiient  of  rest  and  cold  to  the  head,  if 
fever  is  present  or  pain  is  suffered,  we  can  do  little  for  this  condition  except 
we  resort  to  lumbar  puncture  for  the  purpose  of  relie"ving  pressure. 

The  cerebrospinal  fluid  may  also  give  us  valuable  information  as  to  the 
presence  or  absence  of  meningitis,  if  it  be  examined  microscopically  and  a 
quantitative  estimation  of  its  leukocytes  is  made.  As  a  general  rule,  there 
is  a  marked  increase  in  lymphocytes  if  the  inflammatory  process  is  tuber- 
culous, and  of  polymorphonuclear  cells  if  it  is  non-tuberculous.  Exceptions 
to  this  rule  occur,  and  therefore  the  presence  of  either  one  of  these  forms  of 
leukocytes  in  increased  number  is  not  pathognomonic. 

Microscopic  examination  of  the  cerebrospinal  fluid  may  also  be  made 
for  the  purpose  of  discovering  tubercle  bacilli,  or  the  diplococcus  of  pneu- 
monia, or  other  pathogenic  micro-organisms.  The  fluid  for  this  purpose 
should  be  kept  on  ice  for  not  less  than  twelve  hours,  until  a  small  clot  is 
formed.  The  web-like  fibres  of  this  clot  are  transferred  to  a  cover-glass, 
spread  in  as  thin  a  film  as  possible,  and  stained  by  the  methods  commonly 
employed  for  staining  the  tubercle  bacillus.  "\Miere  the  examination  must 
be  performed  at  once,  the  fluid  may  be  put  in  a  centrifuge,  and  the 
sediment  examined  by  the  staining  methods  already  described.  As  with 
examinations  of  the  sputum  in  suspected  tuberculosis^  the  finding  of  tubercle 
bacilli  is  a  positive  sign  of  great  value,  but  the  failure  to  find  them  by  no 
means  proves  that  the  disease  is  not  tuberculous.  Reference  to  the  presence 
of  the  Diplococcus  intercellularis  menlngiiidis  has  already  been  made  in  the 
article  upon  Cerebrospinal  Meningitis.  Occasionally  the  streptococcus  and 
staphylococcus  are  found.  In  African  "sleeping  sickness"  trypanosomes 
have  frequently  been  found  in  the  cerebrospinal  fluid. 


DEMENTIA  PARALYTICA. 

Definition. — Dementia  paralytica,  often  called  "meningoencephalitis," 
"paresis,"  or  "general  paralysis  of  the  insane,"  is  a  state  characterized  ana- 
tomically by  a  widely  diffused  process  of  degeneration  in  the  central  nervous 
system,  particularly  in  the  cerebral  cortex,  with  morbid  changes  in  the  pia 
mater.  The  chief  s}Tnptoms  in  the  early  stages  are  the  development  of 
great  irritability  of  temper,  forgetfulness,  carelessness  as  to  habits,  and  later 
delusions  of  grandeur.  Clinically  it  is  characterized  by  a  progressive  par- 
alysis of  the  body,  associated  with  certain  physical  signs,  and  a  progressive 
loss  of  mental  power  of  a  peculiar  kind.  The  most  striking  symptom  of  this 
disease  is  the  "delusion  of  grandeur." 


DEMENTIA  PARALYTICA  951 

Etiology. — Without  doubt  syphilis  is  a  provoking  cause  in  a  large  propor- 
tion of  cases  (75  per  cent.),  but  it  is  not  present  in  all,  and  in  no  case  is  it  to 
be  regarded  as  a  direct  cause,  in  the  sense  that  the  syphilitic  virus  is  active  in 
a  given  instance.  On  the  contrary,  it  is,  like  locomotor  ataxia,  a  parasyphilitic 
affection,  that  is,  a  sequel  of  that  malady,  appearing  from  five  to  twenty 
years  after  the  initial  lesion.  Alcoholism,  excessive  sexual  indulgence,  and, 
indeed,  excesses  of  every  kind,  are  also  without  doubt  factors  of  importance. 
The  disease  is  a  common  one  among  roues.  Some  cases  seem  to  follow  a 
sunstroke  or  severe  injury. 

The  disease  is  one  of  the  middle  period  of  life,  between  thirty  and  fifty 
years,  but  a  number  of  cases  have  been  recorded  as  occurring  in  children 
who  have  usually  had  hereditary  syphilis. 

Pathology  and  Morbid  Anatomy. — The  primary  change  in  cases  of  this  dis- 
ease takes  place  in  an  increased  blood  supply  to  the  pia  mater  and  in  the 
smaller  vessels  of  the  cerebral  cortex,  associated  with  degenerative  changes 
in  the  bloodvessel  walls.  The  progress  of  these  degenerative  changes  results 
in  the  development  of  fusiform  dilatations  of  the  bloodvessels  and  the  filling 
of  the  lymph  spaces  with  serum.  The  exact  cause  of  these  changes  is  not 
understood,  but  Mott  believes  that  they  are  due,  in  part  at  least,  to  the  forma- 
tion of  a  toxic  substance  called  choline,  which  is  not  only  found  in  the  lymph 
spaces,  but  diffused  through  the  whole  cerebrospinal  fluid.  This  poison 
causes  congestion  of  the  veins  of  the  brain,  and  affects  chiefly  those  which 
empty  into  the  longitudinal  sinus.  Ultimately  the  quantity  of  lymph  present 
in  the  perivascular  spaces  is  so  great  that  a  true  cerebral  oedema  is  produced. 
There  is  an  overgrowth  of  the  neuroglia  about  the  vessels,  and  this  newly 
formed  connective  tissue  sends  fibrils  down  between  the  cells  of  the  cortex, 
with  the  result  that  a  true  sclerosis  develops.  Associated  with  these  con- 
nective-tissue changes  there  are  degenerative  changes  in  the  cerebral  neurones. 
The  body  of  the  neurone  undergoes  hyaline  and  then  fatty  degeneration, 
pigmentation,  and  finally  atrophy.  When  the  disease  has  been  present  for 
a  long  time,  autopsy  reveals  the  presence  of  small  cysts  in  the  white  and  gray 
matter,  and  so  marked  a  decrease  in  the  size  of  the  convolutions  and  of  the 
entire  brain  that  it  is  found  to  be  much  smaller  than  is  normal.  Its  surface 
is  harder  than  is  natural,  pigmented,  and  adherent  to  the  pia  mater,  which 
is  also  found  to  be  the  site  of  overgrowth  of  connective  tissue.  The  ventri- 
cles contain  an  excess  of  fluid,  and  their  lining  membrane,  the  ependyma, 
is  thickened.  It  is  noteworthy  that  the  left  hemisphere  is  usually  more 
affected  than  the  right,  and  that  the  changes  already  described  affect  the 
frontal  lobes  and  the  areas  of  the  motor  cortex  before  the  rest  of  the  brain 
is  involved. 

In  most  cases  of  paresis  degeneration  is  found  in  the  spinal  cord,  so  that 
spinal  symptoms  are  added  to  the  cerebral  signs  and  form  part  of  the  clinical 
picture  of  the  disease.  The  lateral  and  posterior  tracts  are  usually  affected, 
producing  symptoms  of  ataxic  paraplegia.  Sometimes  the  posterior  columns 
alone  are  degenerated,  presenting  symptoms  of  locomotor  ataxia.  Rarely 
disseminated  sclerosis  is  found;  and  recently,  in  one  case,  the  spinal  cord 
in  a  case  of  paresis  was  found  to  be  suffering  from  syringomyelia.  In  a 
few  cases  of  locomotor  ataxia  (tabes  dorsalis),  fully  developed  and  typical, 


952  DISEASES  OF   THE  NERVOUS  SYSTEM 

the  cerebral  signs  of  paresis  came  on,  as  if  the  disease  had  finally  "risen" 
to  the  brain.    These  cases  constitute  the  "ascending  type"  of  paresis. 

Some  authorities  believe  that  paresis  is  identical  in  nature  with  tabes— that 
it  is  a  "tabes  of  the  brain."  A  clinical  picture  of  paretic  dementia  with  tabes 
is,  therefore,  met  with.  Rarely  the  spinal  symptoms  precede  the  cerebral 
symptoms  in  the  development  of  the  disease.  So,  too,  symptoms  of  spastic 
paraplegia  may  develop.  Sometimes  autopsy  reveals  the  fact  that  pachy- 
meningitis and  hematoma  have  occurred  as  the  result  of  the  aneurysmal 
dilatations  of  the  cerebral  and  pial  vessels,  already  described,  leaving  behind 
them  an  organized  membrane  beneath  the  dura,  or  a  mass  of  encysted 
blood  clot. 

Symptoms. — When  the  symptoms  of  dementia  paralytica  are  well  devel- 
oped, they  are  so  characteristic  and  obtrusive  that  there  can  be  little  difficulty 
in  reaching  a  correct  diagnosis  in  regard  to  the  condition  from  which  the 
patient  is  suffering.  It  is  only  when  the  disease  is  in  its  stage  of  onset,  or  in 
an  atypical  form,  that  any  doubt  can  be  present. 

As  a  rule,  the  early  symptoms  are  recognized  in  retrospect  rather  than 
at  the  time  at  which  they  occur,  unless,  perchance,  these  symptoms  are  very 
strongly  developed.  It  is  noticed  that  the  patient  seems  to  be  nervously 
fatigued  or  mentally  fagged,  and  often  this  condition  is  ascribed  to  the 
excesses  which  have  been  committed  in  connection  with  venery,  wine, 
and  other  forms  of  nervous  stress.  The  temper  is  usually  irritable,  and 
the  friends  notice  that  the  patient  takes  offence  at  remarks  which  ordinarily 
he  would  not  notice.  At  times  he  is  remarkably  forgetful.  Naturally  tidy 
as  to  his  habits  and  dress,  he  becomes  careless  and  slovenly.  Occasionally 
sleeplessness  will  be  complained  of. 

Although,  before  the  onset  of  the  symptoms,  he  may  be  apparently  Idnd 
and  faithful  to  his  family,  he  begins  to  be  brutal  in  his  conduct  toward  his 
wife  and  children,  and  perhaps  returns  to  the  alcoholic  and  sexual  excesses 
which  laid  the  foundation  for  his  disease  many  years  before.  The  speech 
becomes  indistinct,  hesitating,  and  if  the  tongue  is  protruded  a  very  fine 
tremor  may  be  seen  in  it.  There  is  also  a  very  marked  tremor  of  the 
hands.  Ataxia  of  station  (Romberg's  sign)  is  a  common  symptom.  The 
pupils  are  generally  unequal  and  irregular,  and  the  pupillary  light  reflex 
may  be  lost,  while  reaction  to  accommodation  is  maintained.  In  other 
words,  the  Argyll-Robertson  pupil  is  present,  for  the  same  reason  that  it  is 
present  in  cases  of  locomotor  ataxia,  because  Meynert's  decussation,  or 
other  fibres,  involved  in  the  light  reflex  arc  are  affected  by  the  degener- 
ative process  already  described.  The  loss  of  consensual  reflex  is  also  fre- 
quently observed. 

The  symptoms  of  onset  are  often  prolonged  over  the  period  of  many 
months,  and  sometimes  for  several  years,  depending  upon  the  rapidity 
with  which  the  pathological  changes  in  the  brain  develop.  The  disease 
is  progressive  and  ultimately  the  symptoms  of  the  later  stages  are  devel- 
oped. These  symptoms  may  consist  in  delusions,  which  are  usually  com- 
posed of  extravagant  ideas.  Thus,  the  patient  may,  on  the  one  hand, 
believe  that  he  is  some  great  historical  character,  or  that  he  is  a  ruling 
potentate,  or,  again,  that  he  is  possessed  of  fabulous  riches.    In  one  instance, 


DEMENTIA   PARALYTICA  953 

for  example,  within  the  writer's  knowledge,  the  patient  took  a  room  at  a 
prominent  hotel,  after  having  provided  himself  with  large  sums  of  money, 
and  from  the  balcony  outside  of  the  room  showered  the  crowd  beneath  with 
coins  of  different  values,  with  the  idea  that  his  wealth  was  limitless.  In 
another  instance,  the  manager  of  a  small  plant  for  making  steel  became 
imbued  with  the  idea  that  his  company  had  obtained  and  could  fill  con- 
tracts for  the  delivery  of  manufactured  steel  on  a  scale  far  beyond  those  ever 
attempted  by  any  corporation,  although  as  a  matter  of  fact  the  business  of 
the  concern  was  at  its  last  ebb,  and  his  delusions  aided  in  causing  its  final 
financial  collapse,  through  its  inability  to  carry  out  the  agreements  which  he 
made  with  other  concerns.  In  this  instance  the  stress  of  business  worry 
combined  with  previous  excess  was  an  active  factor  in  producing  the  dis- 
ease. 

As  the  degenerative  process  in  the  brain  continues,  the  patient's  judg- 
ment becomes  profoundly  impaired.  He  rarely  is  capable  of  continuous 
thought,  and  no  longer  adheres  for  hours  at  a  time  to  his  delusions.  He 
frequently  becomes  exceedingly  emotional,  and  laughs  and  cries  without 
adequate  cause.  At  times  he  is  excessively  depressed;  at  other  times 
exalted,  and  he  may  occasionally  become  frenzied  with  rage,  during  which 
time  he  may  commit  some  crime. 

The  handwriting  is  often  characteristic.  It  may  become  illegible,  either 
because  the  letters  are  badly  formed  or  because  important  words  are 
dropped  out.  Still  later,  loss  of  power  occurs  in  the  limbs  until  total 
paralysis  may  be  present.  Sensation  is  not  so  markedly  disturbed,  but  areas 
of  anaesthesia  and  analgesia  may  be  found.  The  reflexes  may  be  markedly 
increased  or  entirely  lost. 

Naturally,  there  is  an  impairment  of  the  general  health  with  the  progress 
of  the  disease.  Epileptiform  attacks  or  sudden  periods  of  unconsciousness 
(apoplectiform  attacks)  develop,  accompanied  by  paralysis  of  one  limb,  or 
by  hemiplegia.  Death  usually  ends  the  case  by  the  end  of  the  third  to  the 
sixth  year,  the  patient  dying  of  exhaustion  or  of  some  intercurrent  disease, 
such  as  pneumonia,  obstruction  of  the  bowels,  or  of  one  of  the  epileptiform 
or  apoplectiform  attacks. 

Cases  of  paresis  in  which  the  delusion  of  grandeur  is  prominent  are  the 
earliest  recognized,  and  constitute  the  classic  form  of  the  disease.  There 
are  many,  however,  in  which  depression  simulating  melancholia  is  present 
throughout;  that  is,  the  depressed  form  of  paresis.  But  in  a  large  proportion 
of  all  cases  the  mental  symptoms  are  mainly  those  of  progressive  mental 
loss,  without  distinct  delusions  (the  simple  or  demented  form  of  paresis). 
An  alternation  of  excitement  and  depression  (circular  form  of  paresis)  is 
observed  rarely;  delusions  similar  to  those  of  paranoia  or  of  alcoholic 
insanity  may  mask  the  underlying  condition. 

Diagnosis. — Dementia  paralytica  must  be  separated  in  its  early  stages  from 
neurasthenia.  The  patient  suffering  from  nervous  exhaustion  usually  studies 
his  own  symptoms  in  the  greatest  detail,  and  usually  considers  that  he  is  an  ill 
man,  while  the  paretic  has  a  very  much  more  optimistic  view  and  often  insists 
that  he  is  more  than  usually  well,  when  it  is  manifest  that  his  ill  health  is 
extreme.    So,  too,  the  neurasthenic  rarely  has  complete  lapses  of  memory 


954  DISEASES  OF   THE  NERVOUS  SYSTEM 

and  defects  of  speech.  From  cerebral  syphilis  paresis  is  separated  by  the  fact 
that  the  former  disease  usually  manifests  severe  pain  in  the  head  and  true 
aphasia  due  to  a  syphilitic  arteritis  in  the  neighborhood  of  the  speech  centre. 
The  fine  tremor  of  the  tongue  and  of  the  hand  in  paresis  is  absent  in  cere- 
bral syphilis.  Optic  neuritis  is  usually  present  in  cerebral  syphilis,  but 
not  very  common  in  paresis.  So,  too,  the  mental  state  is  one  of  constant 
depression  in  syphilis,  and  not  that  of  excitation.  From  multiple  sclerosis 
paresis  is  separated  by  the  presence  in  sclerosis  of  nystagmus  and  intention 
tremor  and  by  the  absence  of  delusions. 

Prognosis. — This  is  absolutely  unfavorable.  No  cases  ever  recover, 
although  temporary,  and  it  may  be  prolonged;  remissions,  which  cause 
encouragement  on  the  part  of  the  friends,  may  occur. 

Treatment. — It  must  be  evident,  from  the  pathological  condition  already 
described,  that  treatment  can  do  little.  In  paresis  when  there  is  a  clear  his- 
toiy  of  syphilitic  infection,  the  iodides  and  mercury  may  be  freely  used  in 
connection  with  hot  baths.  But  it  must  be  remembered  that  this  disease  is 
the  sequence  of  syphilis  rather  than  the  direct  result  of  it,  and  therefore 
these  remedies  are  in  no  sense  specific.  Their  general  tendency  is  favorable, 
and  they  may  perhaps  arrest  for  the  time  being  the  progress  of  the  vascular 
changes,  but  they  cannot  cure  those  in  existence.  If  the  patient  is  difficult 
to  control,  it  is  far  better  both  for  himself  and  his  friends  that  he  should  be 
committed  to  an  asylum  where  he  can  be  properly  cared  for,  not  only  in  the 
sense  of  being  properly  controlled,  but  of  being  well  fed,  as  the  maintenance 
of  health  and  general  nutrition  is,  of  course,  of  importance.  Sleeplessness 
may  be  treated  by  any  one  of  the  good  hypnotics,  of  which  chloral,  trional, 
and  sulphonal  are  the  best.  Occasionally,  hyoscine  may  be  used.  Care 
must  be  taken  that  the  carelessness  of  the  patient  in  regard  to  his  bowels 
does  not  result  in  obstinate  constipation,  which  may  be  difiicult  to  relieve. 
For  this  reason,  active  purgatives  are  often  necessary.  If  outbreaks  of 
excitement  comes  on,  ^-g-g-  of  a  grain  of  hyoscine  may  be  given  hypo- 
dermically. 

DISSEMINATED  SCLEROSIS. 

Definition. — Disseminated  sclerosis  is  characterized  by  the  development 
of  irregularly  distributed  patches  of  sclerosis  in  different  parts  of  the  brain 
and  spinal  cord.  Similar  changes  also  take  place  in  the  cranial  nerves. 
It  is  sometimes  called  "  insular  sclerosis  "  or  "  multiple  sclerosis."  By  the 
French  it  is  called  sclerose  en  'plaques  disseminees.  It  has  only  been 
recognized  as  a  distinct  disease  for  a  little  more  than  tliirty  years. 

Etiology. — The  essential  cause  of  multiple  sclerosis  is  not  known.  It 
affects  both  sexes  equally,  and  occurs  at  all  ages,  though  very  rarely  in 
childhood.  Its  most  common  period  of  existence  is,  however,  from  the  thir- 
tieth to  the  fortieth  year.  Occasionally  it  has  been  known  to  follow  one  of 
the  acute  infectious  diseases,  and  has  been  regarded  as  a  consequence  of 
disseminated  myelitis  of  infectious  origin  (jNIarie);  but  it  is  doubtful  whether 
this  malady  has  any  direct  productive  effect  in  the  case.  Syphilis,  that 
great  cause  of  organic  nervous  disease,  does  not  seem  to  be  frequently 
present  as  an  etiological  factor. 


DISSEMINATED  SCLEROSIS  955 

Pathology  and  Morbid  Anatomy. — The  lesions  of  disseminated  sclerosis 
consist,  as  already  stated,  in  irregularly  distributed  patches  in  which  the  inter- 
stitial tissues  have  undergone  sclerotic  change.  These  patches  are  found 
chiefly  in  the  white  matter  of  the  brain,  being  comparatively  rare  in  the 
gray  substance  of  the  cortex.  They  are  irregular  in  outline  and  vary  in  size. 
In  appearance  they  are  reddish-gray  and  translucent.  The  surface  of  a  patch 
is  usually  even  with  the  surrounding  brain  tissue,  but  it  may  be  slightly 
depressed.  A  sharp  line  of  demarcation  separates  the  diseased  area  from' 
the  healthy  tissues.  When  touched,  the  patches  seem  harder  than  normal 
gray  matter,  but  they  are  not  usually  met  with  until  section  of  the  brain  or 
cord  is  made,  when  they  appear  in  strong  contrast  to  the  surrounding  white 
tissue.  They  may  be  found  in  considerable  number  in  the  lateral  ventricle, 
in  the  corpus  callosum,  crura,  and  pons.  The  patches  in  the  spinal  cord 
are  not  so  reddish  in  hue  as  in  the  brain,  but  are  more  gray  in  color  and 
extend  vertically  rather  than  transversely;  but  this  rule  is  not  absolute,  and 
at  times  the  transverse  extension  of  a  patch  may  embrace  the  entire  thick- 
ness of  the  cord.  When  one  of  the  cranial  nerves  is  involved,  it  is  found  to 
be  gray  in  color  and  sclerotic  for  a  certain  portion  of  its  length.  In  some 
instances  the  entire  thickness  of  the  nerve  is  involved.  The  olfactory,  optic, 
oculomotor,  trifacial,  and  facial  nerves  are  the  ones  which  are  most  com- 
monly affected,  and  in  the  case  of  the  optic  nerve  the  favorite  seat  is  the 
chiasm. 

The  sclerotic  process  in  this  disease  does  not  differ  very  materially  from 
that  met  with  in  sclerotic  processes  occurring  in  other  organs  of  the  body; 
there  is  an  overgrowth  of  the  true  neuroglia  or  connective  tissue,  and  side 
by  side  with  this  overgrowth  a  corresponding  atrophy  or  disappearance  of 
the  nerve  cells  and  fibres  themselves  takes  place.  When  the  degenerative 
process  is  well  advanced,  we  find  scattered  through  the  connective-tissue 
fatty  granules  and  nerve  cells  which  show  evidence  of  degenerative 
change.  In  the  nerve  fibres  the  chief  change  takes  place  in  the  myelin, 
but  after  the  disease  is  far  advanced  the  axis  cylinder  also  becomes 
affected  and  finally  is  completely  destroyed.  In  the  central  nervous  system 
it  is  usually  found  that  secondary  degeneration  in  the  nerve  fibres  above  or 
below  the  seat  of  the  original  sclerotic  patch  is  only  met  with  when  the  dis- 
ease has  been  sufficiently  severe  to  destroy  the  axis  cylinders.  On  this 
account  secondary  degenerations  are  not  common  in  disseminated  sclerosis, 
the  axis  cylinders  surviving  in  the  midst  of  fully  developed  sclerotic  patches, 

Symptoms. — The  symptoms  of  disseminated  sclerosis  depend  almost 
entirely  upon  the  areas  of  the  nervous  system  which  are  chiefly  affected  by  the 
pathological  changes  just  described.  Among  the  earliest  symptoms  in  many 
cases  is  a  loss  of  power  in  the  extremities.  In  the  legs  the  symptoms  may  be 
ataxic,  but  usually  simulate  those  of  spastic  paraplegia  in  a  striking  degree. 
When  spastic  paraplegia  is  present,  this  indicates  that  the  sclerotic  process 
has  involved  the  pyramidal  tracts,  and  the  knee-jerks  are  found  to  be  exag- 
gerated. In  other  instances  inco-ordination  of  the  hands,  or  of  one  hand, 
may  be  the  first  manifestation  of  the  malady,  and  in  still  others  sensory 
disturbances  in  the  legs  or  arms  are  first  complained  of  by  the  patient.  The 
inco-ordination  of  the  muscles  of  the  arms  is  often  very  marked  indeed. 


956  DISEASES  OF   THE  NERVOUS  SYSTEM 

Often  it  is  impossible  for  a  patient  to  carry  a  glass  of  water  to  his  lips  without 
spilling  it  (intention  tremor).  The  co-ordinated  movements  which  are 
necessary  in  writing  are  impossible  because  of  the  quick  or  spasmodic 
contractions  of  the  muscles  employed  for  this  purpose.  The  cause  of 
these  irregular  movements  is  not  known.  According  to  some  it  is  depend- 
ent upon  the  fact  that  certain  fibres  are  affected,  and  impulses  going  along 
certain  channels,  particularly  the  motor,  are  delayed  in  passing  through  scle- 
rotic areas,  or  that  those  which  pass  along  fibres  still  unaffected  are  made 
inadequate  and,  as  it  were,  embarrassed.  By  others  it  is  thought  that  the 
sclerotic  patches  have  involved  afferent  fibres  of  the  cerebellar  system  which 
are  concerned  with  muscular  sense. 

If  sensory  fibres  in  the  dorsal  columns  are  involved,  areas  of  ancesthesia 
or  hemiancBsthesia,  also  ataxia  of  the  extremities,  will  develop,  the  severity 
of  these  symptoms  depending,  of  course,  upon  the  area  involved  in  the 
sclerotic  process.  The  eye  symptoms  are  usually  well  marked.  One  of 
the  earliest  and  most  constant  of  these  is  nystagmus.  Eyesight  fails 
through  involvement  of  the  optic  nerve  or  because  of  a  sclerotic  patch  at 
the  optic  chiasm.  As  the  disease  advances  pallor  of  the  optic  disk,  partic- 
ularly its  temporal  half,  and  sometimes  optic  atrophy  can  be  recognized 
on  ophthalmoscopic  examination.  One  eye  is  often  much  more  affected 
than  the  other,  and  loss  of  accommodation  may  occur.  In  other 
instances  the  pupillary  reflex  may  be  lost,  yet  the  pupil  will  react  to 
accommodation.  In  other  words,  the  Argyll-Robertson  pupil  is  present. 
The  affection  of  the  external  ocular  muscles,  aside  from  the  production  of 
nystagmus,  consists  most  frequently  in  a  failure  in  convergence  and  in  con- 
jugate deviation.  More  rarely  a  single  muscle  is  affected  and  squint  is  pro- 
duced. When  the  facial  nerve  is  affected,  the  symptoms  in  the  early  stages 
may  consist  in  clonic  spasm  of  the  muscles  of  the  face,  followed  eventually  by 
paralysis.  The  lesions  of  the  cranial  nerves,  which  produce  these  results, 
may,  as  already  pointed  out,  occur  in  the  nerves  themselves  or  involve  their 
nuclei. 

Of  all  the  symptoms  of  disseminated  sclerosis  perhaps  the  most  character- 
istic and  most  frequent  is  the  peculiar  disorder  of  speech  in  which  syllables 
are  enunciated  in  a  measured  manner.  To  this  mode  of  speech  the  term 
staccato  or  scanning  is  applied.  The  exact  cause  of  this  is  not  clear.  It  does 
not  seem  to  be  dependent  entirely  upon  paralysis  involving  the  tongue  or 
the  lips. 

The  mental  condition  of  the  patient  is  usually  not  materially  altered. 
The  memory  may  be  slightly  impaired  and  the  patient  seem  somewhat 
emotional.  Very  occasionally  actual  insanity  develops.  Paroxysmal  attacks 
of  vertigo  and  vomiting  are  occasionally  met  with,  and  in  some  cases  the 
patient  is  seized  with  attacks  which  closely  resemble  an  ordinary  apoplexy. 
These  attacks,  it  will  be  remembered,  sometimes  develop  in  patients  who 
suffer  from  general  paralysis  of  the  insane,  and  they  appear  either  as  ordinary 
coma,  as  Jacksonian  epilepsy,  or  as  a  hemiplegia  which  is  fleeting  in  char- 
acter. All  these  symptoms  of  an  apoplectiform  type  may  recur  frequently, 
and  are  usually  recovered  from,  but  occasionally  death  comes  on  during 
coma.  It  is  a  fact  worthy  of  note  that,  notwithstanding  the  profound  changes 


DISSEMINATED  SCLEROSIS  957 

which  take  place  in  difPerent  portions  of  the  nervous  system,  trophic  changes 
in  the  muscles  are  rarely  met  with,  even  in  advanced  cases. 

Diagnosis. — The  most  characteristic  symptoms  of  disseminated  sclerosis, 
as  just  stated,  consist  in  the  intention  tremor,  the  staccato  speech,  the 
nystagmus,  the  peculiar  jerking,  inco-ordinated  movements  of  the  muscles 
of  the  arms  and  sometimes  of  the  legs,  weakness  of  the  legs,  and  the 
gradual  involvement  of  the  cranial  nerves. 

The  disease  is  to  be  separated  from  locomotor  ataxia  by  the  jerking  character 
of  the  inco-ordinated  movements;  and  by  the  exaggeration  of  the  reflexes, 
which  are  in  contrast  to  the  absent  reflexes  of  ataxia.  From  paralysis  agitans 
it  is  separated  by  the  fact  that  in  the  latter  disease  there  is  a  finer  tremor  of  the 
hand,  or  of  the  parts  of  the  body  which  may  be  affected  (the  tremor  is  passive), 
by  the  peculiar  attitude  of  the  patient  in  paralysis  agitans,  and  by  the  absence, 
as  the  disease  progresses,  of  the  characteristic  symptoms  just  spoken  of  as 
peculiar  to  multiple  sclerosis.  General  paralysis  of  the  insane  is  distinguished 
by  the  presence,  in  the  classic  type  of  this  disease,  of  delusions  of  grandeur, 
by  the  twitching  of  the  muscles  of  the  hps  and  tongue,  which  are  more  con- 
stant and  severe  than  they  are  in  multiple  sclerosis,  and  by  the  other  evidences 
of  mental  change.  In  a  case  of  disseminated  sclerosis,  in  which  the  lateral 
columns  of  the  spinal  cord  are  involved,  it  may  be  difficult  to  differentiate 
multiple  sclerosis  from  spastic  paraplegia,  but  as  the  disease  progresses  the 
development  of  the  other  symptoms  of  disseminated  sclerosis  makes  the 
diagnosis  easy.  From  hysteria  disseminated  sclerosis  is  to  be  separated  by 
the  fact  that  nystagmus  does  not  appear  in  this  functional  nervous  disorder, 
and  by  the  inconstancy  of  the  symptoms  in  many  cases  of  hysteria.  The 
other  characteristic  stigmata  of  hysteria  may  also  be  found.  (See  article  on 
Hysteria.) 

Prognosis. — The  prognosis  in  a  case  of  disseminated  sclerosis  is  absolutely 
unfavorable  as  to  ultimate  recovery.  The  disease  is  characterized  by  various 
remissions  or  periods  of  arrest,  so  that  death  is  sometimes  postponed  for 
a  considerable  period  of  time.  The  prognosis  as  to  duration  of  life  is  worse 
in  those  cases  in  which  the  lesions  involve  nervous  tissues  closely  associated 
with  vital  functions,  as  when  sclerotic  changes  take  place  in  the  pons, 
or,  above  all,  when  they  occur  in  the  medulla.  It  is  noteworthy  that 
pregnancy  or  trauma  increases  the  rapidity  with  which  the  disease  pro- 
gresses. 

Treatment. — Everywhere  in  this  book,  when  we  have  considered  the 
treatment  of  diseases  depending  upon  sclerotic  changes  or  overgrowth  of 
connective  tissue  it  has  been  pointed  out  that  our  therapeutic  resources  are 
inadequate.  We  do  not  know  the  causes  of  this  connective-tissue  over- 
growth, and  so  are  unable  to  combat  it,  nor  do  we  know  why  the  cells  degen- 
erate. Neither  have  we  any  reason  to  believe  that  in  the  future  we  will 
discover  any  remedy  which  will  cause  the  absorption  of  connective  tissue 
when  it  is  once  formed,  and  it  is  certain  that  fibres  which  have  once  degen- 
erated and  have  been  destroyed  cannot  be  regenerated  by  the  action  of  any 
medicine. 


958  DISEASES  OF   THE  NERVOUS  SYSTEM 


DISEASES  IN  WHICH  THE  CHIEF  MANIFESTATIONS   ARE   IN 

THE  SPINAL  CORD. 

LOCOMOTOR  ATAXIA. 

Definition. — Locomotor  ataxia  is  a  disease  characterized  chiefly  by  inco- 
ordination of  gait  and  station,  loss  of  muscle  sense,  and  loss  of  the  deep 
reflexes.  It  is  often  accompanied  by  pain.  The  most  noteworthy  loss  of 
reflexes  is  in  the  patellar  tendon  and  iris.  Pathologically,  it  is  characterized 
by  slow  progressive  lesions  which  affect  chiefly  the  sensory  nerve  roots  and 
the  posterior  or  dorsal  columns  of  the  spinal  cord.  It  is  sometimes  called 
tabes  dorsalis,  or  posterior  spinal  sclerosis. 

History. — Cases  of  locomotor  ataxia  were  recorded  as  a  form  of  paralysis 
many  years  ago,  but  it  was  not  till  1847  that  Todd  clearly  separated  this 
malady  from  other  states  of  paralysis.  In  1840  Stanley  had  recognized  that 
the  affection  was  associated  with  changes  in  the  posterior  columns  of  the 
spinal  cord.  In  1855  Reynolds  first  showed  that  the  disease  was  essentially 
a  state  in  which  the  symptoms  were  due  to  a  loss  of  muscle  sense,  and  not  to 
loss  of  power  in  the  motor  nerves  or  muscles — a  view  confirmed  by  Tiirck, 
who  made  a  microscopic  demonstration  of  the  site  of  the  lesions. 

Etiology. — Males  suffer  more  than  females  in  the  proportion  of  10  to  1. 
In  a  large  hospital  experience  of  over  twenty  years  I  have  never  seen  a  case 
in  a  woman.  Half  the  cases  develop  in  the  decade  of  life  between  thirty  and 
forty  years,  and  80  per  cent,  between  thirty  and  fifty  years.  Gowers  states 
that  it  rarely  develops  after  fifty  years. 

By  far  the  most  common  cause  of  the  disease  is  acquired  syphilis.  Rarely 
the  syphilis  is  hereditary.  Some  writers  have  gone  so  far  as  to  state  that 
locomotor  ataxia  is  due  to  this  cause  in  over  90  per  cent,  of  the  cases  (Sachs). 
Gowers  gives  the  rather  moderate  proportion  of  77  per  cent.;  Starr  70  per 
cent.  It  is,  however,  important  for  the  student  to  remember  that  locomotor 
ataxia  is  not  syphilis  of  the  nervous  system,  but  rather  a  remote  result  of  the 
syphilitic  infection.  In  many  instances  the  ataxic  symptoms  develop  so  many 
years  after  syphilitic  infection  that  the  patient  cannot  believe  that  the  two 
maladies  have  any  relationship  of  cause  and  effect,  the  more  so  as  ataxia  is  more 
frequently  met  with  in  patients  who  have  presented  very  mild  secondary 
symptoms  than  in  those  who  have  had  severe  symptoms  in  the  early  stages. 
Rarely  the  ataxic  symptoms  develop  within  five  years  of  the  primary  sore. 

Next  to  syphilis  as  a  possible  cause  is  traumatism.  Severe  falls,  or  blows 
upon  the  spine,  have  been  followed,  months  or  years  later,  by  tabes  dorsalis, 
but  it  is  impossible  to  tell  whether  the  trauma  is  the  direct  cause  of  the 
malady.  Sometimes  other  diseases  of  the  cord  finally  produce  locomotor 
ataxia. 

Pathology  and  Morbid  Anatomy. — In  studying  the  morbid  anatomy  and 
pathology  of  locomotor  ataxia  it  is  important  for  the  student  to  recall  the 
fact  that  the  primary  lesion  of  the  disease  is  in  the  posterior  ganglia  and 
posterior  roots  of  the  spinal  cord,  and  in  the  ganglia  of  the  cranial  nerves, 
and  not  in  the  posterior  columns  of  the  spinal  cord,  as  was  thought  at  one 


PLATE    VIT. 


hrtSrl  Sensory 
EEEj  Motor 
L^2lH  Association 


XIII 


The  Cervical  and  Sacral  Enlargements  of  the  Spinal  Cord  in 
Cross-section— sho^^^ing  the  various  neurones  in  the  gray  matter, 
the  direction  of  their  axones,  and  the  varieties  of  fibres  in  the 
different  columns  of  the  cord  (Starr).  Blue,  motor-;  red,  sensory-; 
purple,  association-neurones  and  axones. 

I.  Ant.  median  column.  II.  Anterolateral  column.  III.  Gowens'  anterolateral  ascending  column. 
IV.  Marginal  columji.  V.  Lateral  pyramidal  column.  VI.  Direct  cerebellar  column.  VII.  Lissauer's 
tract.  VIII.  Ext.  portion  of  column  of  Burdach.  IX.  Root  zone  of  the  column  of  Burdach.  X. 
Descending  comma-shaped  bundle  of  Schultze.  XI.  Post,  commissural  tract.  XII.  Column  of  Goll. 
XIII.    Septomarginal  tract. 


LOCOMOTOR  ATAXIA  959 

time.  The  sensory  cells  in  the  posterior  ganglia,  outside  of  the  cord,  are 
flask-shaped  bodies,  each  of  which  has  a  process  which  divides  into  two 
axones.  One  of  these  goes  by  the  posterior  nerve  root  to  the  spinal  cord, 
and  the  other  goes  to  the  afferent  nerve,  which  extends  to  the  peripheral 
portions  of  the  body.  (See  Plate  VII.)  Degenerative  changes  take  place 
in  the  proximal  axone  as  well  as  in  the  peripheral  portion  of  the  distal  axone. 
These  changes  are  sclerotic  and  are  carried  into  the  cord,  so  to  speak,  by  the 
proximal  axone.  Therefore,  locomotor  ataxia  consists  primarily  in  disease  of 
the  proximal  axone,  secondarily  in  disease  of  the  distal  axone,  and  finally 
in  disease  of  those  fibres  in  the  posterior  portion  of  the  spinal  cord  which 
have  their  origin  in  the  proximal  axone  just  described.  While  it  is  true 
that  the  primary  lesion  is  not  in  the  cord,  it  is  nevertheless  a  fact  that  the 
chief  manifestations  of  the  pathological  process  are  to  be  found  in  this  por- 
tion of  the  nervous  system.  Indeed,  the  changes  in  the  spinal  cord  are  so 
well  developed  in  typical  cases  that  the  macroscopic  examination  suffices 
for  the  diagnosis  at  the  autopsy. 

The  affected  portions  of  the  cord  are  smaller  than  normal  and  more 
grayish  in  appearance.  The  distribution  of  those  areas  varies  greatly. 
In  some  instances  the  disease  is  so  moderate  in  degree  and  in  distribu- 
tion as  to  be  difficult  of  recognition,  except  by  the  microscope.  In  others, 
if  the  malady  is  far  advanced,  the  whole  length  of  the  posterior  columns 
may  be  affected.  There  are  certain  parts  of  the  cord  which  are  particu- 
larly prone  to  the  development  of  the  disease.  Thus,  the  lesions  are  usually 
well  developed  in  the  posterior  columns  in  the  lumbar  region,  particularly 
in  the  neighborhood  of  the  posterior  root  zones,  and  this  accounts  for  the 
fact  that  the  legs  show  the  earliest  and  most  severe  symptoms.  As  we 
ascend  the  cord,  however,  the  lesions  are  chiefly  found  in  the  postero- 
median columns. 

In  instances  in  which  the  disease  affects  the  arms  as  well  as  the  legs  and 
is  well  developed,  the  posteroexternal  columns  are  affected  even  in  the 
cervical  region   (Fig.  124). 

Under  the  microscope  it  is  found  that  the  connective  tissue  in  the  pos- 
terior columns  of  the  cord  has  undergone  hyperplasia  or  overgrowth.  The 
fibrous  sheath  of  the  bloodvessels  is  particularly  affected  and  is  seen  to  be 
thickened  and  to  project  connective-tissue  fibrils  into  nearby  parts.  The 
nerve  fibres  may  have  disappeared  entirely  or  be  represented  by  atrophied 
or  wasted  fibres.  In  some  cases  the  vessels  of  the  pia  mater  are  also 
thickened,  particularly  in  the  part  covering  the  posterior  columns,  and  these 
vessels  may  also  give  off  fibrils  of  connective  tissue  which  add  to  the  con- 
nective-tissue overgrowth  in  the  superficial  part  of  the  cord. 

The  changes  which  are  found  in  the  posterior  nerve  roots  vary  greatly  in 
their  degree.  In  some  instances  they  are  so  slight  that  they  can  be  recog- 
nized only  by  careful  microscopic  examination;  in  other  instances  they 
are  so  well  marked  that  the  naked  eye  can  detect  them.  Under  these  circum- 
stances they  appear  atrophied  and  the  connective-tissue  elements  may  be 
somewhat  increased.  The  root  fibres  in  the  cord  are  more  affected  than 
those  outside  of  the  cord.  The  ganglia  are  also  affected  by  an  overgrowth 
of  connective  tissue,  and  by  an  atrophy  of  their  nerve  cells.     Beyond  the 


960 


DISEASES  OF   THE  NERVOUS  SYSTEM 


Fig.  124 


ganglia  pathological  changes  in  the  mixed  nerve  are  rarely  seen  as  a  con- 
tinuation of  the  process  found  in  the  nerve  roots,  but  it  is  a  well-recog- 
nized fact  that  marked  primary  changes  are  to  be  found  in  the  peripheral 
nerves,  and  especially  in  the  cutaneous  branches.  These  changes  consist  in 
anatrophy  of  the  myelin  sheath  followed  by  degeneration  and  segmentation 
of  the  axis  cylinder,  and  they  occur  at  the  distal  extremity  of  the  nerve  in 

greater  degree  than  higher  up.  The  main 
nerve  trunks  are  rarely  affected.  It  is 
largely  because  of  these  neural  lesions  that 
sensation  in  the  skin  and  in  the  joints  and 
the  muscular  sense  are  lost. 

In  certain  cases  the  changes  of  locomotor 
ataxia  may  be  well  marked  in  the  cord  and 
slight  in  the  nerve  roots,  and  in  others  the 
nerves  are  chiefly  involved.  It  is  important 
that  this  fact  be  remembered  because  it 
serves  to  fix  in  the  mind  of  the  student  the 
fact  that  locomotor  ataxia  is  not  solely  a 
disease  of  the  posterior  columns  of  the  cord. 
While  locomotor  ataxia  chiefly  affects  the 
spinal  cord  and  its  nerve  roots,  it  also  at- 
tacks quite  frequently  the  cranial  nerves, 
and  of  these  the  optic  nerve  suffers  most 
severely  and  most  frequently.  Its  nerve 
fibres  atrophy  and  its  connective  tissue 
undergoes  proliferation. 

By  no  means  rarely  marked  degenerative 
changes  are  found  in  the  joints.  The  artic- 
ulating cartilages  are  eroded,  the  joint  may 
become  filled  with  fluid,  and  for  these  rea- 
sons dislocations  may  occur.  Trophic 
changes  also  occur  elsewhere.  (See  Symp- 
toms.) 

Symptoms. — In  a  case  of  locomotor  ataxia 
which  is  typical  in  its  course  the  following 
symptoms  are  present,  and  if  they  are  well 
developed  it  is  not  difficult  to  make  a  diag- 
nosis : 

The  patient  often  states  that  his  feet  feel  "  muffled,"  that  is,  as  if  he  had  on 
several  pairs  of  thick  socks.  In  other  cases  he  notices  that  on  arising  at 
night  he  has  difficulty  in  getting  a  proper  "purchase"  with  his  feet  on  the 
floor,  or  the  floor  may  feel  as  if  its  plane  is  at  a  different  angle  from  that  pic- 
tured in  his  mind.  These  awkward  sensations  are  due  to  the  interference  with 
the  sensory  nerve  fibres,  that  is,  with  conduction  of  sensation  to  the  spinal 
cord.  He  also  has  difficulty  in  walking  in  the  dark,  not  only  because  his 
tactile  sense  is  disturbed,  but  because  his  muscle  sense  is  also  impaired,  with 
the  result  that  he  is  in  doubt  as  to  the  position  of  his  limbs  and  as  to  the 
relative  tonicity  of  opposing  muscles.     This  loss  of  muscle  sense  depends 


Sclerosis  of  the  lateral  and  (in  the  ante- 
rior cervical  region)  pyramidal  tracts,  with 
slight  degeneration  of  the  anterior  coruna. 
A,  cervical ;  B,  dorsal;  C,  lumbar  sections. 
(After  Gowers.) 


LOCOMOTOR  ATAXIA  961 

upon  the  fact  that  the  sensory  nerves  supplying  the  joints,  tendons,  and 
fascise  are  impaired  in  function  and  the  tracts  in  the  spinal  cord  which  carry 
these  impulses  which  reflexly  co-ordinate  movement  are  also  involved.  If 
the  impulse  passes  this  area  of  damage  and  reaches  the  cord  it  passes  up 
the  posteromedian  columns  without  decussation,  and  probably  goes  directly 
to  the  cerebellum,  which  presides  over  balance.  These  columns  are  always 
diseased  if  the  ataxia  is  marked,  but  cutaneous  sensibility  is  often  pre- 
served, proving  that  the  muscular  and  cutaneous  sensations  are  carried 
by  different  tracts. 

Closely  related  to  the  disorder  of  muscle  sense  is  inco-ordination,  which 
produces  the  'peculiar  gait.  In  the  ataxic  gait  the  foot  is  raised  awkwardly 
and  then  thrown  down  in  front  of  the  other  foot  with  a  characteristic  uncer- 
tain movement,  the  whole  under  surface  of  the  foot  striking  the  ground  at 
once.  This  uncertainty  of  movement  becomes  still  more  marked  if  the 
surface  over  which  the  patient  has  to  walk  is  uneven,  or  if  a  rug  upon  the 
floor  requires  that  the  feet  shall  be  lifted  slightly  to  clear  it.  In  other  cases 
the  edge  of  the  foot  rests  on  the  floor  instead  of  the  plantar  surface,  and 
in  the  effort  to  correct  this  position  another  clumsy  movement  is  made. 
If  the  light  is  poor  or  if  the  patient  closes  his  eyes,  the  difficulty  in  muscular 
co-ordination  may  be  so  great  that  he  staggers  and  falls.  As  the  involve- 
ment of  the  sensory  pathways  becomes  more  marked,  support  by  means  of 
a  cane,  nearby  objects,  or  another  person,  is  needful  for  locomotion,  and 
finally  all  attempts  at  walking  have  to  be  given  up.  In  cases  in  which  the 
upper  portions  of  the  cord  suffer,  there  is  a  similar  inco-ordination  of  the 
arms,  so  that  the  patient  cannot  carry  food  to  his  mouth  if  the  eyes  are  closed. 
In  other  instances,  however,  even  when  the  legs  are  practically  useless,  the 
arms  entirely  escape.  If  either  the  arms  or  the  legs  are  extended  the  muscles 
do  not  remain  steady,  but  alternately  contract  and  relax,  as  the  patient 
vainly  endeavors  to  maintain  his  balance.  There  is  no  actual  loss  of 
muscle  strength  until  the  disease  has  lasted  so  long  that  the  muscles  waste 
from  disuse. 

The  same  cause  that  produces  the  difficulty  in  gait  also  causes  a  disturb- 
ance of  "station.'"  That  is  to  say,  the  patient  cannot  stand  steadily,  but 
sways  in  the  endeavor  to  keep  his  balance.  If  his  eyes  are  closed  or  if  he  is 
blindfolded  he  sways  so  widely  that  there  is  danger  of  his  falling,  and  he 
may  actually  fall  if  he  cannot  co-ordinate  his  muscles  by  the  use  of  his  eyes, 
which  will  give  him  a  conception  of  the  relative  position  of  surrounding 
objects.  This  instability  is  often  very  marked  when  the  patient  attempts  to 
suddenly  assume  the  erect  posture  after  sitting  in  a  chair  for  some  time. 
As  Romberg  first  called  attention  to  this  loss  of  station,  the  term  "Romberg's 
symptom"  is  applied  to  this  manifestation  of  the  malady. 

Still  another  indication  of  the  disease  in  the  sensory  pathways  in  loco- 
motor ataxia  is  the  diminution  and  final  total  loss  of  the  knee-jerks  when  the 
patellar  tendon  is  tapped.    This  is  called  "WestphaVs  symptom." 

So  far  only  those  disorders  of  motion  which  result  from  the  loss  of  muscle 
sense  have  been  discussed.  There  yet  remain  to  be  considered  the  charac- 
teristic sensory  symptoms  themselves.  These  consist  in  pain  and  loss  of 
sensibility.  Pain  is  a  very  frequent  and  often  a  very  early  symptom,  occur- 
61 


962  DISEASES  OF   THE   NERVOUS  SYSTEM 

ring  in  about  90  per  cent,  of  all  cases,  and  it  may  be  very  severe.  It  occurs 
chiefly  in  the  legs  as  sharp  dartings  called  "lightning  pains."  Unlike  the 
motor  symptoms,  these  pains  are  not  confined  to  the  legs  and  arms,  but  are 
often  present  in  the  body  and  even  in  the  head,  where  other  symptoms  of 
this  disease  are  rare,  except  in  the  eyes.  The  pains  are  often  agonizing  and 
occur  chiefly  at  night.  In  most  instances  they  occur  in  periodic  attacks,  then 
ceasing  for  weeks  or  even  months.  They  may  develop  in  different  parts  of 
the  body  at  each  attack.  They  rarely  have  their  seat  in  large  nerve  trunks, 
but  exist  in  the  more  minute  fibres  of  the  nerves.  When  they  attack  the 
stomach  they  are  called  "gastric  crises,"  a  term  also  applied  to  severe 
attacks  of  vomiting  in  this  disease.  So,  too,  attacks  of  intense  pain  may 
suddenly  develop  in  the  bladder,  "vesical  crises,"  and  in  the  rectum, 
"rectal  crises."    There  may  be  marked  "girdle  sensations"  in  the  trunk. 

The  pains  are  described  as  darting,  rending,  or  burning,  and  the  patient 
may  speak  of  "burning  toes"  as  his  most  troublesome  symptom.  Intense 
hypercesthesia.  of  the  skin  in  the  painful  areas  may  also  be  present.  These 
pains  are  to  some  extent  affected  by  atmospheric  states.  I  have  more  than 
once  known  them  to  be  produced  or  exaggerated  by  constipation,  probably 
because  of  the  absorption  of  intestinal  toxins. 

It  is  important  to  bear  in  mind  the  fact  that  pain  may  be  one  of  the 
earliest  signs  of  this  malady,  and  may  vary  from  tingling  to  an  agony 
without  any  of  the  disorders  of  the  gait  being  as  yet  present.  On  the  other 
hand,  very  severe  ataxia  may  be  present  without  any  pain.  In  addition 
to  these  painful  disorders  various  other  disturbances  of  sensation  also 
develop,  such  as  formication,  tickling,  pricking,  creeping,  sensations  of  heat 
and  cold,  or  hypersesthesia.  When  the  disease  is  well  advanced,  diminution 
of  sensation  in  the  skin  or  even  complete  anaesthesia  may  appear.  The  sense 
of  pain  and  of  touch  may  both  be  impaired.  The  pain  sense  may  be  lost 
and  the  heat  sense  retained,  or,  again,  the  tactile  sense  may  be  interpreted 
by  the  patient  as  pain  or  heat.  A  very  interesting  perversion  of  the  function 
of  sensation  is  the  delay  in  the  transmission  of  the  sensory  impulses,  so  that 
a  very  appreciable  interval  occurs  between  the  moment  at  which  the  foot  is 
pricked  and  the  moment  at  which  the  patient  appreciates  the  fact  that  the 
injury  has  been  sustained.  Obersteiner  has  recorded  a  case  in  which  the 
interval  was  twenty-five  seconds.  So,  too,  the  patient  is  unable  to  readily 
indicate  the  part  touched.  He  may  even  assert  that  it  is  the  left  foot  when 
it  is  really  the  right  one  that  is  irritated.  To  this  symptom  the  term  allo- 
chiria  is  applied.  Ail  these  tests  must  be  made,  of  course,  with  the  patient 
blindfolded.  The  deeper  portions  of  the  body  may  be  as  anaesthetic  as  the 
skin,  and  injury  to  a  testicle,  pleurisy,  and  severe  muscular  inflammation, 
as  after  a  deep  injection  of  mercury,  may  be  painless.  Sexual  power  may 
or  may  not  be  lost. 

The  changes  which  take  place  in  the  eyes  in  locomotor  ataxia  are  so  con- 
stantly met  with  and  are  so  valuable  to  us  from  a  diagnostic  standpoint,  that 
they  are  worth  remembering.  In  about  80  per  cent,  of  the  cases  the  Argyll- 
Robertson  pupil  is  present,  that  is,  the  pupil  reacts  to  accommodation,  but 
not  to  light.  This  state  depends  upon  a  lesion,  somewhere  in  the  path  of 
the  light  reflex,  which  includes  the  optic  nerve  on  the  one  hand  and  the 


LOCOMOTOR  ATAXIA  963 

oculomotor  nerve  and  nucleus  on  the  other,  with  a  connection  between 
these  two  nerves  which  is  not  known.  Some  have  taught  that  Meynert's 
decussation,  between  the  primary  optic  centres  in  which  the  optic  nerve 
ends  and  the  third  nerve  nucleus,  forms  this  connection  and  is  the  seat  of 
lesion  determining  the  Argyll-Robertson  pupil.  Recent  studies  indicate 
that  the  fibres  concerned  pass  from  the  optic  tract  to  the  third  nerve  nucleus 
before  the  former  has  reached  the  primary  optic  centres. 

There  may  be  loss  of  accommodation  in  some  cases.  The  pupils  are 
usually  myotic;  they  may  be  unequal  and  uneven,  especially  during  con- 
traction ;  they  may  also  be  irregular  in  shape. 

The  second  important  ocular  symptoms  are  those  which  depend  upon  the 
nerve  supply  of  the  extrinsic  muscles  of  the  eye.  Diplopia  may  develop  as 
a  fleeting  or  permanent  symptom  due  to  insufficiency  of  one  of  the  ocular 
muscles,  the  external  rectus  muscle  being  the  one  most  commonly  affected, 
although  there  is  diversity  of  opinion  as  to  this  point.  So,  too,  single  or  double 
ptosis  may  develop  and  be  transient  or  permanent.  In  some  cases  all  the 
extraocular  muscles  become  paralyzed  so  that  a  complete  external  ophthal- 
moplegia may  be  present.  The  third  ocular  sign  of  importance  is  atrophy 
of  the  optic  nerve,  which  takes  place  in  about  10  per  cent,  of  all  cases.  It  is 
often  present  before  any  difficulty  of  the  gait  develops,  and  for  this  reason 
the  presence  of  the  disease  may  be  first  recognized  by  the  ophthalmologist 
rather  than  by  the  general  practitioner.  It  is  thought  by  some  writers  that 
this  manifestation  of  locomotor  ataxia  is  more  prone  to  develop  in  the 
instances  in  which  the  arms  are  involved  than  in  those  cases  in  which  the 
lower  portions  of  the  cord  are  affected.  Not  rarely  the  presence  of  optic 
nerve  atrophy  seems  to  be  accompanied  by  an  arrest  of  the  sclerotic  process 
elsewhere.  The  field  of  vision  is  primarily  diminished,  there  may  be  loss  of 
color  vision,  but  sometimes  the  failure  is  marked,  even  from  the  onset,  in  the 
neighborhood  of  the  macula.  The  impairment  of  vision  which  ensues  may 
progress  to  total  blindness  or  become  arrested  and  consist  in  more  or  less 
severe  impairment.  Usually  the  process  is  slow,  but  occasionally  it  is  so 
rapid  that  even  a  few  days  produce  great  changes  in  the  visual  acuity.  As 
is  easily  understood,  when  we  consider  the  nature  of  the  lesions  which  are 
characteristic  of  the  disease  the  loss  of  vision  is  not  always  unilateral. 

When  the  optic  nerve  is  examined  by  the  ophthalmoscope  in  such  cases 
the  disk  is  seen  to  be  pale  and  shrunken,  but  at  times  the  degree  of  blindness 
is  in  excess  of  the  changes  in  the  disk.    Finally,  the  disk  becomes  a  pale  gray. 

Occasionally  deafness  gradually  or  suddenly  developes.  It  may  be  tran- 
sient or  fleeting. 

The  bladder  in  locomotor  ataxia  is  often  greatly  impaired  in  its  functions. 
The  urine  is  often  imperfectly  expelled  and  as  a  result  residual  urine  pro- 
duces cystitis.  More  rarely  retention  of  urine  ensues.  The  sphincter  ani 
is  also  weakened,  and  so  control  of  the  feces  is  diminished. 

There  still  remain  to  be  considered  two  results  of  the  disease  which  are 
of  interest  and  diagnostic  importance.  The  first  of  these  is  the  so-called 
"Charcot  joint,"  to  which  reference  has  already  been  made.  Owing  to  the 
changes  in  the  elbow,  shoulder,  hip,  and  knees  the  landmarks  of  these  parts 
may  be  completely  obliterated,  and  great  swelling  often  is  present.     The 


964 


DISEASES  OF   THE  NERVOUS  SYSTEM 


Fig.  125 


second  of  these  trophic  changes  is  the  so-called  perforating  ulcer  of  the  foot, 
which  may  or  may  not  be  accompanied  by  ulcerations  about  the  toe-nails. 
Diagnosis. — As  already  intimated,  the  most  valuable  diagnostic  symptoms 
and  signs  of  locomotor  ataxia  are  the  loss  of  the  knee-jerk,  the  swaying 
station,  the  Argyll-Robertson  pupil,  the  optic  atrophy,  and  the  lightning 
pains.  No  one  of  these,  however,  enables  us  to  make  a  diagnosis  because 
of    its   presence.      The    disease    must    be    differentiated   from    peripheral 

neuritis  due  to  alcohol,  lead,  and  arsenic,  and 
from  that  due  to  typhoid  fever  and  diph- 
theria. In  these  conditions  there  is  loss  of  knee- 
jerk,  swaying  station,  and  often  severe  pains  or 
anaesthesia  it  may  be,  but  the  Argyll-Robertson 
pupil  is  absent  and  the  history  of  the  patient  as 
to  exposure  to  alcohol,  lead,  or  arsenic  aids  us 
greatly  in  the  differentiation.  To  these  states  the 
term  pseudotabes  has  been  well  applied. 

Locomotor  ataxia  is  separated  from  the  various 
forms  of  paraplegia  by  the  persistence  of  the 
knee-jerk,  which  is  usually  exaggerated,  and  by 
the  actual  loss  of  power  in  paraplegia.  From 
the  spastic  paraplegia  due  to  lateral  sclerosis 
true  locomotor  ataxia  is  separated  by  the  spastic 
state  of  the  muscles  and  the  greatly  increased 
knee-jerk. 

From  general  paralysis  of  the  insane  loco- 
motor ataxia  may  be  difficult  of  separatoin,  for 
in  this  disease  the  Argyll-Robertson  pupil  and 
other  physical  signs  of  locomotor  ataxia  may  be  present.  As  the  case 
advances  the  predominance  of  the  cerebral  symptoms  over  the  spinal  symp- 
toms becomes  marked  and  so  renders  the  diagnosis  possible,  (See  Paretic 
Dementia.) 

The  fact  that  in  rare  cases  of  locomotor  ataxia  severe  pains  are  felt  in 
the  trunk  should  never  be  forgotten,  for  it  has  happened  not  infrequently 
that  they  have  misled  the  physician  into  a  belief  that  caries  of  the  vertebrae 
was  present. 

The  staggering  gait  of  cerebellar  tumor  can  scarcely  be  mistaken  for 
locomotor  ataxia.  If  there  is  doubt  as  to  its  cause  it  can  be  dispelled  by  the 
absence  of  shooting  pains,  by  the  presence  of  headache  and  of  nystagmus. 
Prognosis. — The  prognosis  of  locomotor  ataxia  may  be  best  considered  in 
two  parts.  So  far  as  recovery  is  concerned,  this  is  out  of  the  question.  So 
far  as  rapidity  of  progress  is  concerned,  we  must  always  be  guarded  in 
expressing  an  opinion.  In  the  great  majority  of  cases  the  disease  lasts  for 
years  and  is  characterized  not  only  by  periods  of  rest,  but  of  actual  improve- 
ment of  a  very  marked  character  in  some  cases.  If  there  is  a  syphilitic  his- 
tory the  use  of  the  proper  specific  remedies  may  arrest  the  malady,  but  they 
cannot  cure  the  damage  already  done.  Cases  which  attack  those  young  in 
years  and  progress  rapidly  are  most  unfavorable,  but  even  these  cases  make 
remarkable  "stops"  in  the  advance  of  the  affection. 


Perforating  ulcer  of  the  foot  in  loco- 
motor ataxia.    (Obersteiner.) 


LOCOMOTOR  ATAXIA  965 

Treatment. — There  is  probably  no  grave  disease  of  the  nervous  system  of 
an  organic  nature  which,  in  some  instances  at  least,  yields  such  good  results 
from  treatment  as  does  this  one. 

As  may  be  gathered  from  the  discussion  of  the  pathology  of  locomotor 
ataxia,  it  must  be  evident  that  the  physician  can  only  palliate  the  symptoms 
of  this  disease,  and  that  a  complete  cure  is  practically  impossible.  The  most 
that  we  can  do  is  to  attempt  to  eliminate  from  the  system  the  causes  which 
are  primarily  active  in  the  production  of  the  characteristic  lesions  and  so 
prevent  further  progress  of  the  malady.  What  these  poisons  are  we  do  not 
know,  for,  as  already  pointed  out,  even  in  those  cases  in  which  there  is  a  dis- 
tinct history  of  syphilis,  it  is  probable  that  the  cord  disease  develops  rather 
as  a  parasyphilitic  condition  than  one  depending  directly  upon  syphilis. 
Nevertheless,  in  a  large  proportion  of  cases,  benefit  is  obtained  by  the  pur- 
suance of  a  plan  of  treatment  which  consists  largely  in  the  administration  of 
mercury  and  the  iodide  of  potassium.  If  the  specific  infection  is  of  com- 
paratively recent  date,  the  mercury  should  be  used,  but  in  many  instances 
this  is  not  the  case,  and  the  iodide  of  potassium  is  the  remedy  of  choice. 
The  rule  governing  its  administration,  under  these  circumstances,  is  to  give 
that  quantity  which  the  patient  can  take  without  seriously  impairing  his  diges- 
tive functions  and  general  health.  It  is  a  question  of  the  effect  produced 
rather  than  one  of  grains  of  drug  administered.  Some  patients  can  take 
very  large  doses  without  symptoms  of  iodism;  whereas,  others  are  affected 
even  by  moderate  doses.  The  drug  should  be  given  in  ascending  doses  until 
its  full  physiological  effects  are  manifested,  and  then  the  dose  is  to  be  cut 
down  one-third  or  one-half,  and  continued  for  a  number  of  months.  Very 
often  the  best  results  are  obtained  if  in  addition  inunctions  with  mercurial 
ointment  are  practised  twice  or  thrice  a  week. 

While,  on  the  one  hand,  it  should  be  our  endeavor  to  use  these  two 
specific  remedies  very  freely,  it  must  also  be  remembered  that  the  patient's 
vitality  must  be  kept  at  the  highest  possible  level  by  every  means  in  our 
power.  Poor  health  and  digestive  disturbance  produced  by  the  unwise 
employment  of  mercury  or  iodine  probably  does  the  patient  more  harm 
than  the  drugs  do  him  good.  Often  it  is  advisable  to  give  iodide  of  potas- 
sium for  three  months,  and  then  to  use  mercury  for  three  months.  Starr 
asserts  that  the  use  of  mercury  hastens  the  process  of  optic  nerve  atrophy, 
and  in  those  cases  in  which  this  symptom  is  present  mercurial  treatment 
should  not  be  resorted  to.  In  those  cases  in  which  there  is  no  syphilitic 
history,  or  in  which  the  mercurials  are  badly  borne,  arsenic  may  be  given 
as  a  nerve  tonic.  Nitrate  of  silver  was  at  one  time  thought  to  be  advan- 
tageous, but  there  is  nothing  in  our  knowledge  of  this  drug  or  of  the  disease 
which  makes  its  employment  in  any  way  rational. 

For  the  relief  of  the  pains  in  the  peripheral  nerves,  the  coal-tar  products 
are  our  best  remedies,  acetanilid,  phenacetin,  and  antipyrin  being  commonly 
employed.  In  other  instances  the  salicylates  are  useful.  If  the  pain  is 
excessive,  morphine  must  be  used. 

For  the  twitching  of  the  limbs,  the  bromides,  which  quiet  the  sensory 
portions  of  the  cord,  may  be  employed  in  sufficiently  large  doses  to  pro- 
duce sedation. 


966  DISEASES  OF   THE  NERVOUS  SYSTEM 

A  method  of  treating  these  cases  which  is  of  some  vahie  is  that  introduced 
by  Fraenkel,  of  Berhn.  This  method  is  not  curative  in  the  sense  that  it  is 
supposed  to  influence  the  lesions  in  the  cord,  but  is  employed  with  the 
object  of  training  other  nerve  fibres  than  those  originally  used,  so  that  the 
patient  may  to  some  extent  regain  his  muscle  sense.  This  plan  consists 
in  making  him  take  certain  exercises  which  require  co-ordination.  A 
chalk  line  is  drawn  upon  the  floor  and  he  is  required  to  follow  it  as  closely 
as  possible;  or,  a  series  of  cup-like  depressions  are  made  in  a  plank,  which  is 
placed  across  the  foot  of  the  patient's  bed.  These  depressions  are  num- 
bered from  one  to  ten,  and  he  is  instructed  by  the  nurse  to  raise  his  leg  and 
then  rest  his  heel  in  the  cup  which  she  names.  In  this  way  the  patient  in 
some  instances  is  able  to  speedily  respond  to  the  order,  and  so  is  trained 
to  carry  out  well  co-ordinated  movements.  Still  another  method  consists 
in  supplying  him  with  a  small  double  flight  of  steps  provided  with  railings 
so  that  he  cannot  fall.  The  patient  is  then  required  to  mount  a  few  steps  on 
one  side  and  then  descend  a  few  on  the  other,  using  his  legs  to  lift  himself 
up  on  each  step,  and  not  pulling  himself  up  by  his  hands,  which  rest  upon 
the  rails.  In  other  instances  still,  definite  spaces  are  marked  out  on  the 
floor,  and  he  is  directed  to  take  a  stride  wliich  will  bring  his  heel  on  each 
mark.  It  can  be  readily  seen  that  a  large  number  of  such  exercises  can 
easily  be  devised  if  a  little  ingenuity  is  exercised.  Care  should  be  taken  that 
the  exercises  are  not  continued  so  long  that  the  patient  becomes  in  the 
slightest  degree  exhausted.  For  this  reason  they  should  rarely  be  continued 
more  than  five  minutes  at  a  time,  although  they  may  be  resorted  to  Several 
times  a  day.  Additional  methods  of  treatment  consist  in  the  employment 
of  massage,  which  is  designed  to  maintain  the  nutrition  of  the  limbs  and  to 
keep  in  health  the  bloodvessels  and  lymphatic  system,  thereby  to  a  certain 
extent  compensating  for  the  lack  of  exercise  from  which  the  patient  inevitably 
suffers. 

The  various  forms  of  baths  at  home,  or  at  health  resorts,  may  be  employed 
rather  for  the  mental  effect  which  they  will  exercise  upon  the  patient  than 
with  any  hope  that  they  would  be  in  any  way  curative.  The  great  advantage 
in  resorting  to  the  various  health  resorts  where  baths  can  be  obtained  is  that 
the  patient  goes  away  for  the  purpose  of  getting  well  and  leaves  his  business 
cares  behind  him.  The  great  difficulty  with  cool  baths  is  that  the  patient 
usually  has  not  sufficient  power  of  reaction  to  stand  them,  and  tepid  and 
hot  baths  often  seem  to  exercise  an  enervating  effect.  Where  baths  can  be 
used  with  the  object  of  aiding  in  the  absorption  of  mercury  and  the  iodides, 
and  where  they  do  not  produce  depression,  they  are  valuable. 

So  far  as  exercise  is  concerned,  this  should  be  governed  entirely  by  the 
strength  of  the  patient.  Under  no  circumstances  whatever  should  he  be 
permitted  to  become  exhausted.  Not  infrequently  severe  attacks  of  pains  in 
the  limbs  are  precipitated  by  exercise  which  is  sufficiently  severe  or  pro- 
longed to  diminish  the  nervous  vitality  of  the  patient  or  to  tire  the  nerves 
themselves. 

Electricity  may  be  used  in  the  form  of  the  galvanic  current,  the  positive 
pole  of  the  galvanic  battery  being  placed  at  the  nape  of  the  neck  and  the 
negative  pole  at  the  sacrum  and  at  the  soles  of  the  feet.    The  electrodes 


FRIEDREICH'S  ATAXIA  967 

should  be  large  so  that  the  current  will  be  well  diffused.  As  a  matter  of  fact 
the  condition  of  the  spinal  cord  and  the  nerve  trunks  is  such  that  little  real 
benefit  can  be  expected  from  this  plan  of  treatment  except  for  its  sedative 
influence. 

Some  years  ago  a  method  of  treating  locomotor  ataxia  by  suspension  was 
introduced.  A  harness  was  attached  to  the  patient's  head  and  shoulders, 
and  by  this  means  he  was  gently  swung  free  from  the  chair  in  which  he  was 
sitting.  Under  these  circumstances,  the  weight  of  the  lower  portion  of  his 
body  produced  some  extension  of  the  spine,  and  it  was  claimed  that  in  this 
manner  marked  benefits  were  produced.  Hundreds  of  cases  were  treated 
by  this  method,  but  it  is  worthy  of  note  that  it  has  now  gone  out  of  fashion, 
proving  that  it  does  not  possess  the  value  which  at  first  was  credited  to  it. 


FRIEDREICH'S  ATAXIA. 

Definition. — Under  this  name  a  disease  of  the  nervous  system  is  rarely 
met  with  which  is  hereditary  and  which  depends  for  its  clinical  manifesta- 
tions upon  lesions  in  the  posterior  and  lateral  columns  of  the  spinal  cord. 
It  is,  therefore,  an  ataxic  paraplegia  which  is  peculiar  in  that  it  develops  in 
early  life.  Friedreich's  ataxia  is  also  called  "  hereditary  ataxic  paraplegia," 
"  hereditary  ataxia,"  "  Friedreich's  disease,"  and  "  family  ataxia." 

History. — The  malady  was  first  described  by  Friedreich  in  1861  and 
again  in  1876.  In  the  United  States  the  most  noteworthy  study  is  that  of 
Everett  Smith  in  1885.  Schultze  showed  in  1877  that  the  disease  was  due 
to  a  congenital  defect  in  the  cord. 

Etiology. — The  exact  cause  is  unknown.  Occasionally  there  is  a  distinct 
family  history  of  the  disease,  but  often  no  more  than  one  child  in  a  family 
is  affected.  Sometimes  the  symptoms  develop  after  one  of  the  acute  infec- 
tious diseases  of  childhood,  and  it  is  then  supposed  to  be  due  to  development 
of  the  evidences  of  imperfect  growth  or  to  damage  to  poorly  vitalized  cells 
which  have  never  become  well  developed.  In  some  cases  the  parents  have 
an  alcoholic  history;  in  others  there  is  a  history  of  syphilis.  Neither  of  these 
facts  are,  however,  of  real  etiological  importance.  The  influence  of  age  is 
uncertain.  Rarely  the  malady  manifests  itself  in  infancy;  more  commonly 
it  develops  about  the  sixth  or  eighth  year;  if  not  at  this  period,  then  at 
puberty,  and  if  not  at  puberty,  then  at  about  twenty-one  years  of  age.  The 
two  sexes  suffer  about  equally.  It  has  been  shown  that  defective  develop- 
ment of  the  cerebellum  may  be  a  part  of  the  pathological  findings  in  this 
disease.  Marie,  however,  believes  that  spinal  cord  atrophy  in  these  areas, 
when  due  to  cerebellar  disease,  is  a  separate  malady,  and  the  symptoms  due 
to  agenesis  of  the  cerebellum  are  suflBciently  distinctive  to  constitute  a  sepa- 
rate type  of  hereditary  ataxia. 

Pathology  and  Morbid  Anatomy. — As  already  stated,  the  lesions  of  Fried- 
reich's ataxia  are  chiefly  found  in  the  posterior  and  lateral  tracts  of  the 
spinal  cord,  and  the  disease  may  therefore  be  considered  as  a  combination 
of  two  maladies  so  far  as  the  lesions  and  symptoms  are  concerned. 

When  the  spinal  cord  is  removed  from  such  a  case  at  autopsy  it  is  usually 


968  DISEASES  OF   THE  NERVOUS  SYSTEM 

seen  to  be  smaller  than  normal,  and  the  pia  mater  is  commonly  thickened, 
particularly  over  its  posterior  surface. 

If  the  cord  is  examined  under  the  microscope  with  suitable  staining  (Fig. 
126),  it  is  found  that  the  posterior  dorsal  columns,  particularly  those  of  Goll, 
the  lateral  pyramidal  tracts,  and  the  direct  cerebellar  tracts  all  show  degen- 
erative changes.  These  changes  are  not  chiefly  limited  to  one  portion  of  the 
cord,  as  they  are  in  most  cases  of  locomotor  ataxia,  but  extend  up  into  the 
cervical  region  as  well  as  in  the  lumbar  region.  The  lesions  are  not  only 
posterior  and  lateral,  but  anterior  as  well,  for  the  direct  pyramidal  tract 
on  either  side  of  the  anterior  median  fissure  is  affected.  There  is  also 
atrophy  of  the  cells  in  the  anterior  and  posterior  horns  of  the  gray  matter. 
The  anterior  and  posterior  nerve  roots  are  also  atrophied.  The  cells  in  the 
column  of  Clarke  are  markedly  degenerated,  and  round-cell  infiltration  is 
present  about  the  central  canal  of  the  cord.     In  this  disease,  as  in  other 

Fig.  126 


The  lesion  of  Friedreich's  hereditary  ataxia.    Maldevelopment  and  sclerosis  of  the  lateral  and 
posterior  columns.    (Schultze.) 

maladies,  the  loss  of  nervous  tissue  is  followed  by  overgrowth  of  tltie  neuroglia 
in  the  affected  parts. 

Symptoms. — As  Friedreich's  ataxia  consists,  pathologically,  in  lesions  in 
the  posterior  and  lateral  columns  of  the  cord,  it  necessarily  follows  that  the 
symptoms  are  closely  allied  to  locomotor  ataxia  and  lateral  sclerosis.  The 
onset  of  the  disease  is  characterized  by  gradual  loss  of  co-ordination,  affecting 
the  legs  before  it  affects  the  arms,  which  causes  unsteadiness  in  station,  so 
that  the  feet,  when  the  patient  is  standing,  are  placed  far  apart  to  maintain 
the  balance  of  the  body.  In  some  instances  the  first  symptom  is  that  the 
child  falls  over  objects  which  hitherto  have  not  been  obstacles  in  its  path. 
When  the  child  walks  its  gait  is  tottering,  and  if  it  closes  its  eyes  the  lack  of 
co-ordination  and  consequent  instability  is  so  great  that  it  may  fall.  The 
muscles  of  the  legs  are  often  strongly  contracted  in  an  endeavor  to  maintain 
the  upright  posture,  and  this  condition  of  muscular  rigidity  is  increased  by 


FRIEDREICH'S  ATAXIA  969 

the  disease  in  the  lateral  tracts.  The  child  if  stripped  and  left  standing  is 
seen  to  be  continually  writhing  in  an  endeavor  to  adjust  opposing  muscles 
in  order  to  maintain  its  equilibrium.  The  knee-jerks  are  lost,  but  cases  are 
occasionally  met  with  in  which  the  reflexes  are  exaggerated.  These  cases 
closely  approximate  the  group  called  hereditary  cerebellar  ataxia.  (See 
below.) 

Loss  of  power  is  not  as  early  a  symptom  as  is  inco-ordination.  It  affects 
the  legs  far  more  severely  than  the  arms.  The  extensors  suffer  less  than 
the  flexors,  and  this  may  place  the  feet  in  a  posture  like  that  of  tahpes 
equinus  or  varus.  This  deformity  may  also  be  caused  not  only  by  one 
group  of  muscles  overcoming  others  by  reason  of  their  loss  of  power,  but  by 
the  fact  that  if  the  lesions  in  the  lateral  columns  of  the  cord  predominate, 
a  spastic  paraplegia  develops  which  may  result  in  contractures  as  in  ordinary 
ataxic  paraplegia.  In  those  instances  in  which  the  muscles  of  the  trunk 
become  affected  curvature  of  the  spine  may  develop. 

The  mind  is  not  affected  by  the  disease,  but  nevertheless  the  patient 
rarely  develops  mentally  as  does  the  normal  child. 

When  the  disease  is  well  advanced,  the  movements  of  the  lower  and  upper 
limbs  become  not  only  irregular  from  inco-ordination,  but  jerking  in  charac- 
ter, and  this  jerking  movement  may  extend  to  the  head  and  be  accompanied 
by  tremor.  Speech  hecom.es  impaired,  the  words  are  blurred  because  of  imper- 
fect articulation,  and  the  utterance  may  be  sudden  or  explosive.  The  dis- 
order of  speech  is  a  late  symptom  of  the  malady,  and  may  not  appear  for 
some  years  after  the  ataxic  manifestations  appear.  When  the  eyes  are 
moved  laterally  or  upward  nystagmus  may  be  present,  and  it  is  peculiar 
in  that  it  is  absent  when  the  eyeballs  are  at  rest.  The  extraocular  muscles 
are  rarely  paralyzed,  and  the  optic  nerves  always  escape.  In  these  respects, 
therefore,  the  disease  differs  very  distinctly  from  locomotor  ataxia,  in  which 
malady  these  parts  are  commonly  involved.  Occasionally,  cases  are  met 
with  in  which  the  pupillary  reflex  is  lost.  In  these  cases,  however,  syphilis 
is  the  cause,  and  the  case  is  probably  one  of  tabes  with  Argyll-Robertson 
pupils. 

The  disease  is  usually  characterized  by  an  absence  of  all  disturbances 
of  sensation  save  that  cramp-like  contractions  of  the  muscles  in  the  early 
stages  may  cause  the  patient  some  sii-fjering.  In  rare  instances  severe  darting 
pains  have  been  met  with,  or  the  patient  has  experienced  numbness  in  the 
limbs.     The  symptoms  of  ataxia  are  usually  made  worse  by  prolonged  rest. 

Diagnosis. — The  development  of  the  characteristic  symptoms  just  enu- 
merated during  the  period  of  childhood  renders  the  diagnosis  easy,  for  the 
maladies  which  resemble  Friedreich's  ataxia  are  all  of  them  affections  of 
adult  life,  save  multiple  neuritis,  which  may  cause,  of  course,  pseudotabes 
and  a  disturbance  of  station  and  gait.  From  Marie's  cerebellar  hereditary 
ataxia  Friedreich's  ataxia  can  be  separated  by  a  study  of  the  s}Tnptoms  of 
that  aifection  described  below. 

It  must  be  recalled,  however,  that  cases  of  Friedreich's  ataxia  develop 
which  present  s}Tnptoms  which  do  not  follow  characteristic  lines.  Thus, 
in  some  cases  great  muscular  atrophy  has  occurred.  Nystagmus  may  not 
appear.    Diplopia  may  be  present. 


970  DISEASES  OF   THE  NERVOUS  SYSTEM 

Prognosis. — The  prognosis  is,  of  course,  hopeless.  The  only  thing  favor- 
able which  can  be  said  is  that  the  disease  often  develops  very  slowly  and 
has  long  periods  of  arrest.  The  child,  if  attacked  early  in  life,  rarely  reaches 
adult  years. 

Treatment. — Treatment,  aside  from  that  devoted  to  the  maintenance  of 
good  nutrition,  is  of  little  avail,  for  obvious  reasons. 

Marie's  Cerebellar  Hereditary  Ataxia. — Under  this  name  a  form  of 
hereditary  ataxia  has  been  described  by  Marie  in  which  he  has  shown  that 
a  congenital  defect  exists  in  the  cerebellum.  The  condition  is  characterized 
by  ataxia,  difficulty  in  speech,  and  nystagmus,  and  in  these  points  resembles 
Friedreich's  ataxia.  It  differs,  however,  in  the  presence  of  defective  pupil- 
lary reaction  and  various  ocular  palsies  with  optic  atrophy  and  exaggeration 
of  the  knee-jerks.  Further,  it  develops  in  the  third  decade  of  life,  whereas 
Friedreich's  ataxia  nearly  always  appears  before  the  fourteenth  year. 

L.  F  Barker  has  recently  put  the  matter  thus:  The  direct  cerebellar 
tracts  of  the  cord  which  are  degenerated  in  Friedreich's  disease  end  in  the 
middle  lobe  of  the  cerebellum,  which  is  defective  in  Marie's  type.  The 
ataxia  of  both  these  diseases  therefore  results  from  lesions  of  different  parts 
of  one  system.  In  Barker's  nomenclature  the  spinal  part  of  the  poste- 
rior spinocerebellar  system  is  affected  in  Friedreich's  ataxia,  while  the 
cerebellar  part  of  it  is  involved  in  Marie's  type.  An  analysis  of  the  symp- 
toms in  all  the  reported  cases  of  Marie's  disease  has  led  H.  T.  Patrick  to 
say  that  increase  of  knee-jerk  is  its  sole  distinguishing  feature  from  Fried- 
reich's ataxia.  Probably  the  most  advanced  view  is  that  the  two  conditions 
are  phases  of  one  disease. 


ACUTE  ANTERIOR  POLIOMYELITIS. 

Definition. — This  disease  is  sometimes  called  infantile  spinal  paralysis, 
acute  infantile  palsy,  and  acute  atrophic  paralysis.  It  is  characterized  by 
sudden  loss  of  power  in  one  or  more  of  the  limbs,  most  commonly  the  lower 
extremities.  As  a  rule,  the  loss  of  power  is  complete,  but  occasionally  it  is 
localized  in  certain  groups  of  muscles.  Immediately  after  the  development 
of  the  paralysis  wasting  of  the  muscles  begins  to  take  place  and  may  be 
extreme.    There  is  no  disturbance  of  sensation. 

Etiology. — Within  recent  years  it  has  become  more  and  more  evident  that 
acute  anterior  poliomyelitis  is  due  to  an  infection.  That  the  disease  at  times 
occurs  in  epidemic  form  was  noted  by  Colmar  more  than  sixty  years  ago. 
Since  his  time  a  large  number  of  such  epidemics  have  been  recorded  in  this 
country  and  Europe.  Caverly  has  recorded  144  cases  in  one  epidemic  near 
Rutland,  Vermont,  and  in  1905  Ham  reported  an  epidemic  of  131  cases  in 
Queensland.  These  epidemics  are  often  associated  with  outbreaks  of 
croupous  pneumonia  and  influenza.  The  organism,  if  it  be  one,  has  not 
been  isolated.  Cases  also  occur  which  seem  to  be  non-infectious.  The 
most  severe  case  I  have  ever  seen  followed  a  mother's  attempt  to  punish 
a  child  for  urinary  incontinence  by  placing  its  naked  back  under  a  hydrant 
in  midwinter.    Within  twenty-four  hours  the  disease  was  present  in  full  vigor. 


ACUTE  ANTERIOR  POLIOMYELITIS 


971 


The  disease  is  distinctly  one  of  early  child  life,  the  greatest  number  of 
cases  developing  in  the  first  three  years  of  life,  it  being  very  rare  indeed 
after  the  tenth  year.  It  is  far  more  apt  to  develop  in  the  summer  than  in 
winter,  and  has  its  greatest  incidence  in  July  and  August.  After  this  season 
it  is  most  frequent  in  September  and  in  June. 

Pathology  and  Morbid  Anatomy. — ^The  essential  lesion  of  this  disease  is  an 
acute  inflammatory  process  in  the  anterior  cornua  of  the  spinal  cord,  with 
associated  hypersemia  of  the  membranes  covering  the  anterior  surface  of 
the  cord.  The  branches  of  the  anterior  spinal  artery  (Fig.  127)  bear  the 
brunt  of  the  attack  and  are  intensely  engorged.  Their  finer  branches  are 
ruptured  so  that  extravasations  of  blood  take  place  into  the  gray  matter. 
As  a  result  of  these  changes  the  typical  picture  of  tissues  suffering  from  an 


Fig.  127 


ant, 


a.  spin,  post 


a.  spin  post. 


Scheme  to  show  the  course  and  distribution  of  the  terminal  branches  of  the  arterial  plexus  of  the  pia 
mater:  o.  spin,  post.,  posterior  spinal  arteries:  a.  spin,  ant,  anterior  spinal  arteries-  a.  siL,  anterior 
median  fissure ;  rec.  ant.,  anterior  root  arteries.    (Van  Gehuchten.) 

acute  inflammatory  process  is  presented,  for  serum,  leukocytes,  and  red 
cells  crowed  the  nervous  protoplasm.  The  ganglion  cells  of  the  gray  matter 
in  the  anterior  horns  undergo  marked  degenerative  changes.  They  undergo 
cloudy  swelling  and  the  nuclei  become  granular,  or  if  the  change  is  still  more 
severe  the  nuclei  disappear  and  the  neurones  lose  their  dendrites  and  become 
vacuolated.  As  a  final  stage  the  cell  undergoes  shrinkage,  becomes  a  small, 
granular  mass,  and  finally  disappears.  The  damaged  areas,  in  old  cases, 
are  occupied  by  connective  tissue  and  are  much  shrunken,  so  that  the  affected 
gray  horn  is  much  smaller  than  its  fellow.  The  anterior  nerve  fibres,  which 
have  their  origin  in  this  part  of  the  cord,  also  atrophy.  Associated  with 
these  changes  in  the  anterior  cornua  of  the  cord  there  is  often  some  involve- 
ment of  fibres  in  the  anterolateral  tracts,  because,  it  will  be  recalled,  some 


972  DISEASES  OF   THE  NERVOUS  SYSTEM 

of  the  fibres,  or  axones,  which  leave  the  anterior  horns  pass  upward  and 
downward  in  these  columns  to  enter  the  anterior  horns  above  and  below 
to  associate  their  function,  and  it  is  also  due  to  the  inflammatory  process 
extending  into  the  white  columns. 

The  degree  of  the  inflammatory  process  in  the  gray  matter  varies  very 
greatly  in  different  cases  and  may  involve  the  cells  of  but  a  few  muscles. 
It  may  affect  chiefly  that  part  of  the  gray  matter  which  is  most  anterior  or 
that  nearer  the  commissure.  In  rare  cases  it  would  seem  probable  that  no 
true  inflammatory  process  develops  in  the  cord,  but  that  simple  degenerative 
chano;es  occur  in  the  neurones  in  the  anterior  horns. 

Ssnnptoms. — The  symptoms  of  acute  poliomyelitis  usually  take  the  fol- 
lowing course:  A  child  in  good  health  has  a  restless  and  feverish  night,  and 
seems  on  the  next  day  to  be  somewhat  out-of-sorts.  In  the  course  of  twenty- 
four  or  forty-eight  hours  it  not  infrequently  happens  that  the  parents  con- 
sider the  child  recovered  from  its  acute  illness,  and  it  may  be  some  days  or 
weeks  before  the  mother  notices  that  one  or  both  of  the  lower  limbs  are 
lacking  in  power.  Not  rarely  it  is  found,  as  the  child  sits  in  its  mother's  lap, 
that  one  leg  moves  while  the  other  hangs  like  a  flail,  or  the  mother  notices 
that  the  child  is  unable  to  push  its  leg  into  its  clothing  as  efficiently  as  it 
could  do  before  it  was  taken  ill.  These  may  be  considered  as  the  s}Tiiptoms 
of  a  comparatively  moderate  case. 

In  instances  in  which  the  onset  and  course  of  the  malady  is  more 
severe,  we  find  that  fever  is  quite  marked,  often  rising  as  high  as  102.5°,  and 
continuing  at  this  point  for  several  days.  Occasionally,  at  onset,  it  may 
reach  as  high  as  105°,  and  with  this  febrile  movement  there  may  be  headache, 
loss  of  appetite,  and  vomiting.  Sometimes  diarrhoea  occurs.  In  these 
instances  the  manifestation  of  loss  of  power  is  usually  so  marked  that  its 
presence  is  recognized  within  a  few  hours  of  its  onset.  Even  in  these  cases, 
however,  it  not  infrequently  happens  that  the  child  is  supposed  to  have 
suffered  from  an  attack  of  acute  gastric  catarrh  or  indigestion  until  its 
inability  to  make  certain  movements  calls  attention  to  the  palsy. 

There  is  still  a  third  type  of  cases  in  which  convulsions  appear  at  the  time 
of  onset.  These  convulsions  may  be  cerebral  or  epileptiform  in  character, 
may  be  followed  by  deep  coma  lasting  for  many  hours,  and  the  symp- 
toms may  resemble  an  attack  of  cerebrospinal  meningitis.  Occasionally 
pain  is  a  symptom  of  some  importance,  if,  as  already  pointed  out,  the 
lesions  in  the  anterior  horns  extend  sufficiently  backward  to  involve  some 
of  the  sensory  fibres  beyond  the  commissures.  These  pains  are  usually  felt 
about  the  joints.  In  some  cases  they  come  on  not  as  a  s}Tiiptom  of  onset, 
but  as  a  sequel,  and  seem  to  be  due  to  an  associated  neuritis.  The  degree 
of  the  paralysis  varies  greatly  in  different  cases.  In  some  instances  only  one 
or  two  muscles  seems  to  be  affected.  In  others,  the  whole  limb  may  be 
paralyzed,  or  both  lower  limbs  and  one  upper  limb  may  manifest  loss  of 
power.  Even  when  the  paralysis  is  quite  widespread,  it  is  rare  for  the  cranial 
nerves  to  be  affected,  and  equally  rare  for  the  sphincter  muscles  to  lose 
power. 

In  some  instances  the  disease  seems  to  be  progressive  in  its  t}^e,  the  full 
degree  of  paralysis  not  developing  at  once,  but  beginning  in  one  part  and 


ACUTE  ANTERIOR  POLIOMYELITIS  973 

then  spreading  to  adjacent  parts.  Rarely  one  attack  speedily  follows  another, 
involving  a  different  set  of  muscles. 

In  very  rare  instances  the  paralysis  may  develop  v^^ithout  any  history  of 
the  symptoms  of  onset  already  described.  Cases  are  on  record  in  which 
the  paralysis  has  been  almost  universal,  but  it  is  a  noteworthy  fact,  in  regard 
to  the  paralysis  of  acute  poliomyelitis,  that  it  is  far  more  widespread  in  its 
early  stages  than  later  on,  this  being  due  to  the  fact  that  as  the  inflammation 
subsides  certain  cells  which  have  not  been  irreparably  damaged  regain  part 
or  all  of  their  functions,  and  so  adequately  supply  the  muscles  under  their 
control,  or  collateral  muscles  supply  the  power  needed.  On  the  other  hand, 
it  is  a  fact  worthy  of  note  that  complete  recovery  of  power  in  all  the  muscles 
affected  practically  never  occurs.  The  result  is,  that  impaired  muscles  may 
exist  without  great  loss  of  power. 

The  period  of  recovery  usually  extends  from  one  to  three  months.  The 
muscles  which  fail  to  recover  soon  lose  their  contractility  to  faradism  and 
then  to  galvanic  electricity.  The  loss  of  faradic  responses  may  be  present 
as  early  as  the  eighth  or  ninth  day,  but  in  other  instances  some  response  is 
maintained,  for  a  number  of  weeks.  At  the  end  of  a  few  weeks  the  reactions  of 
degeneration  are  observed.  As  would  be  expected  from  the  lesions  already 
mentioned  and  described  when  discussing  the  pathology  of  the  affection, 
sensation  is  usually  unimpaired.  Reflex  activity  is,  of  course,  diminished 
or  lost  because  of  the  spinal  lesions  and  the  atrophy  of  the  muscles.  As 
secondary  lesions  to  the  paralysis  we  find  shortening  of  the  muscles  with 
consequent  contractures  and  deformities. 

The  legs  are  affected  more  frequently  than  the  arms  in  the  proportion 
of  3  to  1.  The  muscles  below  the  knee  suffer  more  frequently  than  those 
above  the  knee,  and  the  tibial  and  peroneal  muscles  suffer  more  frequently 
than  those  of  the  calf.  In  the  forearms  the  supinators  usually  escape,  but 
the  deltoids  suffer  more  frequently  than  any  other  muscles  in  the  upper 
extremity. 

Diagnosis. — ^The  acute  poliomyelitis  of  childhood  is  readily  diagnosed. 
Care  must  be  taken  that  the  muscular  pains  when  they  occur  are  not  thought 
to  be  due  to  rheumatism.  None  of  the  other  spinal  lesions  of  childhood  have 
such  a  characteristic  onset.  Cerebral  palsies  are  usually  unilateral  and  spastic. 
Pseudohypertrophic  paralysis  develops  very  gradually.  The  characteristic 
feature  of  the  palsy  in  anterior  poliomyelitis  is  the  placidity. 

Prognosis. — This  is  usually  good  so  far  as  life  is  concerned,  although  if 
the  attack  has  been  severe  vital  resistance  may  be  so  diminished  that  other 
affections  may  readily  cause  the  death  of  the  child.  The  degree  of  ultimate 
paralysis  can  only  be  determined  after  two  or  three  weeks  of  careful  obser- 
vation, when  some  idea  as  to  the  number  of  muscles  which  may  recover  can 
be  obtained,  particularly  if  electricity  is  used  to  determine  the  electrical 
contractility  of  the  affected  muscles. 

Treatment.^In  the  treatment  of  acute  poliomyelitis  little  can  be  done  in 
the  way  of  directly  combating  the  disease.  The  child  should  be  put  at 
absolute  rest  in  a  quiet  and  darkened  room.  Sweet  spirit  of  nitre  and  citrate 
of  potassium  should  be  given  in  small  and  frequent  doses  to  diminish  fever 
and  to  cause  mild  perspiration.    It  has  usually  been  held  that  the  adminis- 


974  DISEASES  OF  THE  NERVOUS  SYSTEM 

tration  of  the  salicylates,  particularly  salicin,  is  of  advantage.  This 
may  be  true  with  children  who  have  a  rheumatic  or  gouty  heredity,  but 
there  is  no  reason  to  suppose  that  they  exercise  any  specific  influence  upon 
the  lesions  in  the  cord.  So,  too,  hot  applications  have  been  recommended 
to  be  applied  to  the  back.  It  is  difficult  to  understand  how  they  can  be  of 
much  value.  Some  mild  counterirritant  over  the  spine,  such  as  a  spice 
plaster,  or  a  pepper  plaster,  may  be  advantageous.  The  whole  object  of  the 
physician  must  be  to  produce  nervous  quiet  and  aid  in  diminishing  the  inflam- 
matory process  in  the  cord  by  avoiding  excitement  of  the  nervous  system. 
After  the  acute  stage  of  onset  is  past,  and  the  paralysis  is  present,  that  is 
to  say,  after  sufficient  time  has  elapsed  for  the  acute  stage  of  the  inflamma- 
tion to  have  passed  by,  or,  in  other  words,  in  three  or  four  weeks  after  onset, 
moderately  large  doses  of  strychnine  may  be  given,  but  care  must  be  taken 
that  the  doses  are  not  so  large  as  to  produce  twitching  or  great  nervous 
irritability.  At  this  time,  too,  the  slowly  interrupted  faradic  current  may  be 
applied  to  the  paralyzed  muscles,  and  particularly  to  those  which  are  semi- 
paralyzed,  in  the  hope  that  in  this  way  their  nutrition  may  be  maintained. 
It  must  not  be  forgotten,  however,  that  the  greatest  care  must  be  exercised 
that  the  muscles  are  not  overfatigued,  since  if  they  are  exhausted  they  will 
more  rapidly  atrophy  than  if  no  electricity  was  employed.  If  electricity  is 
used  before  the  spinal  cord  has  recovered  from  the  acute  stage  of  the  inflam- 
mation, it  will  make  the  condition  worse.  In  many  instances  it  is  advisable 
to  use  electricity  on  one  day  and  careful,  gentle  massage  on  the  next.  The 
electrical  current  should  never  be  employed  in  such  strength  as  to  give  the 
child  pain  or  distress. 

As  general  tonics  for  the  nervous  system  the  hypophosphites,  glycero- 
phosphates, cod-liver  oil,  and  iron  may  be  used. 

Should  any  tendency  to  deformity  take  place,  this  must  be  treated  by  the 
methods  commonly  resorted  to  by  orthopedic  surgeons.  Rapid  recovery 
should  not  be  expected  in  these  cases.  Careful  treatment  for  months  is 
necessary  to  get  the  best  results. 


CHRONIC  ANTERIOR  POLIOMYELITIS. 

Definition. — It  is  evident  from  its  name  that  this  disease  closely  resembles 
acute  anterior  poliomyelitis.  A  very  important  difi^erence  lies  in  the  fact 
that  in  the  acute  form  the  damage  takes  place  suddenly,  and  then  ceases  to 
progress,  some  improvement  occurring  in  most  instances,  whereas  in  the 
chronic  form  the  atrophic  process  is  slow  in  onset  and  progressive  and  so 
the  symptoms  get  worse  rather  than  better.  When  the  symptoms  develop 
during  a  period  of  from  two  weeks  to  a  month  the  term  subacute  is  appHed, 
and  when  they  come  on  even  more  slowly,  so  that  several  months  are  con- 
sumed in  their  advance,  the  term  chronic  is  used.  The  dominant  symptoms 
are  muscular  wasting  with  paralysis.  Chronic  anterior  poliomyelitis  is  some- 
times called  "  chronic  atrophic  spinal  paralysis"  or  "progressive  muscular 
atrophy." 


CHRONIC  ANTERIOR  POLIOMYELITIS  975 

Etiology. — This  is  unknown.  Exposure  to  cold  and  wet  has  been  thought 
to  be  a  cause  in  some  cases. 

Pathology  and  Morbid  Anatomy. — The  lesions  of  chronic  anterior  polio- 
myelitis consist  in  atrophy  of  the  nervous  tissues  of  the  anterior  horns  of 
the  gray  matter  of  the  cord.  Not  only  the  cell  bodies  but  their  axones  and 
dendrites  all  undergo  degenerative  change.  There  is  no  acute  inflammatory 
process  present  as  in  the  acute  form  of  the  disease,  and  no  hemorrhages  into 
the  tissues  about  the  vessels.  The  dominant  change  is  a  simple  atrophy 
or  wasting.  The  anterior  nerve  roots  also  suffer  atrophic  changes,  and  the 
so-called  association  fibres  of  the  cord  and  the  cells  which  give  rise  to  them 
also  atrophy.  As  these  association  fibres  pass  to  the  anterior  lateral  columns 
of  the  cord  the  degenerative  process  extends  to  them  as  well,  and  this,  com- 
bined with  the  wasting  of  the  anterior  nerve  roots,  produces  a  shrinkage  in 
the  size  of  these  columns,  which  is,  however,  not  great  enough  to  be  recog- 
nized by  the  unaided  eye.  The  atrophic  process  extends  down  these  tracts 
and  involves  the  motor  nerve  fibres  all  the  way  to  the  nerve  plates  in  the 
muscles,  which  in  turn  undergo  atrophy,  the  muscular  fibres  losing  their 
strise  and  showing  fatty  globules  inside  the  sarcolemma. 

Symptoms. — The  symptoms  of  this  malady  vary  somewhat  with  the  por- 
tion of  the  spinal  cord  which  is  chiefly  affected.  Most  commonly  the  earliest 
manifestations  of  the  disease  appear  in  the  upper  extremities,  and  this  is 
usually  called  the  "Aran-Duchenne  type  of  the  disease."  It  first  manifests 
itself  in  the  adductor  muscles  of  one  thumb.  From  these  it  extends  to  all 
the  small  muscles  of  the  hand,  which  rapidly  become  wasted.  Flexion  of 
the  fingers  upon  the  hand  is  impossible,  and  as  the  interossei  which  flex  the 
first  phalanges  are  paralyzed,  the  long  flexor  and  extensor  muscles  of 
the  forearms  are  unopposed.  As  a  result  we  find  that  the  long  flexors  flex 
the  second  and  third  phalanges  and  the  long  extensors  extend  the  first 
phalanges,  giving  the  so-called  "claw-hand"  deformity.  This  effect  is 
increased  by  the  prominence  of  the  extensor  tendons,  caused  in  part  by  the 
wasting  of  the  smaller  muscles  of  the  hand.  The  hand  or  the  shoulder  on 
the  opposite  side  soon  suffers.  Finally,  all  the  upper  arm  and  shoulder 
muscles  atrophy,  and  later  those  of  the  upper  thorax  as  well.  Still  later 
the  lower  extremities  become  involved.  Often  portions  of  the  latissimus 
dorsi,  the  trapezius,  the  triceps,  the  pectoralis  major,  or  other  muscles 
escape.  When  the  cervical  muscles  fail  the  head  cannot  be  held  erect,  and 
when  the  costal  muscles  are  atrophied  the  act  of  respiration  may  be  solely 
diaphragmatic.     Finally,  symptoms  of  bulbar  paralysis  may  ensue. 

In  that  type  in  which  the  disease  first  affects  the  lumbosacral  portion  of 
the  cord  the  peroneal  muscles  in  one  leg  undergo  paralysis  and  wasting. 
This  condition  then  develops  in  the  muscles  of  the  other  leg.  A  little  later 
the  anterior  tibial  muscles  are  affected,  first  on  one  side  and  then  on  the 
other.  At  this  time  there  is  "  drop-foot "  and  the  patient  has  to  use  his 
thigh  muscles  to  raise  the  leg  so  that  the  toes  will  not  strike  obstructions 
and  cause  stumbling.  As  the  pathological  process  in  the  cord  advances  the 
adductor  muscles  in  the  thighs  and  the  gluteal  muscles  are  paralyzed. 

In  stifl  another  type,  sometimes  called  "Duchenne's  type  of  ascending 
paralysis,"  the  paralysis  and  wasting  extend  upward  from  the  legs  and 


976  DISEASES  OF   THE  NERVOUS  SYSTEM 

speedily  affect  the  muscles  of  the  trunk,  the  arms,  the  forearms,  and  the 
hands  so  that  an  almost  total  paralysis  ensues  and  death  comes  from  involve- 
ment of  the  centres  in  the  medulla  or  by  reason  of  some  intercurrent  disease 
such  as  pneumonia.  Sensation  is  not  disturbed,  but  in  a  few  cases  a  sense 
of  discomfort  may  be  complained  of  in  the  legs.  The  reaction  of  degener- 
ation develops  quite  early  in  the  affected  parts  and  finally  response  to 
electrical  stimulation  is  completely  lost.  The  muscles  present  fibrillary  con- 
tractions if  irritated,  but  the  bladder  and  rectum  are  not  paralyzed.  The 
paralysis  is  due  to  the  wasting.  The  reflexes  are  diminished  or  lost  in 
the  affected  muscles. 

Diagnosis. — It  is  important  to  remember  that  chronic  muscular  atrophy 
may  arise  from  other  diseases  than  chronic  anterior  poliomyehtis,  such  as 
amyotrophic  lateral  sclerosis,  the  muscular  dystrophies,  peripheral  neuritis, 
and  syringomyelia. 

From  amyotrophic  lateral  sclerosis  (which  see)  it  is  distinguished  by  the 
absence  of  spastic  symptoms  and  lack  of  the  exaggerated  knee-jerk  and  of 
Babinski's  reflex. 

From  muscular  dystrophy  by  the  absence  of  fibrillary  tremor  and  of  the 
reaction  of  degeneration  in  the  latter  condition,  and  by  the  fact' that  the 
spinal  form  is  a  disease  of  adult  life.  From  syringomyelia  this  condition 
is  separated  by  the  absence  of  the  dissociated  anaesthesia  and  of  trophic 
lesions  in  the  skin. 

In  neuritis  the  distribution  of  the  paralysis  is  usually  symmetrical; 
whereas,  in  chronic  poliomyelitis  the  paralyzed  parts  are  irregularly  dis- 
tributed. Unless  the  neuritis  be  purely  motor  in  character  there  are  sensory 
disturbances  and  tenderness  on  pressure  over  the  nerve  trunks  and  in  the 
bellies  of  the  muscles.  Moreover,  in  neuritis  there  is  commonly  a  toxic 
cause  recognizable. 

The  Charcot-Marie-Tooth  type  of  muscular  atrophy  may  be  confused  with 
certain  forms  of  progressive  muscular  atrophy.  The  first  of  these,  however, 
is  a  disease  of  early  life,  and  the  paralysis  in  the  legs  does  not  extend  above 
the  knees  or  above  the  elbows,  as  a  rule.  Further  sensation  is  usually 
disturbed  or  impaired  in  the  Charcot-Marie-Tooth  type  and  preserved  in 
this  chronic  muscular  atrophy. 

Prognosis. — The  prognosis  is  grave.  The  future  of  the  case  can  be  deter- 
mined somewhat  by  the  rapidity  of  the  development  of  the  symptoms,  for 
in  the  rapidly  advancing  cases  the  outlook  is  of  course  worse  than  in  others. 
When  the  symptoms  follow  injury  to  the  spine  the  prognosis  is  better  than  in 
the  idiopathic  cases. 

Treatment. — The  rapid  type  of  cases  should  be  treated  as  we  treat  acute 
poliomyelitis.  The  chronic  forms  should  be  cared  for  in  a  manner  practically 
identical  with  that  of  the  advanced  stages  of  acute  poliomyelitis.  The 
treatment,  therefore,  consists  in  hygienic  surroundings,  nutritious  food,  and 
an  abundance  of  fresh  air  and  sunshine.  Care  should  be  taken  that  the 
paralyzed  muscles  are  not  exhausted  by  too  much  rubbing  or  exercise. 
Strychnine  may  be  given  in  moderate  doses  three  times  a  day  for  several 
weeks  at  a  time.  Fowler's  solution,  in  moderate  dose,  is  also  useful  as  a 
tonic.    Therapeutic  measures,  however,  cannot  promise  much  in  this  disease. 


BULBAR  PARALYSIS  977 


BULBAR  PARALYSIS. 

Bulbar  paralysis  is  a  term  applied  to  a  group  of  symptoms  referable  to 
lesions  of  cranial  nerve  nuclei  in  the  medulla  oblongata  or  "  bulb,"  which 
affect  the  tongue,  lips,  and  larynx  in  peculiar  association,  so  that  the  con- 
dition is  called  "  glosso-labio-laryngeal  paralysis."  The  lesions  may  impli- 
cate the  cranial  nerve  nuclei  in  the  pons  and  crus,  and  the  gray  matter  of 
the  spinal  cord,  but  atrophy  of  the  tongue  and  lips  is  the  main  feature  of  the 
disease  which  is  centred  in  the  medulla. 

Etiology. — The  cause  of  this  disease  is  unknown.  It  occurs  most  fre- 
quently between  the  thirtieth  and  fiftieth  years. 

Pathology  and  Morbid  Anatomy. — The  lesions  of  this  malady  consist  in 
degenerative  changes  in  the  nuclei  of  the  motor  nerves  whicli  supply  the 
tongue,  lips,  larynx,  and  pharynx.  As  the  disease  advances,  additional 
nuclei  of  the  cranial  nerves  become  involved  so  that  the  pneumogastric, 
the  facial,  the  motor  fibres  of  the  trifacial,  and  more  rarely  the  abducens 
and  oculomotor  nerves  are  affected.  Occasionally,  it  occurs  as  part  of 
amyotrophic  lateral  sclerosis.  If  the  reader  has  a  clear  conception  of  the 
pathology  of  chronic  anterior  poliomyelitis  he  will  understand  the  pathology 
of  this  affection  as  well. 

Symptoms. — The  symptoms  of  chronic  bulbar  paralysis  usually  begin 
with  difficidty  in  moving  the  tongue  in  speech  so  that  the  patient  is  unable 
to  use  easily  letters  like  v,  n,  r,  f,  and  /.  The  speech  becomes  nasal, 
swallowing  becomes  difficult,  and  when  the  muscles  of  the  lips  become 
affected  labial  sounds  become  imperfect,  letters  like  b  and  p  being  difficult 
to  pronounce.  When  the  laryngeal  muscles  become  paralyzed  speech  is  lost 
completely.  Chewing  becomes  difficult,  owing  to  the  paralysis  of  the  tongue 
and  lips.  There  is  difficulty  in  swallowing,  and  the  food  not  infrequently 
finds  its  way  into  the  larynx,  from  which  it  may  descend  and  cause  septic 
pneumonia.  Owing  to  the  paralysis  of  the  facial  nerves,  the  expression  of 
the  lower  portion  of  the  face  becomes  altered,  the  lips  sag,  and  saliva  may 
flow  over  the  chin.  Fibrillary  contractions  of  the  affected  muscles  also  occur, 
and  the  tongue  lies  relaxed  and  powerless  in  the  floor  of  the  mouth. 

Diagnosis. — True  bulbar  paralysis  must  be  separated  from  that  still  more 
rare  affection  known  as  myasthenia  gravis.  In  this  condition  the  general 
muscular  system  also  suffers  from  feebleness,  but  degeneration  does  not 
take  place  in  the  affected  muscles,  and  they  do  not  undergo  material  wasting. 
Furthermore,  the  condition  in  myasthenia  gravis  is  often  characterized  by 
periods  of  remission  or  partial  recovery.  Autopsy  in  those  cases  of  myas- 
thenia gravis  which  have  come  to  a  fatal  termination  has  always  failed 
to  reveal  the  lesions  which  have  been  described  as  characteristic  of  true 
bulbar  paralysis. 

Prognosis. — This  form  of  paralysis  is  invariably  fatal. 

Treatment. — The  treatment  of  bulbar  paralysis  consists  in  the  adminis- 
tration of  tonics,  and  in  an  endeavor  to  maintain  the  patient's  general  health 
at  the  best  possible  level.    Do  what  we  will,  the  disease  cannot  be  affected 
by  any  plan  of  treatment  yet  devised. 
62 


978  DISEASES  OF   THE  NERVOUS  SYSTEM 


LATERAL  SCLEROSIS. 

Definition.- — Lateral  sclerosis,  also  called  "  spastic  paraplegia,"  is  a  con- 
dition in  which  the  patient  suffers  from  stiffness  or  spasticity  of  the  mus- 
cles of  the  lower  extremities,  with  loss  of  power  which  ultimately  amounts 
to  distinct  paralysis.  The  condition  is  characterized  by  great  reflex  irri- 
tability.   There  are  no  sensory  disturbances. 

History. — Tiirck  described  sclerosis  of  the  lateral  columns  of  the  cord  in 
1856,  and  Charcot  made  further  contributions  as  to  the  symptoms  in  1865. 
Seguin  described  it  still  further  in  1873  as  "  tetanoid  paraplegia,"  an  excellent 
term,  but  it  remained  for  Erb  in  1875  and  1877  to  make  a  full  exposition  of 
the  disease. 

Etiology. — In  many  cases  the  cause  of  lateral  sclerosis  cannot  be  dis- 
covered. Syphilis  may  be  a  cause,  or,  to  speak  more  correctly,  the  malady 
may  be  a  sequel  of  syphilis.  In  some  instances  injuries  to  the  back  are  fol- 
lowed by  these  symptoms.  In  one  case  in  my  experience  a  horse  reared 
and  fell  backward  on  his  rider,  who  at. once  found  his  legs  paraplegic.  This 
passed  away  in  a  few  moments,  but  after  a.  few  months  lateral  sclerosis 
gradually  developed.  In  another  case  under  my  care  a  man  stood  in  very 
cold  water  washing  sheep,  and  dated  the  beginning  of  his  malady  to  that 
exposure.  In  both  of  these  cases,  however,  it  is  quite  probable  that  a  pachy- 
meningitis or  a  hemorrhage  into  the  cord  or  a  myelitis  was  the  cause  of  the 
symptoms  rather  than  a  true  primary  lateral  sclerosis.  In  other  cases  pro- 
longed marches  have  seemed  to  produce  it.  It  is  a  disease  of  the  third  and 
fourth  decades  of  life.  In  some  instances  the  disease  seems  to  depend  upon 
an  hereditary  defect  in  the  lateral  columns  of  the  cord  (Striimpell's  family 
type  of  lateral  sclerosis). 

Pathology  and  Morbid  Anatomy. — ^The  lesions  of  lateral  sclerosis  are  clear 
and  definite.  As  the  name  of  the  disease  implies,  they  are  situated  in  the 
lateral  or  crossed  pyramidal  tracts  of  the  spinal  cord,  and  they  develop 
chiefly  in  their  lower  portions  in  the  early  stages  of  the  disease.  The  axones 
progressively  atrophy  from  below  upward,  and  this  is  associated  with  dis- 
appearance of  the  myelin  and  an  overgrowth  of  the  connective  tissue. 

When  the  disease  invades  the  cervical  region  the  anteromedian  columns  of 
the  cord  may  be  affected  as  well. 

Symptoms. — In  studying  the  symptoms  of  primary  lateral  sclerosis  it  must 
not  be  forgotten  that  they  may  be  simulated  by  secondary  lateral  sclerosis 
following  lesions  higher  up  in  the  cerebrospinal  system.  Thus,  it  is  a  well- 
known  fact  that  a  large  number  of  lesions  in  the  brain  or  cord  may  result 
in  degenerative  changes  in  these  motor  pathways,  and  so  cause  spastic  para- 
plegia. Those  in  the  brain  are  hemorrhage,  abscess,  tumor,  and  softening, 
which,  affecting  the  motor  cortex  or  the  motor  pathways,  induce  a  descending 
degeneration  in  the  pyramidal  tracts.  In  these  cases  the  symptoms  are 
usually  limited  to  one  side,  but  in  the  cerebral  palsies  of  childhood  the 
lesions  are  often  bilateral.  (See  Infantile  Cerebral  Palsy.)  Any  lesion  in 
the  spinal  cord  which  cuts  off  the  fibres  in  the  lateral  tracts  from  their  trophic 
cells  in  the  brain,  also  results  in  lateral  sclerosis.    Thus,  a  transverse  myelitis, 


LATERAL  SCLEROSIS  979 

disseminated  sclerosis,  hemorrhage  into  the  cord,  and  syringomyelia  may 
so  result.  Lateral  sclerosis  is  not  rarely  a  part  of  the  pathology  of  paresis. 
Lesions  outside  the  cord,  such  as  tumors,  disease  of  the  spinal  column,  or 
thickening  of  the  membranes  may  sometimes  cause  these  symptoms. 

The  symptoms  upon  which  we  base  the  diagnosis  of  lateral  sclerosis  are 
the  peculiar  spastic  contractions  of  the  muscles  of  the  legs,  so  that  they  are  in 
a  state  of  extension  as  soon  as  the  patient  attempts  to  move  them.  The 
attitude  of  the  legs  is  that  of  a  person  with  ankylosis  of  both  knees,  and  the 
foot  is  apt  to  be  extended.  When  the  patient  walks  he  has  difficulty  in  bend- 
ing the  knees  and  the  ankles,  and  still  greater  difficidty  in  raising  the  toes 
as  the  foot  is  brought  forward  for  another  step.  For  this  reason  he  is  prone 
to  trip  over  small  obstructions  and  to  have  bad  falls,  because  his  muscles 
are  so  stiff  that  he  cannot  catch  himself  as  he  loses  his  balance.  The  stress 
and  strain  of  walking  are  therefore  very  great,  and  the  muscles  may  become 
so  fatigued  that  they  ache,  but  this  is  the  only  sensory  symptom.  Crossing 
the  legs  when  sitting  becomes  impossible,  and  if  the  patient  is  recumbent  the 
knees  may  be  approximated  owing  to  the  greater  strength  of  the  adductor 
muscles.  This  adduction  of  the  knees  also  interferes  with  walking.  If  the 
patient's  muscles  are  grasped  they  are  found  to  be  hard  and  tense.  On 
further  physical  examination  it  will  be  found  that  the  reflexes  are  all  increased. 
Ankle  clonus  is  marked,  and  the  Bahinski  reflex  is  soon  manifested.  The 
reactions  of  degeneration  do  not  appear  and  the  muscles  do  not  atrophy 
until  the  disease  has  lasted  several  years,  when  they  may  waste  from  disuse. 

Finally,  when  the  malady  has  continued  for  a  very  great  length  of  time 
the  position  of  the  lower  extremities  in  stiff  extension  may  be  changed  to 
that  of  contracture  so  that  they  are  sharply  flexed  at  the  knees  and  fixed  in 
this  position. 

The  upper  extremities  nearly  always  escape,  but  in  the  rare  instances  in 
which  they  are  involved  the  extensor  muscles  suffer  first  and  suffer  most. 

Diagnosis. — As  already  pointed  out,  the  diagnosis  of  this,  disease  should 
not  be  made  till  the  causes  capable  of  producing  secondary  lateral  sclerosis 
are  excluded.  Occasionally  hysteria  may  produce  symptoms  very  like  it. 
A  typical  picture  of  such  a  case  will  be  found  in  my  book  on  Practical 
Diagnosis.  In  such  an  instance  the  sex  of  the  patient  and  the  other  signs  of 
hysteria  should  be  carefully  considered  before  a  diagnosis  of  lateral  sclerosis 
is  made.  When  spastic  paraplegia  is  combined  with  muscular  atrophy  the 
condition  is  one  of  amyotrophic  lateral  sclerosis  (which  see). 

Prognosis. — This  is  bad  as  to  recovery,  but  its  unfavorable  character  is 
modified  by  the  fact  that  the  progress  is  usually  very  slow.  Often  the  dis- 
ease lasts  twenty-five  years  or  more. 

Treatment. — Unfortunately  the  results  which  may  be  obtained  from  the 
treatment  of  lateral  sclerosis  are  not  brilliant.  The  suggestion  that  nux 
vomica  or  strychnine  be  employed  does  not  seem  to  be  based  on  very  rational 
views  of  the  physiological  action  of  this  drug.  Excitation  of  the  motor  tracts 
of  the  spinal  cord  is  already  present,  and  strychnine  rather  tends  to  increase 
this  condition  and  to  exaggerate  the  spastic  condition  of  the  lower  extremities. 
In  some  instances  full  doses  of  the  extract  of  conium  are  advantageous.  In 
others  large  doses  of  chloral  or  one  of  the  bromides  may  be  employed.    The 


980  DISEASES  OF   THE   NERVOUS  SYSTEM 

gentle  forms  of  massage  may  also  relieve  the  sensation  of  tension  and  aching 
in  the  limbs.  Care  should  be  taken  that  the  patient  does  not  walk  far 
enough  to  exhaust  himself.  In  some  instances  a  hot  pack  will  give  relief, 
particularly  if  it  is  taken  at  bedtime,  although  of  course  it  exercises  no 
curative  influence  upon  the  progress  of  the  disease.    Electricity  is  useless. 

Sjrphilitic  Spastic  Spinal  Paralysis. — Under  the  name  of  syphilitic  spastic 
spinal  paralysis  Erb  has  described  a  form  of  lateral  sclerosis  developing 
within  five  years  of  the  primary  sore,  but  differing  from  ordinary  lateral 
sclerosis  by  the  presence  of  some  lack  of  rectal  and  vesical  control  and  mild 
disorders  of  sensation.  This  so-called  syphilitic  spinal  spastic  paralysis  of 
Erb  is  due  to  a  specific  endarteritis,  which  produces  embolism  or  thrombosis 
of  the  vessels  of  the  spinal  cord  and  a  true  myelomalacia,  although  some 
clinicians  have  considered  it  a  meningomyelitis. 


AMYOTROPHIC  LATERAL  SCLEROSIS. 

Definition. — Amyotrophic  lateral  sclerosis  is  a  progressive  form  of  chronic 
spinal  paralysis  characterized  by  advancing  muscular  atrophy  associated 
with  spastic  paraplegia,  or,  in  other  words,  the  symptoms  of  lateral 
sclerosis  are  present.  Although  the  symptoms  are  largely  spinal,  modern 
research  has  shown  that  the  motor  pathway  is  affected  throughout  in 
advanced  cases,  from  the  beginning  of  its  upper  segment  in  the  motor  cortex 
to  the  endings  of  the  lower  segment  in  the  peripheral  nerves.  The  cardinal 
symptoms  depend,  however,  upon  degeneration  of  the  contiguous  parts  of 
these  segments,  namely,  the  pyramidal  tracts  and  the  anterior  horns  of  the 
gray  matter;  and  the  disease  may  be  regarded  as  a  combination  of  lateral 
sclerosis  with  chronic  poliomyelitis.  Not  rarely  the  disease  invades  the 
medulla,  and  symptoms  of  progressive  bulbar  paralysis  are  added  to  the 
clinical  picture. 

Etiology. — Amyotrophic  lateral  sclerosis  is  usually  met  with  in  persons 
between  thirty  and  fifty  years  of  age.  In  some  instances  there  is  a  history  of 
exposure  to  cold  or  of  violent  exertion.  In  still  others,  it  is  found  that  the 
patient  has  been  an  artisan  employed  in  the  handling  of  such  metallic 
poisons  as  mercury,  lead,  or  arsenic,  or  that  he  has  been  addicted  to  the 
excessive  use  of  alcohol.  In  some  instances,  too,  the  disease  has  apparently 
followed  severe  injuries,  but  in  no  instance  has  it  been  proved  that  there  is 
actual  relationship  between  any  of  these  causes  and  the  development  of  the 
disease.  In  all  probability,  these  factors  only  become  active  in  those  cases 
in  which  there  is  a  defective  development  in  the  central  nervous  system, 
which  renders  its  motor  elements  peculiarly  susceptible  to  damage  or  disease. 

Pathology. — The  pathological  conditions  in  amyotrophic  lateral  sclerosis 
may  be  considered  in  three  parts.  The  first  and  most  important  is  the 
advancing  atrophy  which  involves  the  motor  neurones  in  the  anterior  horns 
of  the  gray  matter  of  the  spinal  cord.  Indeed,  the  condition  is  very  similar 
to  that  which  occurs  in  chronic  anterior  poliomyelitis  or  even  identical  with 
it.  As  a  rule,  the  alterations  take  place  chiefly  in  the  cervical  portions  of  the 
cord,  but  in  some  instances,  particularly  if  the  disease  lasts  a  long  time,  the 


AMYOTROPHIC   LATERAL   SCLEROSIS  981 

anterior  portion  of  the  gray  matter  in  the  kimbar  region  is  also  affected. 
Similar  atrophic  changes  take  place  in  the  motor  nuclei  of  the  cranial  nerves 
in  the  pons  and  medulla.  Next  in  importance  to  these  alterations  in  the 
trophic  portions  of  the  spinal  cord  is  the  atrophy  and  degeneration  of 
the  fibres  in  the  lateral  columns  and  the  anterior  median  columns.  These 
changes  extend  to  the  motor  cells  of  the  brain  and  are  not  limited  to  the 
lateral  columns,  the  cortex  being  involved  secondarily  by  "retrograde" 
degeneration  from  the  cord  and  medulla  upward  through  the  pons,  crura, 
capsule,  and  corona  radiata.  In  other  words,  the  degeneration  does  not 
begin  in  the  motor  cortex,  but  in  the  spinal  cord.  Following  the  wasting  of 
the  nervous  elements  of  the  spinal  cord,  there  is  an  overgrowth  of  connective 
tissue  which  not  only  involves  the  lateral  columns  and  the  anterior  median 
columns,  but  also  the  association  fibres  which  are  closely  connected  with  the 
anterior  horns  of  the  gray  matter. 

Symptoms. — ^The  symptoms  of  amyotrophic  lateral  sclerosis  are  quite 
characteristic,  and  depend  in  their  development  to  some  extent  upon  the 
portion  of  the  nervous  system  which  is  first  affected  by  the  disease.  In  those 
instances  in  which  the  lesion  first  affects  the  cervical  portion  of  the  cord  and 
the  anterior  horns  of  the  gray  matter  the  arms  are  first  affected.  These 
extremities  manifest  some  stiffness  in  the  muscles,  and  their  reflex  excitability 
is  increased.  Almost  simultaneously  with  these  symptoms  there  is  wasting 
of  the  muscles  of  one  or  both  hands,  with  associated  loss  of  power.  From  the 
hand  the  paralysis  extends  to  the  forearms,  or  it  passes  directly  to  the  muscles 
of  the  shoulder  and  affects  those  of  the  forearms  afterward.  Fibrillary  con- 
tractions develop  very  early,  and  may  be  produced  by  tapping  the  muscles  or 
by  exposing  them  to  cold.  The  fingers  are  often  in  semi-flexion,  and  if  the 
physician  endeavors  to  straighten  them,  it  is  found  that  the  muscles  are  rigid 
and  resistant,  even  though  the  patient  has  lost  power  in  them. 

When  the  disease  develops  chiefly  in  the  pyramidal  tracts  of  the  motor 
columns  of  the  cord,  the  evidences  of  spastic  paralysis  are  the  first  things  to 
impress  themselves  upon  the  observer,  and  it  may  be  impossible  in  the  early 
stages  of  the  disease  to  separate  the  malady  from  ordinary  lateral  sclerosis, 
since  the  legs  are  stiff  and  move  with  difficulty,  the  knee-jerks  are  exaggerated, 
and  ankle  clonus  and  the  Babinski  reflex  are  usually  present.  When  the 
patient  walks  the  toe  is  dragged  along  the  ground,  the  whole  leg  is  stiff,  and 
one  foot  is  often  placed  awkwardly  in  front  of  the  other,  through  the  contrac- 
tion of  the  adductor  muscles. 

Whether  the  disease  first  begins  in  the  arms  or  in  the  legs,  it  is  worthy  of 
remembrance  that  it  is  often  very  much  more  marked  upon  one  side  than 
upon  the  other. 

As  the  disease  advances  it  sometimes  happens  that  evidences  of  bulbar 
paralysis  develops,  the  speech  becoming  affected,  as  in  ordinary  bulbar  par- 
alysis. Swallowing  may  also  become  difficult.  Owing  to  paralysis  of  the 
uvula  and  palate,  choking  often  takes  place,  and  fluids  when  taken  into  the 
mouth  escape  through  the  nose.  Indeed,  all  the  symptoms  of  bulbar 
paralysis  may  be  present,  and  inequality  of  the  pupils  may  be  noted.  Tap- 
ping the  affected  muscles  in  any  portion  of  the  body  usually  produces  marked 
contractions  in  the  muscle  tapped  and  in  neighboring  groups  of  muscles. 


982  DISEASES  OF   THE  NERVOUS  SYSTEM 

When  contractures  occur  the  hands  may  become  greatly  deformed,  and  the 
feet  may  be  distorted  into  any  of  the  forms  of  tahpes. 

In  tlie  advanced  forms  of  the  disease  the  muscles  of  the  trunk  and  neck 
become  atrophied,  so  that  it  is  impossible  for  the  patient  to  sit  up,  and  the 
head  falls  to  either  side  or  forward.  The  muscles  develop  the  reactions  of 
degeneration  and  lose  their  electrical  excitability.  There  is  no  loss  of  intelli- 
gence, but  sometimes  in  advanced  cases  a  mild  dementia  appears.  When 
the  bulbar  symptoms  are  marked,  palpitation  of  the  heart  is  often  present. 

Diagnosis. — From  bulbar  paralysis  amyotrophic  lateral  sclerosis  is  sepa- 
rated by  the  fact  that  lateral  sclerosis  presents  marked  spinal  symptoms 
with  paralysis  of  the  upper  extremities  and  spastic  paraplegia  of  the  lower 
extremities.  If  in  a  case  of  supposed  bulbar  paralysis  these  symptoms 
develop  later  it  proves  that  the  bulbar  palsy  has  been  due  to  the  oncoming 
of  amyotrophic  lateral  sclerosis.  If  the  symptoms  are  due  to  the  presence 
of  a  meningitis  in  the  cervical  portion  of  the  cord,  there  is  stiffness  and  loss 
of  power  in  the  arms,  and  there  will  also  be  pain  of  a  severe  character.  So, 
too,  injury  or  pressure  upon  the  spinal  cord  in  the  dorsal  and  lumbar  regions, 
producing  a  spastic  paraplegia,  will  also  produce  sensory  disturbances  and 
involve  the  functions  of  the  bladder  and  rectum. 

From  syringomyelia  amyotrophic  lateral  sclerosis  is  separated  by  the  pres- 
ence in  the  former  of  analgesia  and  the  rapid  trophic  changes  which  take 
place  not  only  in  the  muscles,  but  in  the  bones,  the  skin,  and  its  appendages. 
In  many  instances  it  is  almost  impossible  to  differentiate  between  amyotrophic 
lateral  sclerosis  and  ordinary  lateral  sclerosis,  and  it  is  only  by  the  develop- 
ment of  the  symptoms  which  arise  from  involvement  of  the  gray  matter  of 
the  cervical  portion  of  the  spinal  cord  and  the  medulla  that  the  separation 
can  be  made. 

Prognosis. — ^The  prognosis  in  a  case  of  amyotropliic  lateral  sclerosis  is 
absolutely  unfavorable  so  far  as  recovery  is  concerned.  The  duration  of  life 
depends  upon  the  rapidity  with  which  the  vital  centres  in  the  medulla  become 
involved.  In  some  instances  death  comes  within  two  years  after  the  onset  of 
the  malady,  whereas  in  others  it  lasts  for  a  decade  or  even  longer.  The  pro- 
longed cases  are  usually  those  in  which  the  involvement  of  the  lateral  columns 
seems  to  be  the  first  stage  of  the  disease.  As  a  rule,  death  does  not  occur  as 
the  direct  result  of  the  disease,  but  from  complications  which  are  produced 
by  it;  as,  for  example,  the  inhalation  of  particles  of  food  into  the  respiratory 
passages  because  of  the  bulbar  paralysis.  Rarely  there  is  heart  failure  due 
to  involvement  of  the  cardiac  centres. 

Treatment. — ^There  is  no  form  of  treatment  which  can  be  considered  cura- 
tive. Gentle  massage  and  the  use  of  electricity,with  the  hope  that  the  wast- 
ing of  the  muscles  may  be  diminished,  has  been  tried  by  some  clinicians,  but 
it  is  manifest  that  this  plan  of  treatment  must  be  used  with  great  caution, 
since  if  the  trophic  centres  are  destroyed,  the  muscles  must  necessarily 
undergo  wasting  more  rapidly  if  they  are  exercised  than  if  they  are  not 
used.  If  bulbar  symptoms  are  present  the  patient  should  be  fed  by  means 
of  a  stomach  tube.  The  employment  of  nervous  stimulants,  such  as  strych- 
nine, is  inadvisable,  because  it  exaggerates  the  spastic  condition  of  the 
lower  extremities. 


MYELITIS  983 

MYELITIS. 

Definition. — Myelitis  is  a  term  which  at  one  time  was  loosely  applied  to 
all  inflammatory  processes  in  the  spinal  cord.  Its  application  is  becoming 
limited  as  our  conception  of  the  diseases  in  this  part  of  the  body  becomes  more 
definite,  but  it  is  still  used  to  describe  an  inflammatory  process  in  the  cord, 
which  is  general  or  widely  diffused  or  disseminated.  A  myelitis  may  be  acute, 
subacute,  or  chronic.  If  it  extends  across  a  given  segment  of  the  cord  it  is 
called  a  "transverse  myelitis;"  if  it  is  distributed  in  several  foci  through  the 
cord,  it  is  called  "  disseminated  myelitis,"  and  if  it  extends  upward  or  down- 
ward, it  is  called  an  "  ascending  or  descending  myelitis." 

The  term  "  acute  myelitis  "  is  applied  to  those  cases  of  sudden  onset  taking 
but  a  fortnight  to  develop.  The  term  subacute  is  applied  to  those  which  con- 
sume from  two  to  six  weeks  in  onset,  and  the  term  chronic  to  those  which 
develop  so  slowly  that  a  longer  time  elapses  before  the  disease  is  marked. 

"When  the  gray  matter  of  the  spinal  cord  is  affected,  it  is  called  "  polio- 
myelitis," from  the  Greek  word  nohoci,  meaning  gray. 

When  the  brain  and  cord  are  involved  it  is  called  "  encephalomyelitis," 
and  when  the  gray  matter  about  the  central  canal  in  the  cord  is  affected 
it  is  called  a  "central  myelitis." 

Acute  and  Subacute  Myelitis.  Etiology. — The  chief  cause  of  this  condi- 
tion is  without  doubt  an  intoxication,  due  to  the  action  of  toxins  developed 
during  the  course  of  acute  infectious  diseases.  At  one  time  it  was  thought 
that  exposure,  sexual  excess,  and  severe  toil  were  causes,  but  we  now  know 
that  at  the  most  they  are  but  predisposing  factors  in  that  they  diminish  vital 
resistance.  In  addition  to  the  ordinary  infectious  fevers,  myelitis  may  be 
caused  by  gonorrhoea  and  malaria.  Occasionally  severe  vesical  infection 
produces  acute  myelitis.  Myelitis  has  also  been  said  to  follow  concussion  of 
the  spine  and  other  injuries,  but  they  probably  act  solely  as  predisposing 
agencies. 

Pathology  and  Morbid  Anatomy. — If  we  take  transverse  myelitis  as  a  type 
of  the  various  forms  of  this  disease,  we  will  find  on  opening  the  spinal  canal 
that  the  pia  mater  at  the  level  of  the  lesion  is  hypera^mic  and  reddened.  The 
cord  is  also  reddened  and  somewhat  swollen,  and  its  bloodvessels  engorged 
On  section  of  the  cord  the  lines  of  demarcation  between  the  white  and  gray 
matter  are  to  a  great  degree  obliterated.  The  cord  is  softened  and  its  texture 
may  be  actually  diffluent,  this  very  soft  state  being,  however,  at  least  in  part 
a  postmortem  change.  If  this  part  of  the  cord  is  placed  under  the  micro- 
scope it  is  seen  to  be  filled  with  granular  cells,  the  bloodvessels  are  sur- 
rounded by  extravasated  leukocytes,  and  bacteria  may  be  found.  Small 
extravasations  of  blood  into  the  tissue  of  the  cord  may  be  present  from  rup- 
ture of  the  vessels.  The  nerve  cells  are  found  to  have  undergone  granular 
degeneration,  and  their  axones  and  dendrites  have  also  been  destroyed. 
The  axis  cylinder  of  the  nerve  fibres  is  greatly  swollen  and  has  evidently 
undergone  segmentation.  Fatty  degeneration  of  the  myelin  is  found.  The 
connective-tissue  cells  are  swollen,  and  if  any  time  has  elapsed,  an  over- 
growth of  the  neuroglia  is  present. 


984  DISEASES  OF   THE  NERVOUS  SYSTEM 

For  a  clear  understanding  of  the  cause  of  the  symptoms  met  with  in  acute 
myehtis,  myelomalacia,  and  chronic  myelitis  it  must  be  remembered  that 
the  presence  of  a  lesion  in  the  spinal  cord  in  the  motor  tracts  produces  a 
descending  degeneration  in  that  tract,  because  the  nerve  fibre  is  cut  off  from 
its  nerve  cell  or  neurone.  If  the  lesion  be  in  the  sensory  tracts  the  degenera- 
tion is  ascending.  The  ultimate  symptoms,  therefore,  consist  not  only  in 
those  which  arise  from  the  primary  focus  or  lesion,  but  in  those  which  develop 
as  the  result  of  these  secondary  changes.  These  changes  are  demonstrable 
within  a  few  days  after  the  injury,  and  rapidly  progress  so  that  at  the  end 
of  three  weeks  the  degeneration  of  the  affected  fibres  is  at  its  height.  The 
overgrowth  of  the  connective  tissue  is  not  marked  until  a  later  period.  Thus, 
we  find  that  the  chief  degenerative  change  below  the  lesion  is  in  the  anterior 
and  lateral  pyramidal  tracts,  and  above  the  lesion  in  the  dorsal  columns 
of  GoU  and  Burdach,  in  the  direct  cerebellar  tracts,  and  in  the  columns  of 
Gowers  In  addition  to  these  chief  secondary  changes,  there  is  also,  for  a 
short  distance  below  the  primary  lesion,  descending  degeneration  in  the 
anterior  and  anterolateral  colums,  and  in  certain  small  "fields"  of  the 
dorsal  columns  (oval  field  of  Flechsig,  etc.),  which  contain  the  so-called 
association  fibres. 

The  ascending  degeneration  which  takes  place  after  a  transverse  lesion 
affects  chiefly  GoU's  and  Gowers'  columns,  and  the  higher  the  primary  lesion 
the  greater  the  degree  of  the  degenerative  process.  The  column  of  Burdach, 
on  the  other  hand,  while  markedly  degenerated  near  the  site  of  the  lesion,  is 
less  and  less  affected  higher  up  in  the  cord. 

Symptoms. — The  symptoms  of  myelitis  vary  somewhat  with  the  portion 
of  the  cord  which  is  affected  and  with  the  extent  of  the  pathological  process. 

When  there  is  a  transverse  myelitis  of  the  dorsal  portion  of  the  spinal  cord 
the  symptoms  in  the  stage  of  onset  consist  in  wretchedness  and  moderate  fever. 
There  may  be  pain  in  the  back  and  numbness  and  tingling  in  the  lower 
extremities.  Twitchings  or  cramp-like  contractions  of  the  muscles  in  the  legs 
may  occur,  and,  very  rarely  in  adults,  a  convulsion  may  develop.  Sometimes, 
however,  these  prodromata  are  absent,  and  the  first  symptom  complained  of 
is  loss  of  power  in  the  lower  limbs,  which  speedily  develops  into  a  complete 
paraplegia.  Paraplegia  may  become  complete  in  a  few  minutes  or  a  few 
hours.  In  other  instances  of  the  subacute  type  the  onset  is  so  slow  that 
days  and  even  weeks  may  elapse  before  the  loss  of  power  is  complete. 

The  paraplegia  arising  from  a  transverse  myelitis  in  the  dorsal  region  is 
usually  spastic,  and  the  deep  reflexes  are  increased.  The  legs  are  outstretched, 
as  in  ordinary  paraplegia,  unless  degenerative  or  irritative  lesions  arise  in 
the  lateral  pyramidal  tracts  below  the  site  of  the  transverse  lesion,  when  they 
may  become  flexed  by  the  spastic  state  of  the  muscles  of  the  thighs.  In  other 
instances  these  muscles  suffer  from  twitchings  and  temporary  contractions, 
which  may  be  strong  enough  to  prevent  the  examiner  from  eliciting  any  signs 
of  exaggeration  of  the  deep  reflexes.  There  is  always  paralysis  of  the  bladder 
and  rectum  in  transverse  myelitis,  and  retention  or  incontinence  of  urine  and 
feces  may  be  present.  Partly  because  of  pressure  and  unavoidable  unclean- 
liness,  but  chiefly  because  of  trophic  disorders  and  abnormal  blood  supply, 
bed-sores  are  prone  to  develop  on  the  sacrum  and  buttocks.    The  muscles  in 


MYELITIS  985 

the  legs  do  not  rapidly  atrophy,  because  they  receive  trophic  impulses  from 
the  cells  in  the  anterior  cornua  of  a  lower  level  of  the  cord  than  that  of  the 
lesions.  The  skin  of  the  legs  and  of  the  body  below  the  level  of  the  lesion 
is  anaesthetic  to  all  forms  of  irritation,  and  at  the  upper  margin  of  this 
anaesthetic  area  there  is  a  girdle  sensation,  and,  it  may  be,  a  hand  of 
hyper  (Bsthesia. 

When  the  myelitis  affects  the  lumbar  cord  the  paraplegia  is  not  only  ahso- 
lute  as  to  voluntary  movement,  but  as  to  reflex  action  as  well,  all  reflexes  being 
lost.  A  similar  condition  also  occurs  in  some  cases  when  the  injury  is  at  a 
higher  level,  provided  that  the  cord  is  completely  severed  or  the  injury  so 
severe  that  severance  is  practically  complete. 

If  the  lesion  is  in  the  cervical  cord  the  arms  are  not  only  paralyzed,  but 
undergo  atrophy  and  are  flaccid,  the  legs  suffer  from  a  spastic  paraplegia, 
and  the  arms,  legs,  and  body  are  ancesthetic.  There  may  also  be  dilatation 
or  contraction  of  the  pupils.  If  the  lesion  is  high  up  in  the  cervical  area, 
then  the  paralysis  of  the  arms  may  be  spastic  instead  of  flaccid,  and 
they  do  not  undergo  atrophy.  In  such  a  case  respiration  is  very  diffcidt, 
because  of  the  loss  of  power  in  the  diaphragm  and  in  the  other  respiratory 
muscles. 

Prognosis. — While  it  is  a  fact  that  the  prognosis  in  transverse  myelitis  is 
always  grave,  it  is  also  a  fact  that  partial  recovery  sometimes  takes  place. 
Thus,  Oppenheim  states  that  that  form  following  gonorrhoea  always  gets 
better  under  good  treatment,  and  that  that  form  due  to  the  acute  infectious 
fevers  has  good  chances  for  recovery.  On  the  other  hand  the  outlook  in 
syphilitic  cases  is  not  good,  and  in  septicaemia,  tuberculosis,  or  puerperal 
sepsis  it  is  bad.  Again,  the  prognosis  varies  with  the  severity  of  the  symp- 
toms and  the  lesion,  for  manifestly  it  must  be  worse' in  complete  transverse 
myelitis  than  in  that  form  in  which  the  destruction  of  the  cord  is  not  so  com- 
plete. The  cause  of  death  is  usually  bed-sores,  with  exhaustion  and  septic 
cystitis. 

Treatment. — An  understanding  of  the  lesions  of  this  disease  makes  it  evi- 
dent that  treatment  of  a  curative  nature  is  useless.  Careful  feeding  with 
easily  digested  food,  the  maintenance  of  perfect  cleanliness  in  the  parts  pressed 
upon  in  the  dorsal  position,  and  the  cautious  use  of  the  catheter  should  be 
resorted  to.  Hyoscine  may  be  given  to  stop  the  annoying  twitchings  of  the 
muscles. 

Chronic  Myelitis.  Definition  and  Etiology. — Chronic  myelitis  is,  as  its 
name  implies,  a  chronic  form  of  inflammatory  process  in  the  cord  which 
develops  as  a  result  of  a  large  number  of  causes.  Not  only  may  the  causes 
of  acute  myelitis  set  up  a  process  which  may  become  slow  and  chronic  in  its 
progression,  but  other  factors  may  produce  it,  of  which  the  most  important 
are  impairment  of  its  blood  supply  resulting  from  degenerative  changes  in 
the  bloodvessels  from  atheroma  or  syphilitic  arteritis.  Chronic  myelitis  may 
also  arise  as  a  result  of  pernicious  anaemia.  In  some  cases,  too,  the  primary 
cause  lies  in  a  meningitis  of  the  membrane  surrounding  the  cord,  whether 
this  meningitis  be  due  to  an  infection  or  to  injury  followed  by  infection. 
When  syphilis  is  the  cause,  it  not  rarely  happens  that  the  inflammatory 
process  is  limited  to  one  or  more  parts  of  the  spinal  cord,  so  that  the  symp- 


986  DISEASES  OF  THE  NERVOUS  SYSTEM 

toms  of  spastic  paraplegia  due  to  disease  of  the  lateral  pyramidal  tracts 
develops,  or  in  other  instances  the  symptoms  of  locomotor  ataxia  are  present, 
because  the  posterior  tracts  in  the  cord  are  affected.  Rarely  but  one  side 
of  the  cord  may  be  affected,  producing  a  crossed  paralysis  of  motion  and 
sensation  (Brown-Sequard  syndrome). 

Finally,  the  physician  must  recall  the  fact  that  most  of  the  forms  of  chronic 
disease  of  the  spinal  cord,  such  as  disseminated  sclerosis,  amyotrophic  lateral 
sclerosis,  and  the  various  forms  of  poliomyelitis,  may,  in  their  advanced  stages, 
resemble  what  has  been  called  chronic  myelitis.  Indeed,  it  is  so  rare  to  meet 
with  a  case  of  chronic  myelitis  which  cannot  be  placed  under  one  of  these 
headings  that  many  neurologists  are  inclined  to  deny  the  existence  of  chronic 
myelitis  as  a  separate  malady.     (See  below.) 

Pathology  and  Morbid  Anatomy, — The  changes  in  the  spinal  cord  which 
are  found  in  cases  of  so-called  chronic  myelitis  are  not  so  manifest  as  in  the 
acute  form  when  the  cord  is  studied  by  the  naked  eye.  In  one  class  of  cases 
the  appearance  is  quite  like  that  of  disseminated  sclerosis  in  that  areas  of 
overgrowth  of  connective  tissue  are  found  in  both  the  white  and  gray  matter 
of  the  cord.  This  overgrowth  of  the  neuroglia  is  situated  chiefly  around  the 
bloodvessels,  the  walls  of  which  are  also  thickened  and  their  lumen  nar- 
rowed. When  as  a  result  of  the  degenerative  process  an  axis  cylinder  has 
become  distended  or  swollen,  a  small  cavity  is  formed,  and  if  many  of  these 
are  present  they  may  give  the  section  of  the  cord  a  cribriform  appearance. 
The  pia  mater  is  often  found  adherent  to  the  cord. 

In  the  other  type  of  case  a  microscopic  study  of  the  cord  reveals  changes 
which  are  evidently  the  result  of  the  several  diseases  of  the  cord  already 
named,  and  which  are  really  the  cause  of  the  symptoms  presented  by  the 
patient  rather  than  that  a  true  primary  chronic  myelitis  has  been  present. 
Thus,  it  is  found  that  as  a  result  of  a  lesion  in  the  pyramidal  tracts,  a  descend- 
ing degeneration  of  the  fibres  in  that  tract  takes  place,  or  if  the  lesion  has  been 
in  the  posterior  columns,  an  ascending  degeneration  ensues. 

Symptoms. — When  the  condition  of  chronic  myelitis  follows  acute  myelitis, 
the  symptoms  of  that  state  persist  with  gradually  increasing  severity  until 
death  by  exhaustion  or  some  intercurrent  malady  ensues.  If,  however,  the 
process  is  of  the  slow  or  chronic  type  from  the  time  of  onset,  the  primary 
feeling  of  weariness  and  weakness  on  exertion  passes  gradually  into  a  state  of 
paralysis,  more  or  less  complete.  Owing  to  the  degenerative  changes  in  the 
lateral  tracts,  the  paralysis  is  usually  spastic.  There  is  often  an  exaggeration 
of  the  deep  reflexes,  with  anJde  clonus.  In  other  instances  the  character  of  the 
response  to  reflex  stimulation  is  entirely  dependent  upon  the  portion  of  thecord 
which  is  involved.  The  muscles  may  gradually  waste  and  give  the  reactions 
of  degeneration.  Not  rarely  the  loss  of  power  extends  gradually  to  the  trunk 
and  arms.  Sensory  disturbances  are  common.  There  may  be  patches  of 
ancesthesia  and  paresthesia,  and  occasionally  moderately  severe  pains  may 
be  felt  in  the  nerves  in  the  extremities.  Vasomotor  disorders  in  localized 
areas  of  the  skin  may  be  present,  one  part  being  very  pallid  and  another 
hypereemic.      Bed-sores  finally  develop,  as  in  the  acute  form  of  the  disease. 

Diagnosis. — Chronic  myelitis  as  a  separate  disease  is  so  rare  that  a  diag- 
nosis of  its  presence  should  be  made  only  after  a  most  careful  study  of  a  case. 


MYELOMALACIA  987 

From  disseminated  sclerosis  it  is  separated  by  the  absence  of  evidence  of 
lesions  in  the  brain  and  lower  cephalic  centres,  such  as  nystagmus,  intention 
tremor,  and  scanning  speech.  From  lateral  sclerosis  it  is  separated  by  the 
absence  of  vesical  and  rectal  paralysis  in  that  disease.  Then,  too,  lateral 
sclerosis  is  not  characterized  by  loss  of  sensation.  Paralysis  due  to  polio- 
myelitis is  separated  also  by  the  absence  of  anaesthesia,  and  the  fact  that  the 
paralysis  of  the  muscles  is  not,  as  a  rule,  so  general. 

Prognosis. — Recovery  does  not  occur.  Life  may  be  prolonged  for  years 
if  the  process  is  not  progressive  and  no  intercurrent  disease  attacks  the 
enfeebled  sufferer. 

Treatment. — This  is,  of  course,  concerned  entirely  with  the  maintenance 
of  good  health,  with  the  hope  that  a  terminal  infection  may  not  occur.  If 
there  is  a  clear  history  of  syphilis  the  iodides  and  mercury  may  be  used,  but 
they  are  rarely  of  much  value  in  this  state. 


SENILE  PARAPLEGIA. 

Under  this  unsatisfactory  clinical  title  may  be  described  a  condition 
occasionally  met  with  in  old  persons,  and  probably  depending  upon  impaired 
blood  supply  to  the  cord,  resulting  from  degenerative  changes  in  the  vessels 
which  are  not  severe  enough  to  result  in  myelomalacia. 
•  Symptoms. — The  symptoms  consist  in  a  moderate  degree  of  loss  of  fower 
in  the  lower  limbs  so  that  it  is  difficult  for  the  patient  to  move  about.  The 
legs  may  be  shuffled  along  the  floor  instead  of  lifted  clear  of  it.  When  the 
malady  develops  rapidly  and  is  severe  it  may  be  impossible  for  a  time  to 
separate  it  from  true  myelitis. 

Treatment. — The  treatment  consists  in  rest  in  bed,  massage,  and  hydro- 
therapy. Internally,  the  iodides  and  circulatory  stimulants,  such  as  strych- 
nine and  digitalis,  should  be  used. 


MYELOMALACIA. 

This  term  is  applied  to  a  state  of  the  spinal  cord  in  which  it  undergoes 
softening  because  of  embolism  or  thrombosis  of  its  bloodvessels,  with 
the  result  that  its  blood  supply  is  impaired.  The  degenerative  changes 
consist  in  those  which  we  would  expect  to  find  when  necrosis  of  these  parts 
occurs,  namely,  extravasated  red  and  white  blood  cells,  fat-globules,  and 
broken  axones.  When  the  patient  lives  for  a  considerable  length  of  time 
after  this  accident  to  the  circulation  occurs,  a  microscopic  examination  of 
the  cord  will  reveal  an  overgrowth  of  connective  tissue.  The  essential 
difference  between  this  state  and  one  of  acute  myelitis  is  that  in  this 
condition  the  process  is  necrotic;  whereas,  in  the  latter  it  is  primarily 
inflammatory,  and  diapedesis  of  white  and  red  cells  takes  place  as  a  part 
of  a  vital  process. 


988  DISEASES  OF  THE  NERVOUS  SYSTEM 


SYRINGOMYELIA. 

Definition. — Syringomyelia  is  a  condition  of  the  spinal  cord  characterized 
by  the  formation  of  a  cavity  or  cavities  in  its  substance;  by  loss  of  pain 
sense  and  temperature  sense,  with  preservation  of  tactile  sense ;  by  the  devel- 
opment of  progressive  muscular  atrophy  and  paralysis,  and  by  nutritional 
changes  in  the  skin,  muscles,  bones,  and  joints. 

History. — Although  a  very  rare  disease,  it  was  described  before  many 
other  very  common  maladies,  the  state  of  the  spinal  cord  having  been  first 
noted  in  1546  by  Etienne  and  given  its  name  by  Ollivier  in  1824.  We  are, 
however,  able  to  diagnosticate  the  affection  by  reason  of  researches  of 
Schultze  and  other  later  investigators. 

Etiology, — This  is  unknown.  In  some  cases  it  is  probably  dependent 
upon  a  congenital  defect.  In  other  instances  it  has  been  thought  to  be  due 
to  disease  of  the  spinal  arteries,  and  in  some  cases  Van  Gieson  has  shown 
that  it  has  developed  from  a  perforating  hemorrhage  into  the  cord  itself. 

Pathology  and  Morbid  Anatomy. — When  the  spinal  cord  in  a  case  of  syringo- 
myelia is  examined  macroscopically,  the  membranes  are  found  to  be  normal, 
but  the  surface  of  the  cord  may  be  irregular  and  portions  of  it  protrude,  while 
at  other  places  retraction  of  its  surface  seems  to  be  present.  A  closer  exami- 
nation of  the  areas  of  bulging  may  reveal  fluctuation,  and  from  such  areas, 
if  they  be  punctured,  a  clear  serous  fluid  may  run  quite  freely.  This  cystic, 
state  may  extend  very  considerable  distances  up  and  down  the  cord,  and 
may  extend  so  far  transversely  as  almost  to  cut  the  cord  in  two.  The  cavity 
is  usually  largest  in  the  cervical  and  upper  dorsal  regions  of  the  cord,  but  it 
may  be  confined  to  the  lower  part  of  the  cord.  On  the  other  hand,  as  just 
stated,  it  may  extend  from  the  end  of  the  cord  even  to  the  pons.  The  cavity 
may  have  large  dimensions  as  to  length  and  be  so  wide  as  to  convert 
the  cord  into  a  thin-walled  tube. 

It  is  because  of  these  extraordinary  changes  that  the  Greek  words  syrinx, 
a  tube,  and  myelon,  marrow  of  the  spine,  is  applied  to  it.  So  complete 
may  be  the  excavating  process  that  when  the  cord  is  severed  from  the 
medulla  the  fluid  may  escape  and  the  cord  flatten  out  like  a  ribbon.  In 
some  cases  there  are  several  cavities  superimposed.  On  cross-section  the 
cavity  is  usually  found  to  be  just  back  of  the  central  canal  in  the  gray  com- 
missure and  in  the  posterior  cornua,  or  it  may  be  present  where  the  central 
canal  should  be.  Occasionally  it  affects  the  anterior  horns  or  the  lateral  or 
posterior  white  columns. 

The  wall  of  the  cavity  consists  in  a  well-developed  mass  of  neuroglia 
(gliomatosis),  which  in  its  growth  encroaches  upon  surrounding  tissues  and 
may  cause  definite  symptoms  before  its  centre  becomes  broken  down.  Some 
neurologists,  on  that  account,  prefer  to  call  this  disease,  at  least  in  its 
earliest  stages,  spinal  gliomatosis,  or  gliosis. 

The  loss  of  pain  sense  and  temperature  sense  which  is  so  characteristic 
has  been  ascribed  to  pressure  by  the  neuroglia  mass  upon  the  fibers  conduct- 
ing these  sensations  as  they  cross  in  the  central  gray  matter  on  their  way  to 
the  column  of  Gowers.    This  is  at  least  a  good  working  hypothesis. 


SYRINGOMYELIA  989 

Around  the  margin  of  the  connective-tissue  boundary  just  described  theie 
is  usually  an  abnormal  development  of  bloodvessels  which  are  numerous, 
distorted,  and  larger  than  normal. 

Dilatation  of  the  central  canal  by  serous  fluid  is  called  hydromyelia,  and 
is  ordinarily  associated  with  hydrocephalus. 

Symptoms. — The  symptoms  of  syringomyelia  consist  in  loss  of  fain  sense 
and  of  temperature  sense,  so  that  the  patient  may  be  cut  or  burnt  without 
feeling  pain,  although  his  sense  of  touch  in  the  affected  part  is  still  preserved. 
In  some  cases  the  temperature  sense  may  be  preserved,  or  the  sense  of  heat 
is  lost  and  that  of  cold  preserved,  or  vice  versa.  The  areas  in  which  the  loss 
of  pain  sense  exists  are  not  symmetrical,  but  are  irregularly  distributed 
over  the  body.  The  fact  that  the  lesion  usually  affects  the  cervical  portion 
of  the  cord  explains  why  it  is  that  the  areas  of  analgesia  are  usually  found 
in  the  upper  extremities.  Associated  with  this  impairment  of  pain  sense 
there  develop,  as  the  disease  advances,  nutritional  changes  in  the  bones, 
muscles,  and  skin,  and  a  progressive  paralysis  due  to  the  muscle  changes. 

The  outward  evidences  of  trophic  disturbance  are  usually  first  noticed  in 
connection  with  some  injury  which  fails  to  heal  and,  becoming  infected, 
forces  a  recognition  of  its  presence  upon  the  patient,  not  by  pain,  but  by  his 
observation  with  his  eyes  that  healing  does  not  take  place.  In  some  instances, 
however,  nutritional  changes  occur  without  any  history  of  injury.  Felons 
may  develop.  When  they  are  accompanied  by  severe  necrosis  the  condition 
is  usually  called  "Morvan's  disease."  In  still  other  cases  the  finger-nails 
become  deformed,  or  superficial  gangrene  of  the  skin  develops.  The  sJioulder-, 
elbow-,  and  wrist-joints  become  swollen,  filled  with  fluid,  and  absorption  of 
the  articulating  surfaces  takes  place,  the  condition  in  the  upper  extremities 
in  this  disease  being  practically  identical  with  that  seen  in  the  joints  of  the 
lower  extremities  in  certain  cases  of  locomotor  ataxia. 

The  shafts  of  the  long  bones  often  suffer  fracture,  but  these  fractures 
are  painless  and  only  enforce  attention  because  of  the  incapacity  pro- 
duced. Painless  dislocations  may  be  caused  by  insignificant  traumata. 
Curvature  of  the  spine  may  also  occur,  due  to  muscular  atrophy,  and  per- 
haps to  changes  in  the  vertebrae.  Secondary  contractures  may  take  place 
and  produce  great  deformity  of  the  hands,  which,  added  to  the  progressive 
muscular  atrophy  and  the  paralysis,  impairs  the  use  of  the  upper  extremi- 
ties very  much.  In  addition  to  these  symptoms  several  special  symptoms, 
dependent  upon  the  site  of  the  lesion,  must  be  considered.  Thus,  if  the 
lower  part  of  the  spinal  cord  is  affected  there  may  be  vesical  or  rectal  par- 
alysis; whereas,  if  the  upper  cervical  cord  is  affected  there  may  be  unilateral 
retraction  of  the  eyeball,  narrowing  of  the  palpebral  opening,  and  a  slow 
pupillary  reaction  because  of  involvement  of  the  spinal  centre  of  the  cervical 
sympathetic.  When  anaesthesia  is  found  on  the  face  it  is  ascribed  to  impli- 
cation of  the  spinal  root  of  the  fifth  nerve  in  the  cervical  region. 

Diagnosis. — As  already  stated,  the  loss  of  pain  sense  with  preservation  of 
tactile  sense,  the  trophic  changes,  and  the  muscular  atrophy  all  form  a 
picture  which  reveals  syringomyelia.  Before  all  these  symptoms  develop 
the  presence  of  a  slowly  increasing  muscular  atrophy  may  mislead  the 
physician  into  the  diagnosis  of  chronic  poliomyelitis  or  progressive  muscular 


990  DISEASES  OF   THE  NERVOUS  SYSTEM 

atropHy,  Indeed,  in  its  commonest  type,  syringomyelia  presents  tTie  picture 
of  progressive  muscular  atrophy  when  it  is  advanced,  including  the  "claw- 
hand."  Less  frequently  the  white  columns  of  the  cord  are  pressed  upon 
by  the  central  mass  and  symptoms  of  locomotor  ataxia  or  of  lateral  sclerosis 
are  found.  The  true  condition  is  recognized  by  the  dissociated  anaesthesia 
already  described.  Tumor  in  the  cord  usually  produces  so  much  pressure 
that  the  symptoms  of  paraplegia  are  more  marked  than  in  syringomyelia, 
and  a  tumor  is  usually  associated  with  severe  pain.  The  dactylitis  of 
syringomyelia  bears  a  resemblance  to  leprosy,  which,  however,  does  not 
reveal  the  more  general  signs  of  disease  in  the  cord. 

Prognosis. — The  chance  of  recovery  is  of  course  nil,  but  as  the  disease 
progresses  very  slowly  indeed,  hfe  may  be  prolonged  for  years. 

Treatment.— There  is  no  treatment  for  syringomyelia.  The  affected 
extremities  should  be  carefully  protected  from  injury. 


HEMORRHAGE  INTO  THE  SPINAL  CORD. 

Definition  and  Etiology. — Spontaneous  hemorrhage  into  the  spinal  cord 
is  a  very  rare  accident,  so  rare  that  some  writers  have  denied  its  existence 
except  when  it  has  arisen  from  a  direct  traumatism.  Minute  hemorrhages, 
of  course,  occur  in  severe  forms  of  acute  myelitis.  The  most  common  period 
of  life  for  this  accident  to  occur  is  between  the  twentieth  and  fortieth  years, 
but  it  may  occur  in  infants.  Hemorrhage  due  to  injury  may,  of  course, 
develop  at  any  time.  Gowers  cites  a  case  of  hemorrhage  occurring  appar- 
ently as  the  result  of  repeated  sexual  intercourse.  Occasionally  hemorrhage 
into  the  cord  ensues  in  cases  of  asphyxia,  as  in  coal-gas  poisoning,  and  cases 
have  been  reported  in  which  hsemophilia  produced  this  lesion.  The  clot  is 
usually  found  in  these  cases  chiefly  in  the  gray  matter  of  the  cord.  Some- 
times it  is  single;  in  other  instances  there  are  multiple  clots.  If  the  escape 
of  blood  has  been  copious  the  blood  may  perforate  the  white  matter  and 
find  its  way  to  the  pia. 

When  the  clot  is  of  any  size  and  the  cord  is  examined  shortly  after  the 
accident,  changes  resembling  those  due  to  hemorrhage  into  the  brain  are 
present.  The  cord  is  softened  and  infiltrated  with  small  round  cells  and 
with  red  and  white  corpuscles  which  are  seen  to  be  undergoing  granular 
change.  The  tissues  are  also  stained  by  blood-coloring  matter.  If  the  patient 
lives  for  some  weeks  and  then  at  death  the  cord  is  studied,  there  is  found 
fatty  degeneration  of  the  neighboring  tissues  or  a  cicatrix  of  connective  tis- 
sue which  occupies  the  site  of  the  hemorrhage.  Secondary  descending  and 
ascending  degenerations  may  ensue  as  in  myelitis. 

Symptoms. — The  symptoms  of  hemorrhage  into  the  spinal  cord  vary,  of 
course,  with  the  level  at  which  the  lesion  takes  place.  The  general  symp- 
toms are  fara'plegia  with  loss  of  sensation  in  the  paralyzed  limbs,  and  loss 
of  control  of  the  bladder  and  rectum.  These  symptoms  are  those  of  acute 
myelitis  as  well.  In  addition  quite  severe  pain  may  be  felt  in  the  spine  or 
be  referred  to  the  front  of  the  thorax  or  to  the  epigastric  region,  and  even  to 
the  legs. 


HEMORRHAGE  INTO   THE  SPINAL  MEMBRANES  991 

When  the  hemorrhage  is  in  the  cervical  cord  there  is  paralysis  of  the  arms 
as  well  as  the  legs.  The  reflexes  are  usually  lost  at  first  because  of  shock, 
but  soon  reappear  and  are  usually  exaggerated  unless  the  cervical  or  the 
lumbar  enlargement  of  the  cord  is  affected,  when  they  are  permanently 
g^bsent  in  the  arms  or  in  the  legs.  Spastic  contractions  may  develop  later 
from  descending  changes  in  the  crossed  pyramidal  tracts,  as  in  myelitis. 
The  muscles  may  undergo  degenerative  changes  very  rapidly  because  of 
damage  to  the  cells  in  the  anterior  horns  of  the  gray  matter  at  the  level  of 
the  lesion. 

Not  rarely,  if  the  hemorrhage  has  been  at  all  large,  a  stage  of  secondary 
irritation  and  inflammation  develops  as  a  result  of  the  extravasation  of 
blood,  and  this  may  not  only  greatly  increase  the  gravity  of  the  symptoms, 
but  destroy  life.  On  the  other  hand,  it  not  infrequently  happens  that  the 
hemorrhage  in  the  gray  matter  may  not  only  destroy  this  part  of  the  cord, 
but  by  pressure  abrogate  the  function  of  the  white  matter. 

After  the  acute  process  is  over,  the  paraplegia  is  greatly  decreased  as  the 
pressure  is  decreased,  but  complete  recovery  does  not  ensue  because  the 
cord  is  permanently  damaged,  and  so  atrophy  of  the  muscles,  governed  by 
that  part  of  the  gray  matter  which  has  been  damaged,  ultimately  develops 
as  in  acute  poliomyelitis.  Some  degree  of  spasticity  persists  through  loss 
of  fibres  in  the  pyramidal  tracts,  and  various  sensory  defects  if  the  dorsal 
columns  have  not  completely  recovered. 

Diagnosis. — The  diagnosis  of  hemorrhage  in  the  cord  is  not  to  be  made 
until  the  symptoms  are  so  well  defined  that  there  can  be  little  doubt  as  to 
their  cause.  The  onset  of  the  symptoms  must  be  sudden,  that  is,  almost 
instantaneous.  If  several  hours  are  passed  in  their  development  it  is  prob- 
ably a  case  of  acute  myelitis.  Pain  is  also  an  important  symptom,  for,  if  it 
is  present,  it  points  to  hemorrhage. 

Prognosis. — This  depends  upon  the  severity  of  the  symptoms  and  upon 
the  site  of  the  lesion.  If  it  is  in  the  cervical  or  lumbar  enlargements,  the 
prognosis  is  more  grave  than  if  it  is  in  the  dorsal  cord.  If  bed-sores  speedily 
develop  the  outlook  is  correspondingly  bad  not  only  because  their  presence 
shows  grave  lesions  in  the  cord,  but  also  because  their  existence  is  a  menace 
to  the  patient's  life. 

Treatment. — Absolute  rest  in  bed  is  essential.  An  ice-bag  should  be  kept 
over  the  spine,  and  small  doses  of  aconite  and  the  bromides  used  to  allay 
circulatory  excitement.  The  use  of  ergot  in  such  cases  as  commended  by 
Gowers  does  not  seem  to  be  based  upon  a  correct  conception  of  the  physio- 
logical action  of  this  drug.  Some  time  after  the  hemorrhage  the  iodides 
may  be  used  to  aid  in  clearing  up  the  inflammatory  exudate. 

HEMORRHAGE  INTO  THE  SPINAL  MEMBRANES. 

Definition  and  Etiology. — A  hemorrhage  about  the  spinal  cord  may  be 
outside  the  dura  mater  (extrameningeal  or  extradural),  or  inside  the  dura 
mater  (intrameningeal).  If  it  is  between  the  dura  mater  and  the  arachnoid 
it  is  called  subdural,  and  if  it  is  between  the  arachnoid  and  pia  mater  it  is 
called  subarachnoid. 


992  DISEASES  OF   THE  NERVOUS  SYSTEM 

Rupture  of  a  vessel  in  the  spinal  meninges  occurs  usually  in  adult  life, 
and  more  frequently  in  males  than  females.  Its  most  common  cause  is 
iniury  to  the  spine.  It  has  been  known  to  follow  violent  convulsions  and  as 
a  sequel  to  those  infections  which  result  in  purpura.  In  newborn  infants 
the  blood  found  between  the  spinal  membranes  has  its  origin  in  the  meninges 
of  the  brain,  and  follows  the  cord  downward.  Sometimes,  in  cases  of  very 
severe  inflammation  of  the  spinal  meninges,  small  extravasations  of  blood 

take  place. 

In  extradural  hemorrhage  the  blood  comes  from  the  veins  which  lie  between 
the  dura  and  the  bony  canal.  The  quantity  of  blood  which  is  poured  out 
varies  greatly.  In  some  instances  it  reaches  the  full  length  of  the  cord.  In 
other  instances  but  a  small  area  is  covered  by  a  clot.  The  most  common 
seat  for  the  hemorrhage  is  the  cervical  portion  of  the  cord.  The  cord  may 
or  may  not  be  compressed. 

Subdural  hemorrhage,  that  is,  the  escape  of  blood  between  the  dura  and 
the  arachnoid,  also  varies  greatly  in  quantity.  In  subarachnoid  hemorrhage 
the  blood  comes  from  the  vessels  of  the  pia  mater,  and  the  clot  may  surround 
the  cord  for  a  few  inches  or  extend  throughout  the  whole  subarachnoid 
space.  In  very  rare  instances  it  may  actually  force  its  way  into  the  cerebral 
ventricles. 

In  all  cases  of  hemorrhage  into  the  spinal  membranes,  save  the  extra- 
dural type,  the  cerebrospinal  fluid  is  blood-stained.  This  may  be  a  valu- 
able diagnostic  point,  since  lumbar  puncture  may  reveal  the  presence  of 
blood  in  this  fluid. 

Symptoms. — No  symptoms  may  be  present  unless  the  hemorrhage  is 
extensive  enough  to  cause  compression,  or  unless  a  secondary  meningeal 
inflammation  develops.  When  the  effusion  of  blood  is  considerable  there 
is  sudden  severe  fain  in  the  back,  usually  about  the  level  of  the  hemorrhage, 
which  extends  into  the  loins,  and  it  may  be  to  the  anterior  surface  of  the 
body.  There  may  also  be  some  muscular  spasm  in  the  parts  involved  by 
those  nerves,  the  roots  of  which  are  pressed  upon  after  leaving  the  spinal 
cord.  These  spasms  may  be  severe  enough  to  produce  a  convulsion,  local- 
ized or  general.  Immediately  after  these  symptoms  evidences  of  loss  of 
power  develop  and  the  symptoms  resemble  the  early  stages  of  acute  myelitis, 
or  of  hemorrhage  into  the  cord  itself,  save  that  it  is  rare  for  the  paralysis 
of  either  sensation  or  motion  to  be  as  complete  as  it  is  in  those  conditions. 

If  the  hemorrhage  is  in  the  cervical  region,  the  pain  is  felt  in  the  neck  and 
arms.  There  is  difficulty  of  swallowing  and  of  breathing,  and,  it  may  be, 
dilatation  of  the  pupils.  When  it  is  in  the  dorsal  region  the  pain  is  in  the 
chest  and  abdomen,  and  when  in  the  lumbar  region  it  is  chiefly  felt  in  the  legs. 
Consciousness  is  preserved  unless  it  be  lost  through  shock.  Some  hours  or 
days  after  the  hemorrhage  a  secondary  reaction  with  febrile  movement  may 
develop.    In  fatal  cases  death  usually  comes  on  within  a  few  hours. 

From  a  medicolegal  standpoint  it  is  interesting  to  note  that  at  least 
one  case  of  meningeal  hemorrhage  in  the  spine  very  closely  resembled 
strychnine  poisoning.  If  the  symptoms  are  severe,  death  is  very  likely  to 
occur  within  a  few  hours.  If  the  patient  survives  the  first  few  days,  partial 
recovery  from  the  paralysis  may  occur. 


COMPRESSION  OF   THE  SPINAL  CORD  993 

Prognosis. — The  prognosis  as  to  life  is  worse  when  the  hemorrhage  is 
high  up  in  the  meninges  than  when  it  is  low  down. 

Treatment. — The  treatment  of  this  condition  consists  in  absolute  rest, 
the  employment  of  small  doses  of  the  bromides  and  aconite  as  nervous  and 
circulatory  sedatives,  and  counterirritation  over  the  back  in  the  shape  of 
dry  cups  or  leeches.  The  patient  should  be  made  to  lie  on  his  side  or  on 
his  face  rather  than  on  his  back,  in  order  to  prevent  the  accumulation  of 
extravasated  blood  at  the  posterior  portion  of  the  cord.  Where  the  quantity 
of  blood  which  is  poured  out  is  very  large,  and  the  symptoms  so  severe  that 
death  is  threatened,  it  may  be  advisable  to  call  upon  a  skilful  surgeon  to 
relieve  pressure  by  operation. 


COMPRESSION  OF  THE  SPINAL  CORD. 

Definition  and  Etiology. — Compression  of  the  spinal  cord  occurs  as  the 
result  of  disease  of  the  vertebrae,  of  growths  in  the  vertebrae  or  the  meninges; 
of  growths  occurring  within  the  spinal  canal,  inside  or  outside  of  the  dura 
mater;  of  aneurysm  of  the  aorta,  which,  by  pressure  on  the  vertebrae,  cause 
their  absorption;  as  the  result  of  syphilitic  inflammatory  processes  in  the 
spinal  canal,  or  by  the  development  of  a  pachymeningitis,  which  may  involve 
the  cervical  or  lumbar  portions  of  the  cord,  and  which  is  characterized  by  a 
thickening  of  the  parts  involved.  The  result  of  pressure  exercised  by  any  of 
these  causes  interferes  with  the  nutrition  of  the  spinal  cord  and  with  the 
transmission  of  impulses  along  its  tracts,  and  the  symptoms  which  arise  vary 
in  their  character  and  severity  with  the  degree  of  pressure  and  the  alterations 
caused  by  it. 

Disease  of  the  vertebrco  is  most  commonly  the  result  of  tuberculous  infec- 
tion, particularly  in  children.  As  a  result  of  this  process,  the  bones  become 
softened,  give  way  under  the  pressure  which  is  exerted  upon  them,  and  as 
they  do  so  pressure  upon  the  cord  results.  In  other  instances  a  suppurative 
process  results  in  the  development  of  so  much  pus  that  pressure  is  produced 
by  it,  and  not  uncommonly  a  carious  process  in  the  vertebrae  is  associated 
with  an  inflammation  of  the  dura  mater,  with  consequent  thickening  of  this 
membrane,  so  that  pressure  is  produced.  Again,  the  caseous  masses  which 
are  formed,  or  the  overgrowth  of  connective  tissue  which  takes  place,  may  cause 
pressure.  In  some  instances  the  dura  mater  suffers  from  tuberculous  infec- 
tion, and  tubercles  are  found  upon  its  inner  surface,  and  both  the  arachnoid 
and  pia  mater  may  be  involved.  As  a  result  the  nutrition  of  the  spinal 
cord  at  this  point  is  impaired  through  interference  with  the  circulation  in 
its  bloodvessels  and  probably  also  because  of  the  obstruction  to  the  circu- 
lation of  lymph  as  well.  The  cord,  in  the  majority  of  instances,  is  in- 
volved. If,  however,  the  pressure  is  severe,  there  is  apt  to  be  an  overgrowth 
of  connective  tissue  whereby  a  sclerotic  process  is  developed.  The  axis 
cylinders  become  swollen,  and  fatty  globules  can  be  found  in  the  myelin 
sheaths.  If  the  pressure  is  severe  and  is  long  continued,  the  cord  may  be 
markedly  atrophied  and  the  overgrowth  of  connective  tissue  be  very  great. 
In  some  instances  there  may  be  nothing  left  of  the  cord  but  a  band  of  con- 
63 


994  DISEASES  OF   THE  NERVOUS  SYSTEM 

nective  tissue.     If  the  damage  done  to  the  cord  is  of  a  more  severe  type, 
ascending  and  descending  degenerative  changes  occur. 

The  symptoms  produced  by  these  lesions  consist  in  'pain  in  the 
spine  and  in  the  distribution  of  the  nerves  supplying  the  trunk  and  limbs. 
Not  infrequently  pain  will  be  felt  in  the  abdominal  wall  or  in  the  neighbor- 
hood of  the  sternum  because  of  the  irritation  of  the  nerve  trunks  as  they  make 
their  exit  from  the  spinal  cord,  according  to  the  well-known  law  that  pain  is 
frequently  referred  to  the  peripheral  ends  of  the  nerve  affected.  Any  jarring  of 
the  body  by  a  misstep  or  a  sudden  movement  or  even  a  gentle  blow  upon  the 
spinal  column  may  cause  the  patient  suffering.  The  muscles  of  the  back  are 
usually  fixed,  in  order  to  protect  the  spinal  column  as  much  as  possible. 
This  fixation  is  partly  voluntary  and  partly  involuntary.  In  some  instances 
a  girdle  sensation  is  felt  in  the  nerves  which  make  their  exit  from  the  area 
which  is  diseased. 

When  the  lesions  are  high  in  the  cord  there  may  be  painful  sensations  in 
the  arms,  and  if  the  lateral  tracts  are  compressed  there  is  an  exaggera- 
tion of  the  reflexes,  with  a  tendency  to  spasticity  of  the  muscles.  In  other 
instances  the  patient  may  present  all  the  symptoms  of  transverse  mye- 
litis and  develop  bed-sores.  The  rapidity  with  which  these  symptoms 
develop  in  different  cases  varies  very  much,  depending  entirely  upon  the 
activity  of  the  pathological  process  in  the  spinal  column.  In  some  instances 
years  are  consumed  in  the  development  of  the  advanced  stage  of  the  malady. 
In  others  paralysis  of  the  lower  extremities  may  be  produced  in  a  few 
mouths. 

The  diagnosis  of  these  cases  is  not  difficult  if  the  physician  will  carefully 
examine  the  spine. 

The  prognosis  is,  of  course,  not  very  favorable,  but  it  is  a  noteworthy 
fact  that  in  those  stages  in  which  the  process  in  the  spinal  column  becomes 
arrested  a  very  marked  degree  of  recovery  may  take  place.  On  the  other 
hand,  it  sometimes  happens  that  spinal  disease  in  infancy  results  in  later 
life  in  the  development  of  lateral  sclerosis  or  other  diseases  of  the  spinal 
cord.  Much  depends  in  the  way  of  prognosis  upon  what  the  surgeon  is  able 
to  do  for  the  spinal  disease.  The  nervous  symptoms  are  to  be  considered 
purely  secondary,  and  every  effort  made  to  modify  the  pathological  process 
in  the  spine. 

The  treatment  of  compression  of  the  spinal  cord  due  to  disease  of  the 
vertebra  is  entirely  in  the  hands  of  the  orthopedic  surgeon,  who,  by  means 
of  proper  apparatus,  can  often  do  much  good.  The  medicinal  plan  of 
treatment  consists  in  the  use  of  cod-liver  oil,  iron,  and  arsenic,  the  following 
of  a  perfectly  healthy  mode  of  life,  and  the  use  of  good  food.  Pain  is  to 
be  relieved,  if  necessary,  by  opiates,  and  the  nervous  twitchings  by  sedatives, 
like  bromide  and  chloral.  In  some  cases  hydrotherapeutic  measures  are 
advantageous. 

Malignant  growths  of  the  vertebrae,  such  as  carcinoma  and  sarcoma,  are 
rare.  They  are  usually  rapid  in  their  growth  and  produce  symptoms  of 
spinal  compression  as  soon  as  they  invade  the  spinal  canal.  These 
malignant  growths  soon  penetrate  the  dura,  the  arachnoid,  and  the  pia,  and 
speedily  infiltrate  the  spinal  cord  itself,  although  the  dura  mater  is  usually 


COMPRESSION  OF   THE  SPINAL  CORD  995 

capable  of  protecting  the  spinal  cord  from  direct  infection  when  the  disease  is 
tuberculous. 

When  a  tumor  of  the  spinal  cord  develops  it  is  in  the  great  majority  of 
instances  due  to  sarcoma.  Tumor  of  the  spinal  cord  is,  however,  exceed- 
ingly rare.  Schlesinger  found  only  147  spinal  tumors  in  35,000  autopsies, 
and  Starr  states  that  the  ratio  of  tumors  of  the  spinal  cord  to  tumors  of  the 
brain  is  1  to  13. 

Here,  again,  the  symptoms  consist,  as  a  rule,  in  intense  neuralgic  pain 
of  a  shooting  or  stabbing  character  caused  by  pressure  upon  the  nerves 
as  they  leave  the  spinal  canal.  These  pains  are  more  severe  than  those 
produced  by  any  other  form  of  spinal  disease,  and  they  are  felt  in 
different  portions  of  the  body,  according  to  the  portion  of  the  spinal 
cord  which  is  involved.  If  the  lower  cervical  portion  of  the  cord  is  affected, 
the  pain  may  be  felt  in  one  or  both  hands  and  forearms.  If  the  growth 
is  in  the  upper  cervical  region,  they  are  felt  in  the  shoulder  or  neck;  if  it 
occurs  as  low  as  the  sixth  dorsal  segment  the  pain  is  felt  in  the  chest, 
near  the  nipple;  in  the  tenth  dorsal  segment  it  is  felt  in  the  abdomen  and  groin. 
When  a  tumor  compresses  the  cord  in  its  entire  thickness  degenerations 
ensue,  descending  in  the  lateral  columns,  ascending  in  the  dorsal  and  other 
sensory  columns,  just  as  they  arise  in  cases  of  marked  caries  of  the  vertebrae. 
Under  these  conditions  the  symptoms  are  those  of  a  transverse  myelitis.  The 
level  at  which  the  tumor  is  growing  can  largely  be  determined  by  localizing 
the  symptoms,  and  the  fact  that  tumor  is  present  may  be  pointed  to  by 
the  presence  of  growths  elsewhere  in  the  body.  If  the  tumor  is  of  the 
malignant  type  its  growth  is  usually  exceedingy  rapid. 

Spinal  symptoms  due  to  new-growth  differ  from  those  due  to  caries  of  the 
spine  by  the  fact  that  the  stillness  of  the  muscles  of  the  back  and  tendons 
on  jarring  the  spine  is  not  so  marked  in  growths  as  it  is  in  tuberculous  disease. 
In  the  latter  case,  also,  there  may  be  found  a  primary  tuberculous  focus. 

When  compression  is  due  to  tumor  the  treatment  is  operative.  In  many 
instances  it  is  possible  to  give  the  patient  some  relief  by  this  means.  Starr 
has  collected  58  cases  of  tumor  of  the  spinal  cord  in  which  an  operation  was 
attempted.  In  all  his  cases  the  tumor  was  found,  and  in  16  of  them  the 
patients  recovered  If  the  growth  is  malignant  the  possibility  of  doing 
much  good  by  operation  is,  of  course,  remote.  Pain  may,  however,  be 
temporarily  relieved  by  the  removal  of  the  pressure. 

The  compression  of  the  spinal  cord  produced  by  gummatous  growths  or  by 
syphilitic  exudations  about  the  spinal  cord  present  symptoms  which  also 
depend  upon  the  area  which  is  involved,  particularly  upon  the  level  of  the 
lesion.  The  condition  may  arise  either  in  acquired  or  in  hereditary  syphilis, 
and  the  diagnosis  is  made  by  the  history  of  the  patient  and  the  presence  of 
pressure  symptoms.     The  treatment  is  antisyphilitic. 

When  an  aneurysm  of  the  aorta  grows  in  such  a  manner  that  it  erodes  the 
vertebrae,  it  may  produce  symptoms  of  compression  of  the  spinal  cord.  Thus, 
paraplegia  may  be  developed,  or  severe  pain  may  be  felt  in  those  parts  of  the 
body  which  are  supplied  by  the  nerve  trunks  which  have  their  origin  in  that 
portion  of  the  spinal  cord  which  is  affected.  If  the  physical  signs  of  the 
presence  of  aneurysm  are  demonstrable  the  diagnosis  is  not  diflficult,  but  if 


996  DISEASES  OF   THE  NERVOUS  SYSTEM 

the  growth  is  in  a  backward  direction  it  may  present  no  symptoms  which 
indicate  its  presence.  An  examination  of  the  patient's  back  may  not  only 
reveal  signs  of  vertebral  disease,  but  a  bruit  or  a  transmitted  pulsation 
and  a  history  of  syphilis  and  of  trauma,  if  added  to  a  discovery  that 
the  bloodvessels  are  sclerotic,  will  aid  in  discovering  this  cause  of  the 
symptoms. 

A  sixth  cause  of  compression  of  the  spinal  cord  is  hypertrophic  cervical 
pachymeningitis ,  the  pachymeningitis  cervicalis  hypertrophica  of  Charcot. 
This  disease  consists  in  a  thickening:  of  the  dura  mater  to  such  a  degree  that 
the  spinal  cord  and  the  spinal  nerves  as  they  pass  through  the  dura  are  pressed 
upon.  As  a  result  the  spinal  cord  suffers  from  meningomyelitis,  and  the  dura 
mater  becomes  adherent  to  the  pia  mater.  Sometimes  hemorrhagic  extrav- 
asations occur  under  the  dura,  and  there  is  usually  an  overgrowth  of  con- 
nective tissue  about  the  bloodvessels,  both  in  and  about  the  cord. 

The  symptoms  of  this  form  of  meningomyelitis  are  identical  with  those 
already  described  as  occurring  in  cases  in  which  the  cord  is  compressed  by 
other  causes  in  the  cervical  region,  but  they  have  certain  peculiarities  which 
may  aid  in  the  diagnosis  of  the  condition.  There  is  pain  in  the  hack  of  the 
head  and  neck,  with  a  certain  degree  of  stiffness  and  difficidty  in  movement. 
The  pain  radiates  down  into  the  hands  and  arms,  and  is  often  exceedingly 
severe  and  neuralgic  in  type.  Patches  of  ancesthesia  or  paresthesia  may  be 
present  and  localized  muscular  spasms  may  occur,  followed  by  loss  of  power 
and  the  development  of  reactions  of  degeneration,  when  the  disease  has 
lasted  long  enough  to  interfere  mth  the  transmission  of  trophic  impulses 
from  the  cord  to  the  muscles  affected.  Finally,  if  the  pressure  becomes 
great  enough  to  seriously  impair  the  nutrition  of  the  spinal  cord,  there  will 
develop  symptoms  of  spastic  paraplegia  due  to  descending  degenerative 
changes  in  the  lateral  tracts.  If  the  muscles  supplied  by  the  ulnar  and 
median  nerves  are  chiefly  affected,  the  disease  is  present  in  the  lower  part 
of  the  enlargement;  but  if  those  muscles  supplied  by  the  musculospiral  nerve 
lose  power,  the  upper  part  of  the  cervical  enlargement  is  involved.  Loss 
of  power  in  the  triceps,  anconeus,  supinator  longus,  extensor  carpi  radialis 
longior,  and  the  brachialis  anticus,  therefore  indicate  disease  of  the  upper 
segment;  whereas,  a  loss  of  power  in  the  flexor  carpi  ulnaris  and  flexor 
profundus  digitorum  (ulnar  nerve)  and  all  the  muscles  of  the  front  part  of 
the  forearm'  and  thumb  (median  nerve)  indicates  disease  in  the  lower 
segment.  In  some  cases  myosis  from  paralysis  of  the  cervical  sympathetic 
may  be  present. 

Treatment  of  cervical  pachymeningitis  promises  more  than  would  be  sup- 
posed from  the  character  of  the  lesions,  probably  because  the  condition  is 
so  often  due  to  syphilis.  Active  counterirritation  of  the  back  of  the  neck 
by  the  electrocautery  and  the  free  use  of  the  protiodide  of  mercury,  alter- 
nating with  large  doses  of  iodide  of  potassium,  should  always  be  resorted 
to.  Pain  is  to  be  relieved  by  the  use  of  acetanilid  or  phenacetin,  and  if 
these  drugs  fail  to  give  relief  they  must  be  combined  with  morphine. 


SPINAL  MENINGITIS  997 


SPINAL  MENINGITIS. 


Definition  and  Etiology. — A  condition  of  inflammation  of  the  membranes 
covering  the  spinal  cord  is  practically  always  secondary  to  some  lesion  at 
another  part  of  the  body.  In  some  instances  the  specific  micro-organism  of 
croupous  pneumonia,  of  enteric  fever,  of  acute  articular  rheumatism,  or 
septicaemia  finds  its  way  to  these  parts  and  causes  the  pathological  process. 
In  other  instances  tuberculosis  is  the  cause,  whether  it  be  primarily  present 
in  distant  parts  of  the  body  or  in  the  vertebral  column.  In  some  instances  an 
injury  affords  a  means  of  entrance  to  the  body  for  micro-organisms,  which 
attack  the  spinal  meninges,  particularly  if  the  vital  resistance  has  been  low- 
ered by  an  accident.  Spinal  meningitis  may  also  arise  from  cerebral  men- 
ingitis by  direct  extension  of  an  infection. 

Pathology  and  Morbid  Anatomy. — Following  the  stage  of  acute  hypersemia 
present  in  all  acute  inflammatory  processes,  there  is  an  excess  of  serous  fluid 
poured  out  between  the  dura  mater  and  the  pia,  which  fluid  may,  at  autopsy, 
be  found  to  be  purulent.  Patches  of  fibrinous  exudate  are  found  on  the  sur- 
face of  the  pia  mater,  the  bloodvessels  of  which  are  engorged  with  blood  and 
often  suffer  from  small  hemorrhagic  extravasations.  The  spinal  cord,  the 
pia  and  the  dura  mater  are  often  adherent.  After  the  inflammatory  process 
has  been  present  for  some  time,  the  pia  mater  becomes  much  thickened  by 
the  development  of  connective  tissue.  The  secondary  changes  which  ensue 
consist  in  an  inflammatory  process  which  affects  the  superficial  parts  of  the 
spinal  cord  and  causes  degenerative  changes  in  the  spinal  nerve  roots,  the 
axis  cylinders  of  which  become  swollen.  Fatty  globules  appear  in  the  myelin 
sheath.  The  changes  in  the  spinal  cord  are  most  marked  in  the  posterior 
and  lateral  columns,  and  in  subacute  or  chronic  cases  these  areas  are  affected 
by  an  overgrowth  of  connective  tissue,  which  ultimately  produces  sclerotic 
patches. 

Symptoms. — The  onset  of  acute  spinal  meningitis  develops,  as  do  most  acute 
inflammations  of  serous  membranes,  with  fain,  chill,  fever,  and  general 
wretchedness.  The  pain  is  felt  in  the  back  and  limbs,  and  is  greatly  increased 
by  movements.  There  is  also  a  state  of  hyper oesthesia  of  all  the  spinal  nerves, 
so  that  touching  the  patient  may  cause  great  suffering.  It  is  soon  noticed 
that  the  patient  is  stiff  and  more  or  less  fixed  by  muscular  rigidity,  which  is, 
in  part,  due  to  the  pain  produced  by  movement  and  to  the  irritation  of  the 
nerves  as  they  pass  from  the  spinal  cord.  The  stiffness  of  the  muscles  of  the 
back  and  of  the  neck  is  the  most  marked.  At  this  time  "  Kernig's  sign"  is 
developed,  which  consists  in  an  inability  of  the  physician  to  straighten  the 
patient's  leg  at  the  knee  after  the  thigh  has  been  flexed  to  a  right  angle 
with  the  trunk.  This  state  is  due  to  spasm  of  the  flexor  muscles  induced  by 
the  irritation  at  the  point  of  exit  of  the  nerve  trunks.  There  is  often  soon 
developed  an  increase  in  the  reflexes,  chiefly  in  the  legs,  and  this  in  turn  is 
succeeded  by  paralysis  and  final  loss  of  reflexes  if  the  process  is  severe  and 
prolonged.  Along  with  these  symptoms  there  speedily  develops  a  paralysis 
of  the  bladder  and  rectum,  so  that  there  is  retention  or  incontinence  of  urine 
and  incontinence    of   feces.      There    may  also    be    paralytic   incontinence. 


998  DISEASES  OF   THE  NERVOUS  SYSTEM 

Because  of  the  lesions  produced  in  the  nerve  roots  and  in  the  spinal  nerves 
as  they  pierce  the  meninges,  trophic  changes  in  the  skin  may  develop,  as 
shown  by  localized  areas  of  pallor  and  congestion  and  the  speedy  develop- 
ment of  bed-sores. 

If  the  disease  is  severe  and  the  inflammatory  process  spreads  until  the 
upper  portions  of  the  cord  are  involved,  death  may  ensue  by  reason  of  the 
inflammation  reaching  the  level  of  the  medulla  and  causing  fatal  disturbance 
of  the  function  of  respiration  or  of  the  heart.  In  such  cases  Cheyne-Stokes 
breathing  and  irregularity  of  the  pulse  may  be  the  symptoms  of  impending 
dissolution.  Not  rarely  the  development  of  paralysis  of  the  cranial  nerves 
with  convulsions  and  coma  precede  death.  Death  may  come  within  a  few 
days  of  onset  or  after  several  weeks.  In  the  severe  cases  which  recover  the 
patient  often  permanently  suffers  from  localized  palsies,  anaesthesias,  and 
atrophic  lesions  in  the  skin  and  muscles. 

Diagnosis. — Aside  from  the  character  of  the  symptoms  just  described, 
which  points  strongly  to  meningitis,  we  may  resort  to  lumbar  puncture  for 
the  purpose  of  making  the  diagnosis  more  certain.  A  strong,  hollow  needle 
attached  to  a  syringe,  so  that  it  may  be  easily  handled,  or  a  small  trocar  and 
cannula  are  passed  into  the  spinal  canal  between  the  third  and  fourth  lumbar 
vertebrae,  on  a  line  drawn  between  the  crests  of  the  ilia.  The  direction  of 
the  needle  should  be  slightly  to  one  side  and  upward.  (For  further  details 
as  to  this  method  see  Cerebrospinal  Fever.)  As  soon  as  it  enters  the 
spinal  canal  the  cerebrospinal  fluid  will  escape,  drop  by  drop,  or  with  a 
squirt,  if  the  pressure  is  great.  This  fluid  should  be  examined  for  bacteria 
to  determine  the  nature  of  the  infection.  If  the  fluid  contains  disintegrated 
blood,  the  cause  of  the  affection  is  a  pachymeningitis  or  an  injury.  If  fresh 
blood  is  present,  the  blood  is  probably  due  to  the  puncture.  If  the  fluid  is 
clear  there  is  probably  no  true  meningitis  present.  In  cases  of  tuberculosis 
of  the  meninges  it  is  usually  quite  cloudy.  If  it  contains  pus  a  purulent 
meningitis  is  present.  If  inflammation  of  the  meninges  is  present  no  sugar 
will  be  found  in  the  fluid.  A  study  of  the  leukocytes  in  the  cerebrospinal 
fluid  may  throw  light  upon  the  case.  They  are  much  increased  in  number 
in  acute  inflammatory  processes.  In  chronic  conditions  the  mononuclear 
cells  are  particularly  increased. 

Prognosis. — ^Tuberculous  meningitis  is,  of  course,  a  state  giving  a  hopeless 
prognosis.  Septic  cases  are  also  grave.  Those  types  due  to  pneumonia 
and  typhoid  fever  sometimes  recover.  (See  Pneumonia  and  Typhoid 
Fever.) 

Treatment. — The  treatment  of  spinal  meningitis  consists  in  absolute  rest, 
the  patient  being  placed  upon  a  soft  bed.  In  some  instances  if  there  is  any 
sign  of  bed-sores  it  is  essential  that  an  air-bed  or  water-bed  should  be  used. 
The  application  of  blisters  or  the  actual  cautery  has  been  recommended, 
but  in  view  of  the  possibility  of  bed-sores  developing,  it  is  questionable 
whether  their  use  is  safe.  The  same  objection  holds  in  regard  to  such 
forms  of  counterirritation  as  cupping  and  leeching.  Twitchings  or  cramps 
of  the  muscles  are  to  be  relieved  by  the  administration  of  sedatives  to  the 
spinal  cord,  such  as  bromide  and  chloral,  and  if  the  pain  is  very  severe 
morphine  must  be  used.     At  one  time  it  was  believed  that  full  doses  of 


CHRONIC  SPINAL  MENINGITIS  999 

calomel  combined  with  opium  were  exceedingly  valuable  in  the  treatment  of 
acute  inflammation  of  all  serous  membranes,  particularly  those  covering  the 
brain  and  spinal  cord.  At  the  present  time  this  method  of  treatment  has 
almost  entirely  ceased,  but  in  certain  instances  it  would  seem  advisable  to 
have  recourse  to  it.  The  object  is  to  give  enough  mercurial  to  exercise  its 
so-called  antiphlogistic  influence,  and  to  use  the  opium  not  only  for  the  relief 
of  pain,  but  for  the  purpose  of  preventing  the  calomel  from  purging  the 
patient.  The  mercurial  may  be  pushed  until  slight  tenderness  of  the  gums  is 
manifested. 

Chronic  Spinal  Meningitis.  Etiology. — Chronic  spinal  meningitis  is 
said  to  occasionally  have  its  origin  in  an  acute  inflammation  of  the  meninges 
of  the  spinal  cord.  In  all  probability,  however,  such  an  origin  is  exceed- 
ingly rare,  and  in  the  majority  of  instances  it  is  the  result  of  syphilitic  infection, 
whereby  there  is  a  thickening  of  the  dura  and  the  formation  of  an  abnormal 
quantity  of  serum  and  connective  tissue  under  it.  As  the  result  of  the  chronic 
inflammatory  process  in  the  membrane,  a  somewhat  similar  one  is  set  up  in 
the  spinal  cord  near  its  surface,  producing  a  meningomyelitis,  which  is  in  its 
nature  closely  allied  to  the  acute  form  of  meningitis  just  considered.  There 
is  always  present  a  thickening  of  the  bloodvessels,  a  small-cell  infiltration 
about  their  walls,  and,  if  the  process  is  severe,  an  obliterating  endarteritis. 
Sometimes  gummatous  masses  are  formed.  In  most  of  these  cases  there  is 
also  present  cerebral  meningitis  as  well. 

Symptoms. — The  symptoms  of  chronic  spinal  meningitis  consist  in  stiff- 
ness of  the  back  and  extremities,  with  pains  and  cramps.  There  are  also 
disturbances  in  sensibility,  some  portions  of  the  skin  being  hypereesthetic, 
others  anaesthetic.  Motor  power  is  also  impaired,  and  if  the  inflammation  is 
in  the  lower  portion  of  the  spinal  cord  there  may  be  interference  with  the 
function  of  the  bladder  or  rectum. 

Diagnosis. — Chronic  spinal  meningitis  is  to  be  recognized  by  the  presence 
of  the  symptoms  just  described  and  by  the  use  of  lumbar  puncture,  which, 
if  meningitis  is  present,  will  show  an  increased  quantity  of  cerebrospinal 
fluid,  which  is  usually  under  pressure,  and  which  will,  therefore,  escape  from 
the  needle  with  a  spurt.  Care  must  be  taken  that  ordinary  lumbago  with 
spasm  of  the  muscles  of  the  back  and  fixation  and  pain  is  not  confused  with 
this  condition.  Myelitis  is  to  be  separated  by  the  absence  of  severe  pain  and 
of  cramps  in  the  extremities,  and  by  the  presence  of  paraplegia. 

Treatment. — The  treatment  of  chronic  meningitis  consists,  as  must  be  evi- 
dent from  its  cause,  namely,  late  syphilis,  in  the  free  use  of  protiodide  of 
mercury  and  the  iodide  of  potassium,  given  until  a  full  physiological  effect  is 
produced.  In  other  words,  it  is  not  a  question  of  grains  administered,  but 
effects  obtained.  These  cases  are  usually  much  benefited  by  going  to  the 
various  hot  springs,  because,  in  addition  to  the  use  of  mercurials  by  the 
mouth,  they  permit  the  simultaneous  use  of  hot  baths  and  mercurial  inunc- 
tions. Everything  should  be  done  to  keep  the  general  condition  of  the 
patient  at  the  highest  possible  level  approaching  that  of  health. 


1000  DISEASES  OF   THE  NERVOUS  SYSTEM 


ACUTE  ASCENDING  PARALYSIS  (LANDRY'S  PARALYSIS). 

Definition. — This  is  an  acute  ascending  paralysis  beginning  in  the  lower 
extremities  and  rapidly  passing  upward  until  it  involves  the  muscles  of  the 
trunk  and  upper  extremities,  finally  causing  death  by  failure  of  respiration. 
The  condition  is  a  very  rare  one.  It  must  be  clearly  separated  from  those 
forms  of  acute  ascending  paralysis  due  to  an  acute  ascending  myelitis,  or  to  a 
hemorrhage  into  the  spinal  membranes,  and  from  ascending  peripheral  neuritis. 
It  is  a  symptom-complex  which  results  from  a  lesion  of  the  lower  segment 
of  the  motor  pathway,  either  in  the  cord  and  bulb  or  in  the  peripheral  nerves. 
It  is  sometimes  called  acute  progressive  paralysis,  or  Landry's  paralysis, 
having  been  first  described  by  Landry  in  1859.  Rare  cases  have  been 
recorded  in  which  the  disease  has  begun  in  the  arms  and  passed  to  the  legs. 

Etiology. — The  exact  etiological  causes  of  this  malady  are  not  understood. 
The  disease  occurs  more  frequently  in  males  than  in  females,  and  its  most 
common  period  of  occurrence  is  between  twenty  and  forty  years  of  age.  In 
all  probability  every  case  is  due  to  an  infection  of  the  peripheral  nerves  and 
spinal  cord,  for  it  sometimes  follows  an  acute  illness  due  to  a  micro-organism, 
as,  for  example,  influenza,  smallpox,  erysipelas,  typhoid  fever,  and  pelvic  peri- 
tonitis. The  excessive  use  of  alcohol  has  seemed  in  some  cases  to  be  a 
powerful  predisposing  cause,  and  cases  have  been  recorded  in  which,  in  the 
presence  of  a  history  of  syphilis,  the  malady  has  been  arrested  by  the  use 
of  specific  remedies. 

Pathology  and  Morbid  Anatomy. — The  lesions  found  at  autopsy  in  a  case 
of  Landry's  paralysis  are  by  no  means  constant  in  all  cases.  In  some 
instances  the  chief  lesions  have  been  found  in  the  spinal  cord,  in  others  in 
the  peripheral  nerves  and  nerve  roots.  In  the  spinal  cord  the  lesions  described 
in  some  cases  have  been  practically  identical  with  those  of  acute  dissemi- 
nated myelitis,  and  in  others  they  have  been  identical  with  those  met  with 
in  severe  peripheral  neuritis.  In  every  case,  however,  it  is  evident  that  the 
peripheral  motor  neurones  are  the  portions  of  the  nervous  system  most 
affected. 

Symptoms. — In  some  cases  of  acute  ascending  paralysis  the  onset  of  the 
paralytic  symptoms  is  preceded  for  a  few  hours  by  a  sense  of  general  wretched- 
ness, with  tingling  or  'pain  in  the  limhs  or  hack.  This  is  followed  by  a  rapidly 
increasing  weakness  in  the  lower  limhs,  which  may  amount  to  a  complete  loss 
of  power  in  from  a  few  hours  to  several  days.  The  muscles  of  the  lower  part 
of  the  trunk  are  next  involved,  and  finally  the  muscles  of  the  arms  and  of 
the  upper  thorax  fall  victims  to  the  rapidly  spreading  malady.  The  respira- 
tion becomes  difficult,  the  speech  indistinct,  and  dysphagia  may  be  present. 
Sensation  in  the  paralyzed  parts  may  be  impaired,  but  it  is  not  lost.  The 
reflexes  are  decreased,  and  perhaps  lost,  but  they  may  be  restored  later  on 
and  ultimately  become  excessive.  Muscular  atrophy  does  not  develop 
even  when  the  patient  survives  for  weeks,  and  the  sphincters  usually,  but 
not  always,  retain  their  power.  Bed-sores  do  not  develop.  The  mind  nearly 
always  remains  clear,  and  the  temperature  is  usually  not  elevated.  Very 
rare  cases  have  been  reported  in  which  the  paralysis  has  been  of  the  acute 


CAISSON  DISEASE  1001 

descending  type,  the  arms  being  the  parts  first  affected.  In  such  cases  fatal 
bulbar  paralysis  may  occur  before  the  lower  parts  of  the  body  are  affected. 

Diagnosis. — Acute  ascending  paralysis  is  to  be  separated  from  acute 
poliomyelitis  by  the  absence  of  rapid  atrophy.  From  the  paralysis  due  to 
an  acute  hemorrhage  into  the  spinal  meninges  it  is  separated  by  the  absence 
of  pain  and  of  spasm.  From  an  acute  ascending  myelitis  it  is  separated  by 
the  fact  that  there  is  no  loss  of  sensation,  that  the  sphincters  are  unaffected, 
and  that  the  paralysis  progresses  more  rapidly. 

Prognosis. — The  prognosis  depends  upon  the  state  of  the  respiratory  cen- 
tre and  the  lungs,  and  upon  the  condition  of  the  centres  governing  cardiac 
action.  If  these  parts  are  involved,  death,  of  course,  speedily  ends  the  case. 
Death  may  come  in  a  few  hours  or  days,  or  not  for  several  weeks.  Cerebral 
and  bulbar  symptoms  are  always  grave.  A  fatal  ending  usually  occurs, 
but  cases  sometimes  improve  and  recovery  may  occur. 

Treatment. — The  treatment  of  a  patient  suffering  from  Landry's  paralysis 
should  be  almost  identical  with  that  advised  in  cases  of  acute  myelitis.  A 
warm  bath  may  be  given  to  draw  the  blood  to  the  surface,  and  moderate 
counterirritation  should  be  applied  over  the  vertebrae.  It  is  absolutely  essen- 
tial that  perfect  rest  be  obtained,  and  that  the  patient  shall  lie  upon  the  side 
rather  than  upon  his  back,  since  the  dorsal  position  may  increase  the  ten- 
dency to  congestion  of  the  cord.  As  the  disease  is  probably  dependent  upon 
infection  and  toxaemia,  the  skin  should  be  kept  active  by  mild  diaphoretics, 
and  the  kidneys  should  be  stimulated  to  activity  by  the  use  of  the  vegetable 
salts  of  potash  or  other  mild  diuretics.  Some  writers  recommend  the  admin- 
istration of  salicylate  of  sodium,  although  they  do  not  seem  to  be  able  to 
explain  how  it  can  do  good.  Gowers  speaks  highly  of  the  use  of  ergotin, 
and  mentions  the  case  of  a  man  of  fifty-seven  who  developed  symptoms  of 
Landry's  paralysis  after  exposure  to  cold  and  wet.  To  this  patient  ergotin 
was  given  every  hour  till  20  grains  had  been  taken,  when  the  symptoms 
became  markedly  improved  and  the  patient  speedily  recovered,  so  that  by 
the  end  of  a  week  he  was  well.  One  can  not  help  feeling  that  in  all  probability 
the  ergotin  had  little  to  do  with  this  remarkable  recovery,  as  it  is  hard  to 
see  how  this  drug  could  be  useful  in  combating  an  infection  which  was 
so  severe  in  its  nervous  effects.  When  there  is  a  history  of  syphilis  the 
protiodide  of  mercury  should  be  administered  freely. 


CAISSON  DISEASE. 

Caisson  disease  is  a  condition  met  with  in  persons  who  have  been  exposed 
to  high  atmospheric  pressures  for  a  number  of  hours,  and  is  particularly 
prone  to  develop  if  severe  toil  has  been  maintained  during  the  exposure. 
The  disease  is  usually  met  with  in  artisans,  or  laborers,  who  are  engaged  in 
the  building  of  piers  or  foundations  many  feet  under  water,  where  it  is 
necessary  to  have  a  pressure  of  several  atmospheres  in  order  to  keep  the 
caisson  dry.  In  some  instances  the  pressure  is  as  great  as  ninety  pounds  to 
the  square  inch.  The  atmosphere  in  the  caisson  often  has  a  high  proportion 
of  humidity,  and  the  temperature  may  also  be  quite  high.    The  symptoms 


1002  DISEASES  OF   THE  NERVOUS  SYSTEM 

develop  when  the  workman  leaves  the  caisson  and  is  exposed  to  normal 
atmospheric  pressure.  In  mild  cases  nothing  more  than  a  feeling  of  dizziness 
and  vertigo  develop,  associated,  it  may  be,  with  neuralgic  pains  in  the  head. 
In  severe  cases  the  neuralgic  pains  become  excruciating,  so  that  the  patient 
feels  as  if  his  muscles  were  being  stripped  from  his  bones,  and  this  pain  is 
followed  by  a  loss  of  both  motion  and  sensation  in  the  lower  limbs,  although 
the  patient  still  complains  of  the  pain.  Often  nausea  and  vomiting  are 
present,  accompanied  by  violent  epigastric  paroxysms  of  pain.  Occasionally, 
there  is  loss  of  power  in  the  sphincters.  In  some  instances  pain  is  absent, 
but  paralysis  is  present,  paralysis  being  the  more  constant  symptom.  In  still 
more  severe  cases  coma  develops,  in  which  case  death  invariably  results. 
The  prognosis  is  generally  favorable  unless  the  symptoms  of  paralysis  and 
pain  are  unusually  severe.  The  mildest  cases  rarely  last  over  twelve  hours, 
and  sometimes  only  three  or  four;  but  in  severe  cases,  recovery  may  not  take 
place  for  days  or  weeks. 

The  pathology  of  this  curious  condition  is  not  well  understood.  (A  dis- 
cussion of  many  of  the  views  concerning  it  will  be  found  in  the  author's 
Fiske  Fund  Prize  Essay  for  1886.^)  It  would  seem  probable  that  the  symp- 
toms are  largely  dependent  upon  disorder  of  the  circulation  in  the  central 
nervous  system.  Air  emboli  were  found  in  the  small  arteries  of  the  postero- 
lateral tracts  of  the  spinal  cord,  also  secondary  softening  was  observed. 
Those  who  have  had  the  most  experience  with  the  disease  in  this  country  are 
Jaminet,  Bauer,  and  Woodward,  who  made  many  observations  during  the 
building  of  the  St.  Louis  Bridge,  and  A.  H.  Smith,  of  New  York,  who  studied 
it  during  the  building  of  the  Brooklyn  Bridge. 

Treatment. — The  treatment  is  both,  prophylactic  and  palliative.  The 
prophylaxis  consists  in  having  superimposed  air  chambers,  each  one  having 
a  different  pressure  so  that  the  workmen  may  pass  by  degrees  from  the  high- 
pressure  caisson  to  the  pressure  of  atmospheric  air.  It  is  also  advisable  to 
have  the  workmen  brought  to  the  surface  with  as  little  muscular  effort 
as  possible.  In  the  building  of  the  St.  Louis  Bridge,  thirteen  of  the  men 
who  were  employed  in  the  building  of  the  east  pier,  which  was  sunk  127  feet 
below  high-water  mark,  died ;  but  in  building  the  east  abutment,  which  was 
sunk  five  feet  deeper,  only  one  man  died.  In  the  latter  case  the  workmen 
were  lifted  to  the  surface  by  an  elevator  instead  of  having  to  climb  a 
ladder. 

When  the  symptoms  come  on,  morphine  should  be  given  hypodermic- 
ally  in  adequate  dose.  A.  H.  Smith  considered  that  ergot  is  of  value. 
Hot  compresses  should  be  wrung  out  and  applied  to  the  feet  and  spine. 
Jaminet  recommends  a  draught  of  a  strong  alcoholic  stimulant,  with  ginger. 

The  whole  object  of  the  physician  should  be  to  re-establish  and  equalize 
the  circulation.  If  the  pulse  is  full  and  the  heart  laboring,  venesection 
should  be  freely  employed.  Sometimes  relief  can  be  obtained  by  returning 
the  patient  to  the  caisson.  In  some  instances  a  small  caisson  for  the  resus- 
citation of  workmen  has  been  built  on  the  surface,  with  advantageous  results. 

'  New  and  Altered  Forms  of  Disease  due  to  the  Advance  of  Civilization  in  the  Last  Half  Century. 


NEURITIS  1003 


DISEASES   IN  WHICH  THE   CHIEF  MANIFESTATIONS  ARE 

IN  THE  NERVES. 

NEURITIS. 

Definition. — Neuritis  is  an  inflammation  of  a  nerve.  When  the  in- 
flammatory process  chiefly  involves  the  perineurium  it  is  called  "  perineu- 
ritis;" if  the  tissues  surrounding  the  nerve  bundles  and  between  the  nerve 
fibres  are  affected,  it  is  an  "  interstitial  neuritis,"  and  if  the  nerve  fibres  them- 
selves are  primarily  affected,  it  is  said  to  be  a  "parenchymatous  neuritis." 
The  latter  condition  is  usually  a  subacute  or  chronic  process  and  is  charac- 
terized by  degenerative  changes  in  the  nerve  fibres.  The  distinction,  how- 
ever, between  these  different  forms  is  theoretical  rather  than  clinical,  because 
it  is  not  possible  to  draw  a  definite  line  between  them  in  most  cases. 

Etiology. — The  causes  of  neuritis  are  very  numerous.  Any  injury  to  a 
nerve  trunk,  as  by  a  blow,  stretching,  or  a  wound,  may  give  rise  to  the  inflam- 
matory process,  as  may  also  tumors,  which  by  pressure  cause  irritation. 
Sometimes  the  use  of  a  tool  or  a  crutch  may,  by  constant  pressure  on  a  nerve, 
produce  neuritis.  Various  infectious  diseases  and  the  abuse  of  alcohol  may 
produce  it,  as  may  also  many  of  the  metallic  poisons.  In  those  cases,  how- 
ever, in  which  the  malady  arises  as  the  result  of  a  poison,  the  neuritis  is 
usually  a  multiple  neuritis  and  does  not  affect  one  nerve  alone.  (See  Multiple 
Neuritis.)    Gout,  and  lithaemic  states,  also  cause  it. 

Pathology  and  Morbid  Anatomy. — The  nerve,  which  is  acutely  inflamed, 
is  found  on  examination  to  be  red  and  swollen  and  lacking  its  usual  lustre; 
the  bloodvessels  supplying  it  are  hypersemic  or  congested.  If  the  process 
has  been  present  for  some  time  the  nerve  may  be  marked  by  swellings  due 
to  overgrowth  of  connective  tissue  and  its  endoneurium  may  be  infiltrated 
by  small  cells.  At  this  time  one  of  three  processes  develops.  Either  the 
results  of  the  acute  inflammatory  process  undergo  resolution  or  the  inflam- 
mation becomes  so  severe  that  the  nerve  is  destroyed,  or  if  the  process  is 
more  moderate,  but  continued,  there  is  an  overgrowth  of  connective  tissue 
and  gradual  atrophy  and  loss  of  function.  Microscopically,  the  inflamed 
nerve  presents  additional  changes  which  serve  to  separate  the  parenchyma- 
tous form  of  the  disease  from  that  in  which  the  perineurium  and  interstitial 
tissues  are  chiefly  affected.  In  the  parenchymatous  type  the  myelin  is 
opaque  and  swollen  and  soon  undergoes  segmentation  with  granular  material 
between  the  segments.  The  axis  cylinder  may  be  continuous  or  broken  into 
segments  corresponding  to  the  breaks  in  the  myelin.  Finally,  the  myelin 
and  cylinder  entirely  disappear  and  only  the  nerve  sheath  containing  a  little 
granular  matter  is  left.  This  last  state  may  also  arise  as  a  result  of  the 
interstitial  form  of  neuritis,  but  in  this  form  the  nerve  is,  in  the  early  stage 
of  the  inflammation,  more  swollen  and  congested  and  the  sheath  filled  with 
serum  or  purulent  exudate. 


1004  DISEASES  OF   THE  NERVOUS  SYSTEM 

Symptoms. — The  symptoms  of  neuritis  vary  over  a  wide  range  in  severity. 
When  the  inflammatory  process  is  very  mild  so  that  the  normal  function  is 
but  slightly  perverted,  as  from  moderate  pressure,  a  tingling  sensation  is 
felt  or,  in  its  place,  a  sense  of  numbness  is  experienced.  This  is  called  par- 
cesthesia  and  can  scarcely  be  said  to  be  due  to  any  real  change  in  the  nutri- 
tion of  the  nerve. 

When  the  change  in  the  nerve  is  more  severe  the  symptoms  are  more 
definite.  Tingling  or  pricking  sensations  may  be  present  not  only  at  the 
site  of  the  lesion,  but  at  the  peripheral  part  of  the  nerve.  If  the  damage  is 
the  result  of  pressure  there  is  rarely  any  pain,  and  motor  paralysis,  more  or 
less  complete,  is  present  instead.  If,  on  the  other  hand,  the  lesion  is  asso- 
ciated with  any  wound,  and  an  infection  of  the  nerve  has  taken  place, 
then  pain  is  usually  present  and  is  often  severe.  Pressure  upon  the  inflamed 
nerve  trunk  by  the  finger-tips  also  increases  the  pain  not  only  at  the  point 
of  pressure,  but  at  the  end  of  the  nerve  as  well.  After  the  process  in  the 
nerve  is  so  advanced  that  its  function  is  greatly  impaired,  trophic  changes 
occur  in  the  muscles  and  skin,  the  former  wasting  and  the  skin  becoming 
glossy.  The  muscles  cease  to  respond  to  faradic  electricity  and  later  fail  to 
respond  to  galvanic  electricity,  the  reactions  of  degeneration  being  first 
developed.  Injuries  to  parts  supplied  by  the  nerve  affected  may  result  in 
sloughing,  but  sores  rarely  develop  unless  an  injury  is  suffered. 

When  recovery  begins  the  electrical  contractility  to  galvanic  stimulation 
first  returns  in  part  and  later  the  power  of  voluntary  movement. 

Diagnosis. — The  diagnosis  of  neuritis  involving  a  single  nerve,  or  several 
nerves  in  nearly  related  parts,  is  not  difficult,  for  the  pain  is  limited  to  the  area 
of  the  nerve,  as  is  also  the  ansesthesia  or  hypersesthesia  and  loss  of  power.  The 
condition  is  also  pointed  to  by  the  history  of  injury  or  of  some  diathetic  state 
which  produces  the  affection.     Pressure  on  the  nerve  trunk  will  elicit  pain. 

Prognosis. — The  outlook  for  recovery  in  most  cases  of  neuritis  is  quite 
good  because  of  the  extraordinary  power  of  regeneration  possessed  by  nerves. 
Even  if  the  damage  to  the  nerve  has  been  so  severe  that  its  function  is 
abolished  by  the  division  of  all  its  conducting  fibres,  the  function  can  be 
restored  by  the  surgeon,  who,  by  excising  the  destroyed  portion  and  joining 
the  distal  and  proximal  ends  together,  may  re-establish  the  pathway  for 
both  sensory  and  motor  impulses.  So  rapid  is  the  regeneration  that  if  a  nerve 
is  severed  by  accident,  and  immediately  sewed  together,  power  may  return 
in  two  weeks.  When  the  damage  has  been  done  by  pressure  or  inflamma- 
tion the  recovery  rarely  ensues  in  less  than  six  weeks,  and  even  eight  months 
or  a  year  may  be  consumed  in  the  regenerative  process.  When  recovery 
fails  to  occur  and  it  is  believed  that  only  a  small  part  of  the  nerve  is  diseased 
surgical  procedures  are  necessary,  but  if  there  is  reason  to  believe  that 
permanent  damage  to  a  large  part  of  a  nerve  has  taken  place,  then  the  prog- 
nosis is  hopeless.  Sometimes  the  mere  exposure  of  the  nerve  and  the  break- 
ing up  of  adhesions  or  exudates  that  cause  pressure  is  sufficient  to  produce 
recovery. 

Treatment. — The  treatment  of  neuritis  may  be  divided  into  two  parts, 
that  devoted  to  the  relief  of  pain  and  that  to  the  abatement -of  the  inflam- 
mation and  to  the  regeneration  of  normal  function.    For  the  relief  of  pain  the 


NEURITIS  1005 

part  affected  may  be  wrapped  in  lint,  which  is  heavily  smeared  with  equal 
parts  of  an  ointment  of  ichthyol  and  lanolin,  outside  of  which  is  placed 
some  oil-silk  to  retain  moisture.  In  some  instances  a  hot  poultice  of  flaxseed 
or  hot  compresses  may  be  used  in  the  earlier  stages  to  diminish  the  activity 
of  the  inflammatory  process.  If  the  pain  is  so  severe  that  sleep  is  interfered 
with,  the  various  coal-tar  products  may  be  employed,  of  which  the  most 
valuable  are  phenacetin  in  the  dose  of  5  grains  four  or  five  times  a  day,  if 
need  be.  Acetanilid  may  be  given  in  similar  dose,  and  antipyrin  in  slightly 
larger  dose.  In  other  cases  better  results  accrue  if  to  these  products  of 
the  coal-tar  group  are  added  small  doses  of  codeine  or  morphine.  If  the 
pain  does  not  yield  to  these  remedies,  hypodermic  injections  of  morphine 
may  be  necessary  for  a  short  time,  but  their  continued  use  is  dangerous,  as 
the  patient  only  too  readily  develops  the  morphine  habit.  If  the  neuritis 
affects  the  arm  or  some  portion  of  the  body  which  does  not  by  its  disability 
force  the  patient  to  lie  in  bed,  it  is  essential  that  the  part  involved  shall  be 
placed  at  rest.  Thus,  if  the  arm  is  affected  it  should  be  carried  in  a  sling, 
and  it  may  be  necessary  to  protect  it  by  a  splint. 

For  the  restoration  of  function  no  therapeutic  measure  should  be  insti- 
tuted beyond  those  already  named  until  the  acute  stage  of  the  inflammatory 
process  has  ceased.  When  it  is  evident  that  the  acute  process  is  no  longer 
present,  strychnine  or  nux  vomica  may  be  given  internally  in  full  doses. 
These  may  also  be  combined  with  phosphorus  and  small  quantities  of  quinine. 
The  area  of  the  skin  which  is  supplied  by  the  affected  nerve  should  also  be 
stimulated  by  the  application  of  faradic  electricity,  care  being  taken  that 
the  current  employed  is  not  so  strong  as  to  damage  the  part.  It  is  a  good 
rule  never  to  use  a  current  so  strong  as  to  produce  suffering.  This  method 
of  treatment  not  only  tends  to  rapidly  restore  sensation  in  the  paralyzed 
part,  but  also  to  bring  back  faradic  contractility  in  the  muscle,  and  so  ulti- 
mately restore  motor  power.  If,  however,  the  parts  fail  to  respond,  then 
galvanic  electricity  must  be  used,  and  the  current  interrupted  so  as  to  pro- 
duce a  stimulant  effect.  In  some  instances  the  muscle  seems  to  respond 
better  to  the  negative  than  to  the  positive  pole,  much  depending  of  course 
upon  the  stage  of  degeneration  which  is  present.  Care  should  be  taken  that 
the  applications  of  electricity  are  not  prolonged  for  more  than  a  few  minutes 
at  a  time,  and  that  they  are  not  made  oftener  than  once  a  day.  Additional 
measures  for  improving  the  nutrition  of  the  part  are  massage  and  manipula- 
tion. None  of  these  measures  should,  however,  be  employed  if  there  is 
tenderness  in  the  nerve  trunk  or  if  they  produce  exhaustion  in  the  parts 
affected.  Indeed,  it  is  possible  in  some  instances  to  produce  injuries  of 
the  nerve  by  too  active  manipulation.  It  must  be  remembered  that  the 
electricity,  the  massage,  and  the  Swedish  movements  only  do  good  by 
increasing  the  circulation  and  modifying  the  nutritional  processes  in  the 
parts  affected.  If  anaesthesia  of  an  extremity  exposes  it  to  injury,  by  reason 
of  the  patient  being  unconscious  of  the  presence  of  heat  or  cold,  or  of  objects 
which  are  capable  of  doing  damage,  the  part  should  be  carefully  protected 
by  a  splint  or  soft  dressing. 


1006  DISEASES   OF   THE   NERVOUS   SYSTEM 


Special  Forms  of  Neuritis. 

Cervicobrachial  Neuritis. — Cervicobrachial  neuritis  follows  injuries  to 
the  neck  and  shoulder,  and  is  usually  produced  by  falls  or  severe  blows. 
Symptoms  may  also  arise  as  the  result  of  disease  of  the  vertebrae  or  from  an 
aneurysm.  In  other  cases  the  acute  infectious  diseases  or  gouty  or  rheu- 
matic conditions,  associated  with  exposure  to  cold,  seem  to  be  responsible 
for  the  condition.  The  symptoms  depend  to  a  large  extent  upon  the  portion 
of  the  cervicobrachial  plexus  which  is  affected.  If  the  four  upper  cervical 
nerves  are  involved,  severe  pain  in  the  neighborhood  of  the  occiput  is  felt, 
and  the  head  is  held  in  a  fixed  position  because  movement  increases  the 
suffering.  When  the  fifth  or  sixth,  cervical  nerves  are  involved,  the  pain  is 
in  the  neck  and  the  upper  portion  of  the  shoulder  and  axilla,  and  it  may  be 
felt  down  the  back  of  the  arm.  Whereas,  when  the  lower  cervical  nerves 
are  affected,  including  the  branches  of  the  first  dorsal,  the  pain  is  clavicular 
and  axillary  in  the  area  of  its  distribution  and  extends  down  the  front  of  the 
arm  and  forearm  into  the  fingers.  There  is  also  loss  of  power  in  all  the  mus- 
cles which  are  supplied  by  the  nerves  making  up  the  cervicobrachial  plexus 
when  their  fibres  are  involved.  Because  of  the  fact  that  the  cervical  sympa- 
thetic nerve  receives  fibres  fron  this  part  of  the  spinal  cord  it  sometimes 
happens  that  ocular  symptoms  accompany  manifestations  of  the  neuritis 
in  the  lower  portions  of  the  cervicobrachial  plexus,  with  the  result  that  there 
may  be  retraction  of  the  eyeball  and  narrowing  of  the  palpebral  fissure,  with 
a  mild  degree  of  myosis  and  some  pallor  of  the  side  of  the  face  affected. 
The  skin  on  this  side  is  dry  and  does  not  become  flushed  on  exercise.  Cases 
of  neuritis  of  the  cervicobrachial  plexus  show  marked  evidences  of  pain  when 
pressure  is  made  over  the  plexus  or  when  the  arm  is  moved  away  from  the 
body. 

In  some  instances  of  cervicobrachial  neuritis  of  very  sudden  onset  actual 
hemorrhage  may  occur  into  the  sheath  of  the  nerves,  the  so-called  "apo- 
plectic neuritis."  The  same  numbness  and  tinghng  as  has  been  described 
under  neuritis  in  general,  followed  by  loss  of  sensation  and  of  motor  power, 
occurs  in  cervicobrachial  neuritis.  Trophic  changes  in  the  skin  and  muscles 
take  place,  and  the  reactions  of  degeneration  develop. 

A  form  of  cervicobrachial  neuritis  which  affects  children  is  sometimes 
called  obstetrical  paralysis,  or  birth  palsy,  and  is  due  to  damage  of  the 
cervicobrachial  plexus  in  parturition. 

Prognosis. ^^The  prognosis  in  cases  of  cervicobrachial  neuritis,  like  that 
of  neuritis  in  general,  is  good  provided  the  injury  has  not  been  so  severe  as 
to  sever  the  nerve  fibres,  and  provided  the  condition  has  not  lasted  too  long. 

Treatment. — The  treatment  consists  in  absolute  rest,  the  employment  of 
hot  compresses  if  the  condition  is  seen  early  in  its  course,  and  later  on  the 
constant  use  of  counterirritation.  Rubbing  the  parts  with  some  stimulating 
liniment  like  that  of  chloroform  or  ammonia  is  of  value.  Electricity, 
massage,  and  Swedish  movements  are  to  be  resorted  to  after  all  evidence 
of  acute  inflammation  is  passed.  The  rest  of  the  treatment  is  identical  with 
that  given  for  neuritis. 


NEURITIS  1007 

Obstetrical  or  Birth  Palsy. — A  paralysis  of  brachial  nerves  is  a  frequent 
occurrence  in  difficult  and  protracted  labors,  especially  in  cases  of  breech 
presentation.  Pressure  with  the  finger  or  tenaculum  introduced  into  the 
axilla  in  order  to  facilitate  deUvery  will  injure  the  nerves  and  produce 
paralysis.  In  birth  palsy  the  following  muscles  are  affected:  deltoid,  biceps, 
supinator  longus,  and  infraspinatus.  This  leads  to  inward  rotation  of  the 
arm,  extension  of  the  forearm,  and  pronation  of  the  hand.  The  paralysis 
is  soon  followed  by  atrophy  of  the  muscles.  The  prognosis  of  birth  palsy 
is,  generally  speaking,  favorable,  except  when  reaction  of  degeneration 
exists.  As  to  treatment,  massage  and  electricity  are  the  only  means,  and 
should  commence  as  early  as  possible. 

Multiple  Neuritis.  Definition  and  Etiology.— Multiple  neuritis,  sometimes 
called  "  polyneuritis"  or  "  peripheral  neuritis,"  is  a  condition  in  which  a  large 
number  of  the  peripheral  nerves  of  the  body  suffer  from  subacute  or  chronic 
inflammation  as  a  result  of  the  action  of  some  toxic  agent.  These  toxic 
agents  may  be  derived  from  external  or  internal  sources.  The  external 
agents  are  alcohol,  lead,  arsenic,  copper,  mercury,  anilin,  carbon  monoxide, 
and  carbon  bisulphide.  The  internal  agents  are  the  poisons  developed  in  the 
various  acute  infectious  fevers,  as  typhoid  fever,  smallpox,  scarlet  fever, 
influenza,  erysipelas,  pneumonia,  diphtheria,  dysentery,  and  other  infectious 
maladies.  Occasionally,  too,  a  multiple  neuritis  develops  as  a  complication 
of  septic  infection,  either  that  following  a  wound  or  occurring  during  the 
puerperal  period.  Cases  have  also  been  recorded  in  which  the  toxic  sub- 
stance apparently  has  arisen  from  decomposition  changes  in  the  intestines. 
In  some  instances  syphilis,  tuberculosis,  diabetes  mellitus,  and  malarial  fever 
have  seemed  to  be  provoking  agents,  but  in  all  probability  these  affections 
act  indirectly  by  rendering  the  nerve  trunks  susceptible  to  the  action  of  the 
poison.  A  special  form  of  multiple  neuritis  is  that  which  is  known  as  beri- 
beri or  "  kakke."  (See  Beriberi.)  In  several  instances  small  epidemics  of 
multiple  neuritis  have  been  described.  Multiple  neuritis  occurs  most  fre- 
quently between  the  twentieth  and  the  fiftieth  year  of  age,  and  is  very  rare  in 
children,  unless  it  is  due  to  diphtheria.  Whatever  may  be  the  cause  of  an 
attack  of  multiple  neuritis,  the  pathological  changes  which  are  found  in 
the  affected  nerves  do  not  differ  greatly  from  those  already  described  as 
occurring  in  ordinary  neuritis  of  a  more  limited  extent. 

Symptoms. — The  symptoms  of  multiple  neuritis,  be  the  cailse  what  it  may, 
are  fairly  constant,  although  slight  variations  in  the  character  of  the  symp- 
toms occur  according  to  the  peculiar  influence  exercised  by  the  poison.  As 
alcoholic  neuritis  is  the  type  most  frequently  met  with,  a  description  of  this  dis- 
ease may  be  used  for  all  forms  of  multiple  neuritis.  At  the  beginning  of  the 
malady  there  may  be  some  slight  elevation  of  temperature,  but  in  many  cases 
this  does  not  occur.  The  patient  first  complains  of  tingling  or  numbness  in 
the  feet  and  fingers.  In  other  cases  dull  pain  may  be  experienced.  Rarely 
this  pain  may  be  severe.  These  disturbances  of  sensation  are  usually 
increased  by  moving  the  affected  limb  and  by  deep  or  superficial  pressure 
over  the  nerve  trunks,  and  especially  by  deep  pressure  upon  the  muscle  bellies 
of  the  forearms  and  of  the  calves. 

Following   these   symptoms  weakness  develops,  and  it  may  become  so 


1008  DISEASES  OF  THE  NERVOUS  SYSTEM 

severe  that  the  patient  is  unable  to  move  his  hands  or  feet,  and  foot-drop  or 
wrist-drop  may  develop.  After  the  paralysis  has  lasted  for  some  little  time, 
some  wasting  of  the  muscles  of  the  affected  parts  takes  place.  The  reflexes 
are  diminished  or  altogether  arrested. 

A  peculiarity  of  the  paralysis  of  peripheral  neuritis  is  that  very  often  it  does 
not  involve  all  the  nerves  of  a  limb.  Thus,  it  not  infrequently  happens  that 
the  peroneal  nerves  suffer  chiefly.  In  other  instances  the  tibialis  posticus  is 
chiefly  affected;  and  it  is  only  when  the  condition  is  unusually  severe  that  a 
complete  paraplegia  is  present.  In  the  arms  the  musculospiral  nerve  is  most 
commonly  affected.  It  is  a  noteworthy  fact  that  the  paralysis  is  usually 
symmetrical.  In  some  instances  the  sjmiptoms  are  more  sensory  than  motor, 
but  this  is  rarely  the  case.  Sensory  symptoms  are,  however,  very  con- 
stant in  alcoholic  neuritis,  and  in  most  of  the  other  forms.  They  may,  how- 
ever, be  absent  or  be  very  slight,  as  in  neuritis  due  to  lead,  and  in  such  forms 
of  infectious  disease  as  diphtheria  and  influenza.  These  forms  of  neuritis 
are  often  spoken  of  as  "  motor  neuritis  "  to  indicate  that  the  sensory  functions 
escape. 

In  addition  to  the  numbness  and  tingling  already  mentioned,  patches 
of  anaesthesia  and  hypersesthesia  are  often  found  existing  near  one  another 
or  even  coinciding.  So,  too,  there  may  be  a  hypersensitiveness  to  pain  and 
a  loss  of  the  sense  of  touch,  or  vice  versa. 

Not  infrequently  the  affection  develops  a  train  of  symptoms  which  are  so 
exactly  like  those  met  with  in  locomotor  ataxia  that  even  the  most  skilful 
neurologist  may  have  difficulty  in  differentiating  the  two  diseases.  In  other 
words,  a  so-called  "pseudotabes"  due  to  multiple  neuritis  is  present.  This 
resemblance  depends  upon  the  fact  that  the  fibres  of  "  muscle  sense  "  which 
are  affected  in  their  spinal  course  (posterior  columns)  in  tabes  are  implicated 
in  such  cases  of  multiple  neuritis  at  their  origins  in  the  joints  and  muscle 
fasciae.  The  presence  of  the  Argyll-Robertson  pupil  in  true  ataxia,  how- 
ever, usually  determines  that  the  case  is  not  one  of  peripheral  neuritis. 
As  an  illustration  of  how  closely  multiple  neuritis  may  resemble  locomotor 
ataxia,  cases  have  been  reported  in  which  perforating  ulcer  of  the  foot 
occurred. 

Aside  from  the  trophic  changes  already  spoken  of  as  occurring  in  the  mus- 
cles, local  disorders  of  blood  supply  and  secretion  are  often  present.  There 
may  be  areas  of  skin  which  suffer  from  excessive  sweating-  In  other  cases 
localized  patches  of  oedema  are  found,  and  rarely  the  joints  become  swollen, 
so  that  the  case  resembles  acute  articular  rheumatism.  Actual  breaking 
down  of  the  skin  as  the  result  of  trophic  changes,  however,  rarely  occurs. 
The  bladder  and  rectum  are  usually  unaffected,  and  this  aids  materially 
in  separating  the  paraplegia  of  severe  neuritis  from  that  due  to  myelitis. 
Occasionally,  however,  this  valuable  aid  to  differentiation  fails  us,  and 
retention  or  incontinence  of  urine  or  feces  is  present. 

Associated  with  these  evidences  of  impairment  in  function  in  the 
peripheral  nerves  it  is  not  infrequent  for  disturbances  to  occur  in  connec- 
tion with  intellection.  Confusion  of  thought  and  impairment  of  memory 
are  frequently  present,  occasionally  in  a  peculiar  form  characterized 
by  fabrication  or  "pseudoreminiscence,"  the  patient    relating    imaginary 


NEURITIS  1009 

recent  experiences.  This  mental  condition,  combined  with  multiple 
neuritis,  is  sometimes  called  "Korssakoff's  disease." 

The  cranial  nerves  also  share  in  the  malady.  Indeed,  in  some  instances 
they  suffer  most.  Nystagmus,  or  squint,  may  be  present,  but  the  optic 
nerve  is  not  often  affected,  although  occasionally  it  may  suffer  very  slight 
atrophy.  The  paralysis  of  the  cranial  nerves  may  be  symmetrical.  Thus, 
Oppenheim  has  reported  cases  of  double  facial  palsy  due  to  this  cause. 

Tachycardia  and  interference  with  the  function  of  the  diaphragm  may  be 
manifested  from  the  infection  involving  the  pneumogastric  and  phrenic 
nerves.  Mannaberg  asserts  that  'the  multiple  neuritis  may  be  confined 
entirely  to  the  cranial  nerves. 

When  the  multiple  neuritis  is  due  to  lead,  it  is  a  noteworthy  fact  that  the 
inflammatory  process  is  not,  as  a  rule,  very  widely  distributed,  and  that  the 
sensory  nerve  fibres  usually  escape.  In  association  with  the  symptoms  of 
neuritis,  already  described,  there  may  be  a  history  of  lead  colic,  which  will  aid 
in  determining  the  cause  of  the  paralysis.  The  presence  of  a  blue  line  on  the 
gums  is  also  pathognomonic.  Anaemia  is  often  marked.  Aside  from  the 
fact  that  sensation  is  usually  not  involved,  the  multiple  neuritis  caused  by 
lead  is  noteworthy,  in  that  it  chiefly,  and  it  may  be  exclusively,  affects  the 
extensor  muscles  of  the  hand  and  fingers.  Indeed,  the  paralysis  may  be  so 
localized  in  mild  cases  that  only  the  extensor  communis  digitorum  may  be 
involved,  so  that  the  ring  and  little  finger  cannot  be  extended.  When  the 
paralysis  is  very  marked,  double  drop-wrist  is  present.  Another  peculiarity 
of  lead  palsy  is  that  the  supinators,  especially  the  supinator  longus,  and  the 
triceps,  escape.  The  deltoid,  however,  may  be  partially  paralyzed,  and  the 
abductor  pollicis  longus  and  the  interossei  may  be  palsied.  Occasionally, 
however,  the  supinators  are  affected,  as  is  also  the  biceps.  Muscular  atrophy 
is  nearly  always  marked  in  lead  paralysis,  and  the  reaction  of  degeneration 
usually  speedily  develops.  Muscular  tremor  may  also  be  present.  The 
noteworthy  fact  that  sensation  is  not  disturbed  in  most  cases  may  be  well 
reiterated.  Drop-foot  is  rarely  seen  in  cases  of  lead  paralysis.  Paralysis 
of  the  cranial  nerves  due  to  lead  is  exceedingly  uncommon.  (See  Lead 
Poisoning.) 

When  the  paralysis  is  due  to  arsenic,  it  is  not  infrequently  associated  with 
gastrointestinal  disturbances,  and,  unlike  that  due  to  lead,  it  is  usually  asso- 
ciated with  marked  disturbances  of  sensation  in  the  affected  parts.  W^asting 
of  the  muscles  supplied  by  the  affected  nerves  usually  develops  quite  early. 
Not  only  are  the  extensors  affected,  as  they  are  in  lead  poisoning,  but  the 
flexors  are  also  involved.  Another  point  of  difference  between  arsenical 
paralysis  and  that  due  to  lead  lies  in  the  fact  that  the  lower  extremities  are 
quite  as  frequently  affected  as  the  upper  extremities,  so  that  quadriplegia, 
that  is,  a  paralysis  of  all  four  extremities,  is  present.  Reactions  of  degenera- 
tion speedily  develop.  The  pulse  is  apt  to  be  rapid.  Disturbances  of  the 
psychic  functions  are  said  to  occur,  which  is  rare  in  lead  poisoning,  unless 
encephalopathia  saturnina  is  present.  Symptoms  of  ataxia  are  usually 
marked.  The  reflexes  are  lost,  and  these  two  factors  may  make  the  case 
more  closely  resemble  true  locomotor  ataxia  than  any  other  form  of  multiple 
neuritis.  Nutritional  changes  in  the  skin  are  quite  frequent  in  arsenical 
64 


1010  DISEASES  OF  THE  NERVOUS  SYSTEM 

neuritis.  In  some  instances  herpetic  eruptions  develop.  In  others  the  skin 
becomes  glossy,  and  there  may  be  falling  out  of  the  hair.  It  is  exceedingly 
rare  for  the  cranial  nerves  to  be  involved. 

Of  all  the  forms  of  multiple  neuritis  due  to  toxic  substances  having  their 
origin  in  the  body,  that  due  to  the  poison  of  diphtheria  is  most  frequently 
met  with.  As  diphtheria  is  essentially  a  disease  of  childhood,  it  is  evident 
that  diphtheritic  multiple  neuritis  must  be  more  commonly  met  with  in 
young  persons.  The  peculiarity  of  this  form  of  neuritis  is  that  it  most  fre- 
quently affects  the  muscles  of  the  soft  palate,  changing  the  character  of  the 
speech  and  rendering  swallowing  difficult.  This  paralysis  is  both  motor  and 
sensory,  and  is  often  accompanied  by  wasting.  Sometimes  the  external 
ocular  muscles  are  paralyzed.  In  other  instances  the  internal  ocular 
muscles  suffer  chiefly,  and  accommodation  may  be  paralyzed  as  the  result 
of  oculomotor  involvement.  The  pupillary  reflex  is,  however,  usually  pre- 
served. In  other  instances  the  paralysis  produced  by  diphtheria  is  almost 
universal.  I  have  seen  more  than  one  instance  in  which  the  child  was  not 
only  paralyzed  in  all  its  extremities,  but  was  unable  to  exercise  any  control 
over  the  movements  of  its  head,  and  could  only  svv-allow  when  put  in  such  a 
position  that  the  liquids  could  readily  pass  down  the  gullet.  Such  cases  are 
usually  characterized  not  only  by  loss  of  motor  power,  but  by  loss  of  sensa- 
tion as  well.  The  bladder  and  rectum  usually  escape  the  general  paralysis, 
but  they  may  be  involved.  It  is  a  noteworthy  fact  that  diphtheritic  paralysis 
is  not  a  concomitant  symptom,  but  a  sequel  to  an  attack  of  diphtheria,  and  the 
full  severity  of  the  symptoms  may  not  be  present  for  several  weeks  after  the 
diphtheria  has  ceased.  In  some  instances  the  diaphragm  is  paralyzed,  and 
if  the  nerve  supply  of  the  heart  becomes  affected  sudden  death  may  occur. 
(See  Diphtheria.) 

Diagnosis. — The  presence  of  numbness  and  tingling  followed  by  more  or 
less  impairment  of  motion  and  sensation  in  certain  nerve  trunks,  with  com- 
plete or  partial  escape  of  other  nerve  trunks,  of  course,  points  to  multiple 
neuritis  as  the  cause  of  the  malady,  particularly  if  the  history  of  the  patient 
reveals  the  fact  that  he  or  she  has  been  exposed  to  one  of  the  provoking  causes 
already  named.  In  some  instances  more  than  one  of  these  causes  has  been 
effective,  and,  therefore,  the  precise  factor  in  determining  the  neuritis  cannot 
be  relied  upon.  Thus,  I  have  known  more  than  one  instance  in  which  the 
administration  of  very  large  quantities  of  alcohol  as  a  stimulant  during 
typhoid  fever  has  produced  a  multiple  neuritis,  which  was  attributed  to  a 
typhoid  toxin,  when  in  reality  the  alcohol  was  the  active  agent.  In  those 
cases  in  which  the  paralysis  comes  on  very  rapidly  and  is  severe,  the  differ- 
entiation must  be  made  between  this  condition  and  Landry's  paralysis  (which 
see),  and  this  is  the  more  important  because  Eichhorst  has  described  a  neu- 
ritis acutissima  progressiva.  A  so-called  apoplectiform  type  has  been 
described  by  other  observers-  The  presence  of  the  Argyll-Robertson  pupil, 
optic  nerve  atrophy,  and  the  history  of  exposure  to  a  poison  may  be  the  only 
means  by  which  we  can  differentiate  between  true  locomotor  ataxia  and 
multiple  neuritis. 

Prognosis. — The  prognosis  is  favorable  in  nearly  every  case,  unless  the 
patient  has  been  exposed  to  the  evil  influences  of  lead  or  arsenic  or  alcohol 


NEURITIS  1011 

for  so  long  a  time  that  the  nerves  cannot  undergo  regenerative  change.  In 
cases  of  profound  alcohoHc  intoxication  sudden  death  may  take  place 
when  the  pneumogastric  nerve  becomes  involved.  In  nearly  all  instances 
recovery  is  exceedingly  slow  The  first  symptom  of  improvement  is  a 
diminution  in  the  pain  and  a  decrease  in  tenderness  of  the  nerves  on  pal- 
pation. In  other  instances  the  power  of  motion  returns  before  the  sensory 
functions  are  restored  to  their  normal  condition,  and  inability  to  get  about 
may  be  caused  by  the  intense  hypersensitiveness  of  the  feet.  Even  if  the 
patient  does  not  recover  for  eighteen  months  or  two  years,  the  condition  is 
by  no  means  hopeless.  Care  should  be  taken,  however,  that  complete 
recovery  should  not  be  promised  in  cases  which  have  been  exposed  to  the 
poisons  for  very  long  periods  of  time.  Not  infrequently  great  disappoint- 
ment is  caused  by  periods  in  which  no  improvement  takes  place,  or,  indeed, 
in  which  a  relapse  seems  to  be  threatened. 

The  prognosis  in  multiple  neuritis  due  to  lead  is  good  so  far  as  the  preserva- 
tion of  life  is  concerned.  It  is  bad  in  direct  proportion  to  the  duration  of  the 
condition  and  of  the  exposure  to  the  poison.  The  same  facts  hold  true  in 
regard  to  the  peripheral  neuritis  due  to  arsenic. 

Occasionally  secondary  contractures  occur  as  the  result  of  the  contraction 
of  non-paralyzed  muscles,  whereby  deformities  are  produced. 

After  diphtheria,  even  in  those  cases  in  which  the  paralysis  is  most  severe, 
the  prognosis  is  not  necessarily  very  grave.  The  immediate  danger  is  that 
some  nervous  mechanism  connected  with  a  vital  function  may  be  involved. 
If  this  does  not  occur,  partial  or  complete  recovery  of  motion  or  sensa- 
tion nearly  always  takes  place,  although  twelve  months  may  pass  before 
recovery  occurs.     Usually,  however,  two  or  three  months  is  sufficient. 

Treatment. — The  treatment  of  multiple  neuritis  gives  better  results  than 
that  devoted  to  the  relief  of  any  other  form  of  paralysis.  If  the  cause  of  the 
malady  is  one  of  the  metallic  poisons  already  named,  the  patient  must  be 
removed  from  further  exposure  to  the  poison.  Thus,  workers  in  lead  and 
arsenic  must  cease  following  such  occupations.  For  the  purpose  of  aiding  in 
the  elimination  of  any  of  the  poisons  which  may  remain  in  the  body,  moderate 
doses,  20  to  30  grains,  of  iodide  of  potassium  may  be  given  twice  or  thrice  a 
day.  If  the  patient  uses  alcohol  to  excess,  this  agent  must,  of  course,  be 
withdrawn.  While  the  nerves  are  hypersensitive  to  pressure  and  while  pain 
is  present,  strychnine  and  faradic  electricity  should  not  be  applied  to  them, 
since  they  tend  to  increase  irritation;  but  when  there  is  anasthesia  and  loss 
of  power,  full  doses  of  strychnine  and  phosphorus  are  often  useful,  and  the 
rapidly  interrupted  faradic  current  may  be  used  to  stimulate  the  affected 
nerve  fibres.  Muscles  which  are  suffering  from  loss  of  power  may  be  exer- 
cised by  the  use  of  the  slowly  interrupted  faradic  current.  Massage  may  also 
be  employed,  but  it  is  of  vital  importance  that  no  form  of  exercise  shall  be 
used  to  the  point  of  exhaustion  of  the  affected  parts.  In  other  words,  only 
healthy  exercise  designed  to  improve  the  nutrition  of  the  parts  affected  should 
be  resorted  to. 

If  it  is  thought  that  the  neuritis  is  due  to  toxic  materials  arising  inside 
the  body,  these  should  be  removed,  if  possible.  The  administration  of  laxa- 
tives or  purges  is  usually  needful.     If  ansemia  is  present,  particularly  if  it 


1012  DISEASES  OF   THE  NERVOUS  SYSTEM 

is  associated  with  septic  conditions,  such  as  are  met  with  in  sepsis  and  puer- 
peral fever,  iron  and  arsenic  are  useful.  If  the  patient  is  rheumatic  or  of  gouty 
tendency,  hot  baths,  or  a  visit  to  any  of  the  well-known  hot  springs  may  be 
resorted  to,  and  the  various  salicylates  or  iodides  should  be  administered 
in  sufficiently  full  doses  to  produce  mild  physiological  effects.  For  the  pur- 
pose of  aiding  in  the  elimination  of  toxic  materials,  pure  water  should  be 
drunk  freely  to  flush  the  kidneys,  and  Turkish  baths  may  be  taken  to  produce 
sweating.  Pain  is  to  be  relieved  by  the  use  of  such  remedies  as  phenacetin  or 
acetanilid,  and  by  hot  applications  to  those  areas  which  suffer  most.  Some- 
times the  application  of  splints  to  provide  perfect  rest  for  the  painful  part  is 
useful. 

In  those  forms  of  multiple  neuritis  which  depend  upon  infection,  such  as 
diphtheria,  smallpox,  or  typhoid  fever,  the  heart  should  be  carefully  exam- 
ined, and  if  any  evidences  of  tachycardia,  bradycardia,  or  arhythmia  are 
present,  the  patient  should  be  warned  against  sitting  up  in  bed,  and  should 
be  protected  from  all  causes  which  may  throw  an  increased  strain  upon  the 
circulation.  This  is  particularly  important  in  diphtheritic  multiple  neuritis. 
Contractures  should  be  prevented  by  massage  and  Swedish  movements  and 
remedied,  if  they  occur,  by  tenotomy. 


DISEASES  OF  THE  CRANIAL  NERVES. 

The  Olfactory  Nerve. — Disease  of  the  olfactory  nerve,  of  course,  inter- 
feres with  the  special  sense  of  smell,  and  if  this  sense  is  entirely  lost  the 
condition  is  called  anosmia.  Partial  or  complete  loss  of  this  sense  results 
from  lesions  of  the  peripheral  ending  of  the  nerve  in  the  nasal  mucous 
membrane  and  from  pathological  states  of  the  tissues  beneath  it,  such  as 
morbid  growths  or  disease  of  the  ethmoid  bones.  Similar  loss  of  function 
results  from  meningitis,  from  injury  of  the  bones  forming  the  base  of  the 
skull,  or  morbid  growths  affecting  these  bones.  Tumors  of  the  brain  may 
destroy  the  olfactory  nerves  or  the  olfactory  bulbs.  When  complete  loss  of 
the  sense  of  smell  occurs  and  no  local  lesion  in  the  nasal  bones  or  mucous 
membranes  is  present,  it  is  usually  an  evidence  of  a  tumor  or  abscess  in  the 
anterior  cranial  fossa. 

The  Optic  Nerve. — The  optic  tract  of  either  side  arises  by  two  roots  from 
structures  in  the  midbrain  called  the  primary  optic  centres.  These  struc- 
tures are  the  external  geniculate  body,  the  posterior  part  (pulvinar)  of  the 
optic  thalamus,  and  the  anterior  quadrigeminal  body. 

It  is  important  to  remember  that  the  fibres  from  the  optic  tract  undergo 
partial  decussation  in  the  chiasm.  The  outer  fibres  do  not  decussate  and  they 
connect  the  outer  half  of  the  retina  with  the  primary  optic  centres  of  the  same 
side.  The  inner  fibres,  on  the  other  hand,  all  cross  to  the  opposite  side,  and 
they  connect  the  inner  half  of  the  retina  with  the  nuclei  on  the  opposite  side. 
It  is  evident,  therefore,  that  the  right  optic  tract  contains  fibres  which  carry 
impulses  from  the  right  halves  of  both  retinae  to  the  right  side  of  the  brain, 
and  that  the  left  optic  tract  contains  fibres  which  convey  impulses  from  the 
left  halves  of  both  retipse  to  the  left  side  of  the  brain.    It  is  essential  to  remem- 


DISEASES  OF   THE  CRANIAL  NERVES  1013 

ber  these  facts  in  order  to  understand  the  condition  known  as  hemianopsia, 
which  will  be  described  shortly. 

Optic  neuritis,  sometimes  called  papillitis,  is  an  inflammatory  condition 
which  is  manifest  in  the  intraocular  end  of  the  nerve,  and  it  may  be  due 
to  several  causes.  In  the  great  majority  of  cases  it  is  due  to  brain  tumor. 
Choked  disk  is  an  oedematous  state.  The  degree  of  neuritis  has  no  direct 
relationship  to  the  size  of  the  tumor,  nor  to  the  area  of  the  brain  which  it 
affects,  although  a  tumor  of  the  corpora  quadrigemina  seems  to  cause  the 
condition  more  commonly  than  do  growths  elsewhere.  Tumor  of  the  parieto- 
occipital region  and  of  the  cerebellum  also  produces  papillitis  in  a  large 
proportion  of  cases  in  which  these  growths  occur,  while  a  tumor  of  the 
frontal  lobes  of  the  cerebrum  very  rarely  causes  it.  The  condition  is  not 
materially  affected  as  to  frequency  or  severity  by  the  character  of  the  growth. 
Meningitis  in  any  of  its  forms  may  cause  papillitis,  but  tuberculous  meningitis 
does  so  more  commonly  than  any  other  form.  Rarer  causes  are  cerebral 
softening,  inflammation,  and  atrophy,  or  any  cause,  such  as  aneurysm  or 
hydrocephalus,  which  produces  an  increase  in  intracranial  pressure.  Very 
rarely  disseminated  sclerosis,  general  paresis,  or  myelitis  may  cause  papil- 
litis, as  may  the  various  acute  infectious  diseases,  or  the  excessive  use  of 
alcohol,  or  lead  poisoning. 

Symptoms. — There  are  often  no  symptoms  whatever  which  point  to  optic 
neuritis,  at  least  in  so  far  as  the  patient  complains  of  impairment  of  vision. 
The  diagnosis  rests  solely  upon  the  use  of  the  ophthalmoscope  and  upon  a 
study  of  the  fields  of  vision.  The  ophthalmoscope  reveals  an  indefinite  out- 
line of  the  head  of  the  nerve,  with  redness,  followed  by  swelling  of  the  papilla, 
which  becomes  grayish  in  hue.  Finally,  the  disk  protrudes,  its  outlifies 
become  lost  and  whitish  patches  may  be  seen  upon  its  surface.  The  retinal 
arteries  are  contracted  and  the  veins  congested  and  tortuous.  At  the  point  of 
exit  and  entrance  of  the  vessels  this  part  may  seem  devoid  of  vessels,  because 
they  are  hidden  in  the  infiltrated  mass.  Small,  narrow,  flame-like  hemor- 
rhages may  be  seen  along  the  vessel  walls.  The  field  of  vision  is  concentrically 
contracted,  and  the  perception  of  red  and  green  is  lost  before  the  other  color 
senses  are  destroyed.  Hemianopsia  is  present  if  the  lesion  is  so  situated  as 
to  cause  this  symptom. 

Another  form  of  optic  neuritis,  called  retrobulbar  neuritis,  exists  in  which 
the  inflammatory  process  develops  in  the  optic  nerve  in  the  orbit.  In  the 
acute  form  the  symptoms  consist  in  dimness  of  vision  which  always  occurs 
in  the  centre  of  the  field,  and  which  may  end  in  complete  blindness  in  from 
one  to  eight  days.  With  the  ophthalmoscope,  when  the  disease  is  well 
developed,  the  edges  of  the  disk  are  seen  to  be  indistinct,  its  surface  hyper- 
semic,  and  its  main  bloodvessels  shrunken.  The  cause  of  the  acute  form  is 
usually  some  one  of  the  acute  infections,  such  as  influenza,  scarlet  fever, 
or  one  of  the  diathetic  diseases,  such  as  rheumatism,  gout,  and  sometimes 
syphilis. 

The  treatment  of  retrobulbar  neuritis  consists  in  the  production  of  profuse 
sweating  by  pilocarpine,  the  use  of  large  doses  of  the  salicylates  if  gout  or 
rheumatism  is  present,  or  the  employment  of  mercury  and  the  iodides  if 
syphilis  is  suspected.     Counterirritation  on  the  temple  is  also  advisable. 


1014  DISEASES  OF  THE  NERVOUS  SYSTEM 

The  chronic  form  of  retrobulbar  neuritis  is  usually  a  toxic  condition  pro- 
duced, in  the  majority  of  instances,  by  tobacco,  alcohol,  arsenic,  lead,  or 
poisons  made  by  infectious  diseases.  Its  symptoms  consist  in  diminution 
of  vision  and  in  color  scotomata.  The  prognosis  when  the  cause  is  tobacco 
and  alcohol  is  good,  if  the  patient  will  give  up  these  drugs  and  if  he  does  so 
in  the  early  stages  of  the  disease;  otherwise  the  prognosis  is  bad. 

The  treatment  consists  in  the  elimination  of  the  causes  as  far  as  possible, 
in  the  use  of  massive  doses  of  strychnine,  and  the  employment  of  the  iodides 
and  free  sweating. 

Treatment. — -This  depends  upon  the  cause.  If  it  is  due  to  brain  tumor  or 
abscess,  operative  treatment  is  required,  unless  a  gummatous  growth  is 
present,  when  mercury  and  the  iodides  are  needful.  Trephining  of  the 
skull  to  relieve  pressure  may  be  resorted  to  as  a  palliative  measure  in  cases 
where  a  growth  cannot  be  removed. 

Optic  Atrophy. — Atrophy  of  the  optic  nerve,  as  its  name  implies,  is  a 
condition  in  which  a  degenerative  process  affects  its  fibres.  It  is  divided 
into  five  forms:  the  primary,  secondary,  consecutive,  retinitic,  and  choroi- 
ditic  atrophy.    The  last  two  forms  are  really  of  the  consecutive  class. 

Etiology. — Primary  atrophy  of  the  optic  nerve  has  been  thought  to  be 
due  to  impaired  nutrition,  sexual  excesses,  and  to  such  diseases  as  chronic 
malarial  infection,  diabetes,  syphilis,  and  to  the  overaction  of  certain  drugs. 
The  most  important  causes  of  primary  optic  atrophy  are  diseases  of  the 
spinal  cord,  notably  locomotor  ataxia.  It  is  also  seen  in  cases  of  general 
paresis  and  disseminated  sclerosis.  In  many  instances  the  optic  atrophy 
may  be  one  of  the  early  symptoms  of  ataxia.  It  has  also  been  met  with  in 
cases  of  lateral  sclerosis,  chronic  myelitis,  and  bulbar  palsy. 

Secondary  atrophy  arises  from  causes  which  produce  pressure  upon  the 
optic  tract  and  the  optic  fibres,  as,  for  example,  the  growth  of  a  tumor  or  an 
aneurysm,  or  meningitis.  So,  too,  injuries  to  the  head  sometimes  produce 
atrophy.     Consecutive  atrophy  follows  the  various  forms  of  optic  neuritis. 

Pathology. — ^The  axones  lose  their  medullary  sheaths  and  are  converted 
into  fine  fibrils,  between  which  are  interspersed  numerous  fatty  granules. 
When  the  condition  is  far  advanced,  the  nerve  elements  entirely  disappear 
and  there  is  a  marked  increase  in  connective-tissue  formation. 

Symptoms. — The  subjective  symptom  complained  of  by  the  patient  is 
diminution  in  the  acuity  of  vision.  The  other  symptoms  are  developed  by 
the  use  of  the  ophthalmoscope.  When  this  instrument  is  used  it  is  found 
that  the  optic  disk  is  gray  or  greenish-gray,  or  actually  white  in  color,  although 
there  may  be  patches  of  red  throughout  it.  The  centre  of  the  disk  is  depressed 
in  direct  proportion  to  the  degree  of  atrophy  which  has  taken  place.  The 
margin  of  the  disk  is  distinct,  and  in  some  cases,  when  the  condition  of  the 
optic  nerve  is  due  to  disease  of  the  spinal  cord,  there  is  broadening  of 
the  normal  scleral  ring.  The  bloodvessels  are  narrowed,  but  in  some  cases 
only  the  arteries  seem  to  be  affected,  the  veins  escaping.  An  examination 
of  the  central  vision  shows  that  it  is  markedly  impaired,  or  absolute  blindness 
may  be  present.  The  field  of  vision  is  greatly  narrowed  and  there  may  be  a 
cerdral  scotoma  or  hemianopsia.  The  color  fields  are  markedly  diminished, 
the  green  being  most  affected;  after  it  the  red,  and  then  the  blue  and  yellow. 


DISEASES  OF  THE  CRANIAL  NERVES  ]015 

Sometimes  the  field  for  red  is  first  affected.  The  pupil  usually  manifests 
some  degree  of  paralytic  dilatation,  and  when  the  nerve  is  completely  atro- 
phied the  pupil  is  dilated  and  the  iris  motionless.  In  secondary  atrophy 
the  disk  is  apt  to  be  whiter  than  in  the  primary  forms,  when  it  is  usually  gray. 
In  that  form  of  optic  nerve  atrophy  called  retinitic  and  choroiditic  atrophy, 
the  disk  is  often  slightly  yellowish  in  hue,  but  its  borders  are  not  distinct. 

Diagnosis, — The  mere  discovery  that  the  optic  disk  is  grayer  than  normal 
and  that  its  margins  are  sharply  defined,  does  not  justify  the  diagnosis  of 
optic  atrophy.  If,  however,  any  of  the  diseases  so  far  named  are  also  present, 
such  a  diagnosis  is  usually  correct. 

Prognosis. — The  prognosis  as  to  complete  recovery  is  bad.  On  the  other 
hand,  it  must  be  remembered  that  the  atrophic  process  is  often  a  slow  one 
which  may  last  for  years.  Indeed,  the  prognosis  in  secondary  cases  depends 
largely  upon  the  rapidity  with  which  the  underlying  disease  is  advancing. 

Treatment. — The  treatment  consists  in  the  administration  of  full  doses  of 
mercury  and  the  iodides  if  there  is  any  suspicion  that  a  recent  or  ancient 
syphilitic  infection  has  been  present.  Strychnine  in  large  doses  combined 
with  nitroglycerin  is  also  useful. 

Of  the  functional  disorders  of  the  optic  nerve  the  most  important  are 
blindness  due  to  uraemia,  that  due  to  diabetes,  malaria,  profound  ana:mia, 
and  the  abuse  of  drugs.  When  uraemia  is  the  cause  the  presence  of  the 
symptoms  of  that  condition,  in  association  with  dimness  of  vision  or  blind- 
ness, make  the  diagnosis  clear.  The  so-called  albuminuric  retinitis  may  be 
present,  but  the  ophthalmoscope  may,  however,  reveal  no  morbid  changes. 
If  the  patient  survives,  vision  usually  returns. 

When  the  dimness  of  vision  is  due  to  diabetes,  the  prognosis  is  unfavorable 
because  the  disease  is  incurable.  That  form  which  is  due  to  malarial  infec- 
tion has  associated  with  it  other  symptoms  of  this  disease.  Recovery 
usually  takes  place  if  proper  treatment  is  administered.  So,  too,  in  cases 
of  dimness  of  vision,  due  to  hemorrhage  and  profound  ansemia,  the  prog- 
nosis is  good,  unless  the  anaemia  is  one  of  the  so-called  essential  anaemias 
which  always  go  from  bad  to  worse.  The  treatment  in  such  a  case  consists, 
of  course,  in  the  use  of  drugs  designed  to  combat  anaemia. 

Hemianopsia. — Hemianopsia,  or  blindness  of  one-half  of  the  visual  field, 
occurs  in  three  forms:  that  known  as  bitemporal  hemianopsia,  binasal  hem- 
ianopsia, and  homonymous  hemianopsia,  each  variety  being  named  not 
from  that  part  of  the  retina  which  is  blind,  but  from  the  visual  field  which  is 
affected.  In  the  first  there  is  loss  of  vision  in  both  temporal  fields,  in  the 
second  in  the  nasal  half  of  each  eye,  and  in  the  third  form  the  same  side  of 
each  eye  is  lacking  in  function — that  is,  for  example,  the  outer  half  of  the 
left  eye  and  the  inner  half  of  the  right  eye.  When  the  left  half  of  each  retina 
is  inactive,  the  condition  is  called  right  homonymous  bilateral  hemianopsia, 
and  when  the  right  half  is  functionless  it  is  designated  left  homonjTnous 
bilateral  hemianopsia.  Homonymous  hemianopsia  is  the  most  common. 
Binasal  hemianopsia  is  very  rare.  Bitemporal  hemianopsia  is  produced  by 
a  lesion,  such  as  a  tumor  or  an  aneurysm,  which  presses  upon  the  middle  of 
the  chiasm.  Homonymous  lateral  hemianopsia  is  produced  by  a  lesion  of 
one  optic  path  at  any  point  back  of  the  chiasm,  either  in  the  neighborhood 


1016 


DISEASES  OF   THE  NERVOUS  SYSTEM 


of  the  calcarine  fissure  (occipital  lobe),  in  the  optic  radiations,  including  the 
point  where  they  pass  just  back  of  the  internal  capsule,  in  the  primary  optic 


Fig.  128 


j^eft  Eye 


Tisu^FYela 


The  visual  tract.  The  result  of  a  lesion  anywhere  between  the  chiasm  and  the  cuneus  is  to  produce 
homonymous  hemianopsia.  H.  Lesion  at  chiasm  causing  bilateral  temporal  hemianopsia.  N.  Lesion  at 
chiasm  causing  unilateral  nasal  hemianopsia.  T.  Lesion  at  chiasm  causing  unilateral  temporal  hemi- 
anopsia. SN.  Substantia  nigra  of  crus.  L.  Lemniscus  in  crus.  RN.  Red  nucleus.  III.  Third  nerves. 
P,  Q,  R,  S,  U.  Lesions  in  the  occipital  lobe  and  in  front  of  it,  producing  left  homonymous  lateral 
hemianopsia. 

centres,  or  in  the  optic  tract.     (See  Fig.  128.)    It  is  important  to  remember 
that  the  lesion  in  cases  of  hemianopsia  is  on  the  opposite  side  to  that  of  the 


DISEASES  OF   THE  CRANIAL  NERVES 


1017 


dark  field.^  (See  Fig.  129.)  De  Schweinitz  has  condensed  the  following 
rules  as  to  the  significance  of  various  forms  of  hemianopsia  from  a  series 
prepared  by  Dr.  Seguin: 

(a)  The  lesion  in  hemianopsia  is  on  the  opposite  side  of  the  dark 
fields. 

(b)  If  the  preserved  fields  are  accompanied  by  concentric  contraction, 
the  smaller  half-field  will  be  in  the  eye  opposite  to  the  lesion;  contraction  of 
the  preserved  half-field  is  most  common  with  lesions  of  the  cortex,  but  also 
may  occur  in  lesions  of  the  tractus. 

Fig.   129 

I4EFT  VISUAL  FIELD.    RIGHT  VISUAL  FIELD , 
Fixation  Point.  Fixation  Poi/if. 


Diagram  illustrating  why  it  is  that  the  lesion  is  on  the  opposite  side  to  the  dark  field.    (Oliver.) 

(c)  If  the  hemianopsia  is  relative,  the  lesion  is  probably  in  the  cortex; 
but  cortical  lesions  are  not  excluded  by  absolute  hemianopsia. 

(d)  A  lesion  confined  to  the  cuneus,  or  to  it  and  the  gray  matter  immedi- 
ately surrounding  it,  on  the  mesial  surface  of  the  occipital  lobe,  produces 
homonymous  lateral  hemianopsia  without  motor  or  sensory  symptoms,  at 
least  without  these  as  a  direct  consequence  of  the  lesion,  although  they  may 
appear  as  indirect  or,  as  they  are  sometimes  called,  distant  symptoms. 
Slight  motor  symptoms  such  as  deviation  of  one  eye  inward  may,  however, 
be  added  to  the  visual  symptoms  of  a  lesion  in  the  occipital  lobe  (Mills). 

(e)  A  iCsion  producing  typical  hemiplegia,  aphasia,  if  the  right  side  is 


1  For  a  more  complete  study  of  the  significance  of  this  difficult  subject  see  the  author's  Practical 
Diagnosis,  fifth  edition. 


1018 


DISEASES  OF   THE  NERVOUS  SYSTEM 


IV 


paralyzed,  little  or  no  anaesthesia,  and  lateral    hemianopsia,  is  probably 
due  to  disease  in  the  area  supplied  by  the  middle  cerebral  artery. 

(/)  A  lesion  causing  hemiplegia,  hemianaesthesia,  and  lateral  hemianopsia 
is  probably  situated  in  the  posterior  portion  of  the  internal  capsule. 

(g)  A  lesion  causing  hemiansesthesia,  ataxic  movements  of  one-half  of  the 
body,  no  distinct  hemiplegia,  and  lateral  hemianopsia,  could  be  situated  in 
the  posterior  lateral  part  of  the  optic  thalamus. 

(h)  A  lesion  causing  the  symptoms  of  disease  of  the  base  of  the  brain, 
associated  at  the  same  time  with  changes  in  the  pupil,  changes  in  the  nerve 

head,     and     lateral     hemianopsia, 

^^°^  ^^^  could  be  situated  in  one  optic  tract 

or  in  the  primary  optic  centres  on 

one  side. 

-  f  (i)   Incomplete  hemianopsia,  as- 

'  ~  suming  usually  a  quadrant-shaped 

defect,  may  be  present  on  account  of 

a  lesion  confined  to  the  lower  half  of 

the  cuneus.    It  may  also  occur  with 

less  definite   limitations  in  lesions 

,     y  j^       t^-    \  III  of  the  subcortical  substance  of  the 

occipital  lobe,  and  then  may  be 
associated  with  other  symptoms, 
as  hemiplegia  and  hemianaesthesia. 
Finally,  it  may  occur  from  a  lesion 
of  the  tract,  but  then  will  be  accom- 
panied by  other  symptoms  indicating 
basal  disease,  or  from  a  lesion  of 
the  external  geniculate  body. 

(j)  A  hemianopsia  in  which  there 
is  preservation  of  the  light  sense,  but 
loss  of  either  the  color  sense  or  the 
form  sense,  indicates  that  the  lesion 
is  in  the  visual  centre  of  the  cortex. 
The  Third  or  Oculomotor  Nerve. 
— The  third  nerve  has  its  origin 
from  groups  of  cells  in  the  floor  of 
the  aqueduct  of  Sylvius.  It  then 
passes  through  the  tegmentum  of  the 
crus  cerebri,  and  makes  its  exit  in  a 
bundle  on  the  inner  side  of  the  crus. 
(Fig.  130;  see  also  Plate  IX.)  It 
then  passes  from  the  crus  to  the 
sphenoidal  fissure  and  so  into  the 
orbit,  where  its  fibres  divide  and  go 
to  supply  the  ciliary  muscle,  the  sphincter  of  the  iris,  the  superior  rectus, 
internal  rectus,  inferior  rectus  and  inferior  oblique  muscle.  (See  Plate  VIII.) 
It  also  sends  fibres  to  the  levator  palpebrae  muscle.  As  it  is  a  motor  nerve, 
paralysis  follows  its  injury.    The  causes  of  disturbance  in  its  function  are 


Showing  the  nearness  of  origin  of  the  oculomotor 
(3),  pathetic  (4),  and  abducens  (6).  The  roots  ot 
these  nerves  are  shown  by  an  incision  which  has 
divided  the  pons.  III.  The  third  nerve,  arising  from 
several  roots.  IV.  The  fourth  nerve.  VI.  The  sixth 
nerve,  arising  from  three  roots.  (Modified  from 
Arnold.) 


PLATE  VIII. 


Shio>A'^ing  the  Distribution  of  the  Troehlearis,  Oculomotor,  and 
Trifacial  Nerves.     (Modified  from  Riadinger.) 

1.  The  troehlearis  nerve. 

2,  3,  4,  5,  6,  7.     The  oculomotor  nerve  fibres. 
8,  9,  10,  11.     The  trifacial  fibres. 


PLATE  IX. 


Base  of  Brain,  sh.o"wing  the  Superficial  Origin  of  the  Cranial 

Nerves. 


The  Roman  numerals  refer  to  the  twelve  cranial  nerves. 


DISEASES  OF   THE  CRANIAL  NERVES  1019 

numerous.  They  may  exist  at  the  base  of  the  brain,  where  the  nerve  leaves 
the  crus,  in  the  sphenoidal  fissure,  in  the  orbit,  and  even  in  its  peripheral 
filaments  in  the  eye  itself,  although  change  in  its  functional  activity  in  the 
latter  area  is  usually  due  to  the  effect  of  drugs.  Of  the  causes  which  pro- 
duce disturbance  of  its  function  at  its  origin  in  the  crus,  we  find  tuberculous 
meningitis  or  that  due  to  some  acute  infectious  disease,  abscess  of  the  brain, 
and  hemorrhage.  For  this  reason  meningitis  of  either  form  in  infancy  very 
frequently  involves  this  nerve,  and  so  produces  symptoms  which  call  the 
attention  of  the  physician  to  the  existence  of  the  disease  at  the  base 
of  the  brain.  In  adults,  aside  from  tuberculous  meningitis,  there  may  be 
syphilitic  exudation,  or  the  nerve  itself  may  be  inflamed,  owing  to  the 
presence  of  this  same  disease.  Tumors  or  abscess  at  the  base  of  the 
brain  may  press  upon  it.  When  the  nerve  is  injured  in  its  passage  through 
the  sphenoidal  fissure,  the  cause  is  usually  some  traumatism  which  results 
in  fracture  of  the  bone,  or  very  rarely  a  severe  blow  which  damages  the 
nerve  by  pressure  against  the  bone.  In  a  case  which  came  to  the  writer's 
attention,  a  severe  blow  with  the  hilt  of  a  sword  upon  the  forehead  caused 
paralysis  of  this  nerve,  probably  in  this  manner. 

In  the  orbit  a  tumor  may  press  upon  the  nerve  fibres.  Occasionally  the 
nerve  loses  power  through  the  action  of  the  poison  produced  by  diphtheria 
or  typhoid  fever. 

Symptoms. — The  dominant  symptoms  of  paralysis  of  the  oculomotor 
nerve  are  ptosis,  mydriasis,  and  consequent  loss  of  pupillary  reaction  to  light 
and  accommodation.  As  it  supplies  the  internal  rectus,  external  squint  may 
be  present.  The  paralysis  of  the  ocular  muscles  also  results  in  diplopia. 
If  the  patient  is  directed  to  look  upward,  downward,  or  inward  he  is  unable 
to  do  so.  The  inability  of  the  pupil  to  contract  when  light  is  thrown  into  the 
eye  may  be  due  to  a  lesion  of  the  nerve  before  it  enters  the  orbit,  or,  as 
already  stated,  to  the  action  of  a  drug  upon  its  peripheral  filaments.  It  will 
be  remembered  that  pupillary  contraction,  when  produced  by  the  entrance 
of  light  into  the  eye,  is  due  to  a  reflex  impulse  which  passes  along  the  optic 
nerve  to  the  neighborhood  of  the  corpora  quadrigemina,  thence  to  the  third 
nucleus  and  along  the  fibres  of  the  third  nerve  to  the  ciliary  ganglion,  from 
which,  by  way  of  the  ciliary  nerves,  it  goes  to  the  iris  and  causes  contraction 
of  its  circular  muscular  fibres.  A  lesion  in  any  portion  of  this  reflex  arc 
interferes  with  pupillary  reaction.  In  addition  to  those  injuries  of  the  oculo- 
motor nerve  already  mentioned  which  cause  paralysis,  a  loss  of  pupillary 
reaction  may  occur  in  locomotor  ataxia,  in  multiple  sclerosis,  in  general 
paresis,  in  bulbar  palsy,  and  in  myelitis  when  that  disease  involves  the  fibres 
of  the  arc.  When  these  diseases  are  responsible  for  the  loss  of  pupillary 
reaction,  the  lesion  is  supposed  to  exist,  in  the  majority  of  instances,  in 
fibres  which  connect  the  optic  tracts  in  front  of  the  corpora  quadrigemina 
with  the  oculomotor  nuclei.  When  drugs  produce  paralytic  mydriasis, 
their  action  is  usually  exercised  upon  the  peripheral  ends  of  the  nerve. 

Diagnosis. — The  diagnosis  of  paralysis  of  the  oculomotor  nerve  is  readily 
made  if  the  symptoms  just  described  are  kept  in  mind. 

Prognosis. — The  prognosis  depends  upon  the  underlying  cause  of  the 
paralysis.     In  diphtheria  and  typhoid  fever  recovery  usually  takes  place, 


1020  DISEASES  OF   THE  NERVOUS  SYSTEM 

and  unless  the  damage  produced  by  an  injury  is  very  great,  the  outlook  is 
favorable.  On  the  other  hand,  if  the  cause  is  tuberculous  meningitis,  tumor, 
or  abscess,  or  any  one  of  the  progressive  nerve  diseases  just  named,  recovery 
is,  of  course   impossible. 

The  Fourth  or  Trochlearis  Nerve.  This  nerve  supplies  the  superior 
oblique  muscle  of  the  eye  (1,  Plate  VIII.).  Interference  with  the  action  of  this 
nerve  is  not  uncommon  and  is  rarely  recognized  by  the  general  practitioner. 
The  symptoms  are  not  developed  until  the  eye  is  tested  bymeansof  placingacol- 
ored  glass  over  one  eye,  when  it  will  be  found  that  the  object  which  is  placed 
before  the  patient  stands  in  its  normal  position  as  seen  by  the  normal  eye,  but  is 
displayed  outward  and  obliquely  when  seen  by  the  eye  supplied  by  the  im- 
paired pathetic  nerve.  As  the  nerve  arises  from  an  area  almost  identical  with 
that  of  the  third  nerve,  the  centric  causes  of  trochlearis  paralysis  are  practically 
identical  with  the  causes  of  oculomotor  paralysis.  It  is  important  to  remem- 
ber that,  should  paralysis  of  the  fourth  nerve  be  present  without  involvement 
of  the  third  or  sixth  nerve,  it  probably  indicates  a  growth  in  the  cerebel- 
lum or  an  inflammatory  exudate  upon  the  under  surface  of  its  middle 
lobe 

The  Fifth  or  Trifacial  Nerve. — The  trifacial  nerve  contains  motor  and 
sensory  fibres,  the  sensory  fibres  being  by  far  the  more  numerous.  The 
motor  fibres  have  their  origin  in  the  pons,  a  little  above  its  middle,  receiving 
also  the  root  descending  from  the  midbrain;  they  pass  out  in  a  bundle  sepa- 
rate from  the  sensory  fibres  until,  outside  the  cranial  cavity,  they  take  part 
in  forming  the  inferior  maxillary  division  of  the  nerve,  through  which  they 
supply  the  muscles  of  mastication. 

The  sensory  fibres  of  the  fifth  nerve  arise  from  a  nucleus  at  about  the 
middle  of  the  pons,  and,  in  addition,  by  the  spinal  root,  from  a  chain  of  cells 
descending  through  the  medulla  as  far  as  the  first  cervical  segment  of  the 
cord;  they  emerge  from  the  pons  in  a  heavy  trunk,  which  passes  to  the 
Gasserian  ganglion  (8,  Plate  VIII.)  and  then,  beyond  the  ganglion,  divides 
into  three  branches:  ophthalmic  (9),  superior  (10),  and  inferior  maxillary 
(11).  In  addition  to  providing  sensation  to  the  greater  portion  of  the 
face,  it  also  supplies  the  anterior  two-thirds  of  the  tongue. 

Symptoms. — When  the  fifth  or  trifacial  nerve  is  paralyzed  in  its  motor 
fibres,  the  patient  is  unable  to  contract  his  masseter  muscles  and  there  is 
dropping  of  the  lower  jaw.  Unless  the  paralysis  is  bilateral,  however,  it  may 
not  be  easily  discovered,  since  the  muscles  on  the  unaffected  side  may  hold 
the  jaw  in  position.  And,  moreover,  if  the  lesion  be  in  the  brain  the  function 
of  mastication  is  maintained  from  the  other  side  by  bilateral  innervation. 
In  some  instances  of  paralysis  of  the  fifth  nerve,  deafness  arises  as  the  result 
of  interference  with  the  function  of  the  tensor  tympani  muscle,  for  a  small 
branch  from  the  motor  fibres  of  the  fifth  nerve  passes  through  the  otic 
ganglion  and  supplies  this  muscle.  When  this  muscle  is  paralyzed,  the 
tympanic  membrane  is  relaxed  and  this  interferes  with  its  function.  Motor 
paralysis  of  the  fifth  nerve  is  rarely  met  with.  Certain  poisons  like  gelsemium 
may  cause  dropping  of  the  jaw  by  paralyzing  the  muscles  of  both  sides. 
When  the  sensory  portion  of  the  nerve  is  affected  there  is  anaesthesia  of  the 
skin  of  the  face  in  the  areas  supplied  by  the  particular  branches  affected. 


DISEASES  OF  THE  CRANIAL  NERVES  1021 

If  the  area  be  that  of  the  forehead,  the  upper  eyelid,  the  conjunctiva,  and 
the  nostril,  the  ophthalmic  branch  of  the  fifth  nerve  is  at  fault,  and  the 
lesion  is  probably  at  the  sphenoidal  fissure  or  within  the  orbit,  reflex  wink- 
ing of  the  eye  no  longer  takes  place  because  the  conjunctiva  is  anaesthetic, 
and  for  the  same  reason  a  flow  of  tears  does  not  occur  upon  irritating  the 
conjunctiva,  because  the  lachrymal  reflex  is  abolished. 

If  the  skin  of  the  upper  part  of  the  face  is  anaesthetic,  the  superior  maxil- 
lary branch  is  involved;  and  if  the  skin  of  the  temporal  region  and  that  of 
the  jaw  and  the  under  lip  are  anaesthetic,  the  inferior  maxillary  branch  is 
diseased.  When  both  of  these  branches  are  paralyzed  there  is  probably  a 
tumor  of  the  superior  maxillary  bone;  and  if  the  entire  area  of  the  three 
branches  is  anaesthetic,  the  Gasserian  ganglion  may  be  the  part  affected, 
and  this  will  be  accompanied  by  trophic  changes  in  the  anaesthetic  parts. 
The  most  common  cause  of  anaesthesia  of  the  trifacial  is,  however,  neuritis. 

Romberg  makes  the  following  differential  statement: 

(a)  The  more  the  anaesthesia  is  confined  to  single  filaments  of  the  tri- 
geminus, the  more  peripheral  the  seat  of  the  cause  will  be  found  to  be. 

(6)  If  the  loss  of  sensation  affects  a  portion  of  the  facial  surface,  together 
with  the  corresponding  faucial  membrane,  the  disease  may  be  assumed  to 
involve  the  sensory  fibres  of  the  fifth  pair  before  they  separate  to  be  dis- 
tributed to  their  respective  destinations;  in  other  words,  a  main  division 
must  be  afi^ected  before  or  after  its  passage  through  the  cranium. 

(c)  When  the  entire  sensory  tract  of  the  fifth  nerve  has  lest  its  power,  and 
there  are  at  the  same  time  derangements  of  the  nutritive  functions  in  the 
affected  parts,  the  Gasserian  ganglion,  or  the  nerve  in  its  immediate  vicinity, 
is  the  seat  of  the  disease. 

(d)  If  the  anaesthesia  of  the  fifth  nerve  is  complicated  with  disturbed  func- 
tions of  adjacent  cerebral  nerves,  it  may  be  assumed  that  the  cause  is  seated 
at  the  base  of  the  brain. 

When  the  fifth  nerve  is  paralyzed  the  mucous  membrane  of  the  nose 
and  mouth  are  also  ancesthetic  and  usually  dry.  The  sense  of  taste  is  lost 
and  trophic  lesions  may  develop,  although  it  is  questionable  as  to  whether 
these  depend  upon  affection  of  the  sensory  fibres.  These  lesions  consist  in 
ulceration  of  the  cornea,  loosening  of  the  teeth,  atrophy  of  the  gums,  and  the 
development  of  herpes  zoster.  As  the  sensation  in  the  anterior  two-thirds  of 
the  tongue  is  impaired,  this  organ  is  often  damaged  by  the  teeth.  The 
dryness  of  the  mucous  membrane  of  the  nose  also  interferes  with  the 
sense  of  smell,  and  irritating  substances  may  be  inhaled  through  the  nostrils 
without  pain,  because  of  the  lack  of  sensation  in  the  nasal  mucous  mem- 
brane.   Paralysis  of  this  nerve  is,  however,  very  rarely  met  with. 

In  the  great  majority  of  instances  in  which  a  physician  is  called  on  to 
treat  a  lesion  of  the  trifacial  nerve,  the  patient  complains  of  severe  neuralgic 
pain,  which  in  most  cases  arises  from  the  Gasserian  ganglion  (8,  Plate 
VIIL).  When  trophic  changes  are  very  well  marked,  they  result  in  hemi- 
atrophy of  the  face.  In  those  cases  in  which  the  motor  fibres  of  the  fifth 
nerve  are  irritated,  there  may  be  lockjaw  as  in  true  tetanus,  and  so-called 
masseter  spasm  may  have  a  reflex  origin  because  of  the  presence  of  dental 
irritation. 


1022  DISEASES  OF   THE  NERVOUS  SYSTEM 

Paralysis  of  the  Sixth  Abducens  Nerve. — The  sixth  nerve  has  its  origin 
from  cells  in  the  floor  of  the  fourth  ventricle,  passes  through  the  pons,  and 
makes  its  exit  in  the  groove  between  the  pons  and  the  medulla  (Plate 
IX.),  whence  it  passes  through  the  sphenoidal  fissure.  It  is  subject  to 
the  same  lesions  at  the  base  of  the  brain  as  is  the  oculomotor  nerve,  such 
as  tuberculous  meningitis  and  syphilitic  exudation,  tumor  and  fracture  of 
the  base  of  the  skull.  Injury  may  occur  to  it  in  the  sphenoidal  fissure. 
The  sixth  nerve  supplies  the  external  rectus  and  its  paralysis  thus  causes 
internal  squint,  the  patient  being  unable  to  rotate  the  eye  outward. 

The  exact  lesion  which  produces  paralysis  of  the  sixth  nerve  can  only 
be  determined  by  a  study  of  the  associated  symptoms.  In  those  cases 
in  which  there  is  facial  palsy  on  the  same  side  as  the  squint,  and  paralysis 
of  the  arm  and  leg  upon  the  opposite  side,  in  other  words,  "crossed  hemi- 
plegia," the  lesion  is  in  the  pons  or  at  the  base  of  the  brain  in  such  a  position 
that  it  produces  pressure  on  the  pons  on  one  side  and  above  its  lower 
third. 

Disturbances  of  Motility  in  the  Ocular  Muscles  Depending  on  the 
Third,  Fourth,  and  Sixth  Nerves. — The  movements  of  the  eyeballs  depend, 
of  course,  upon  the  associated  action  of  different  muscles  supplied  by  different 
nerves.  When  the  axes  of  the  eyeballs  converge,  they  do  so  by  the  action 
of  the  internal  recti  muscles  supplied  by  the  third  nerve,  and  when  they 
diverge  they  move  in  these  directions  by  the  external  recti  supplied  by  the 
sixth  nerve.  If,  however,  there  is  conjugate  deviation,  then  a  much  more 
complicated  nervous  mechanism  is  brought  into  play,  for  if  the  axis  of  each 
eyeball  is  turned  to  the  right,  for  example,  this  motion  is  made  by  contraction 
of  the  external  rectus  of  the  right  eye  and  the  internal  rectus  of  the  left 
eye,  each  being  supplied  by  different  nerves,  the  right  sixth  and  the  left 
third,  and  yet  it  is  essential  that  they  shall  act  in  accord.  This  is  accom- 
plished by  the  presence  of  association  fibres  which,  by  joining  together  the 
nuclei  of  the  nerves,  enable  them  to  act  in  unison.  If  by  disease  these  asso- 
ciation fibres  are  destroyed  (in  the  posterior  longitudinal  bundle),  conjugate 
deviation  of  the  eyes  becomes  impossible.  When  the  eyeballs  are  deviated 
by  reflex  action,  the  pathway  of  the  nervous  impulse  is  through  the  optic 
nerve  by  connecting  fibres  to  the  motor  nuclei  of  those  nerves  governing 
the  ocular  movements,  which  not  only  join  the  nuclei  of  the  different  nerves 
of  one  side,  but  connect  them  with  the  nuclei  of  the  opposite  side  as  well. 
When  they  are  moved  by  voluntary  action,  the  impulse  leaves  the  motor 
centres  in  the  anterior  part  of  the  motor  area  of  the  cortex,  and  thence  passes 
down  through  the  anterior  part  of  the  knee  of  the  internal  capsule,  thence 
through  the  crus  cerebri,  and  finally  crosses  in  the  raphe,  passing  to  the 
nuclei  of  the  oculomotor  nerves  and  of  the  fourth  and  sixth  nerves.  When 
the  impulse  for  conjugate  deviation  arises  in  the  motor  cortex,  it  passes  first 
to  the  nucleus  of  the  opposite  sixth  nerve,  and  thence  is  sent  along  the  associa- 
tion fibres  through  the  posterior  longitudinal  bundle  to  the  nucleus  of  the 
third  nerve  on  the  opposite  side,  just  as  it  is  in  reflex  deviation.  When  a 
nervous  explosion  takes  place  in  the  motor  cortex,  as  in  cases  of  epilepsy, 
it  often  happens  that  there  is  conjugate  deviation  of  the  eyes  away  from 
the  side  on  which  the  lesion  exists,  and,  conversely,  if  the  ocular  centres  in 


PLATE  X, 


Showing  Exit  of  Facial  Nerve  ( 1 )  from  Stylomastoid  Foramen  and 
its  Distribution  to  the  Muscles  of  the  Face.      (Riidinger.) 


DISEASES  OF   THE  CRANIAL  NERVES 


1023 


the  cortex  are  destroyed,  there  is  conjugate  deviation  of  the  eyes  toward  the 
side  on  which  the  lesion  exists.  This  has  given  rise  to  the  statement  that 
in  the  coma  of  ordinary  apoplexy  the  patient  "looks  toward  his  lesion"  at 
least  in  those  instances  in  which  an  apoplexy  destroys  these  centres.  (See 
Apoplexy.) 

There  are  two  states  which  give  rise  to  an  erroneous  diagnosis  in  connec- 
tion with  these  symptoms,  namely,  '  rheumatic  palsy"  of  the  ocular  muscles, 
which  disappears  under  the  free  use  of  the  iodides  and  salicylates,  and  so- 
called  "recurrent  oculomotor  paralysis,"  which  is  probably  the  result  of 
congestion  and  oedema,  and  which  is  accompanied  by  sick  stomach,  diplopia 
and  fever. 

Ophthalmoplegia  or  Paralysis  of  the  Internal  and  External 
Muscles  of  the  Eyeball). — This  condition  depends  not  upon  disorder 
of  function  of  any  single  cranial  nerve,  but  upon  interference  with  the  action 
of  the  third,  fourth,  and  sixth  nerves.  As  already  stated,  the  third  nerve 
supplies  the  ciliary  muscle,  the  circular  fibres  of  the  iris,  the  superior  rectus, 
internal  rectus,  inferior  rectus,  inferior  oblique,  and  the  levator  palpebrse. 
The  fourth  nerve  supplies  the  superior  oblique,  and  the  sixth  the  external 
rectus.  When  morbid  changes  take  place  in  the  nuclei  of  these  nerves  the 
normal  co-ordinated  movements  of  the  eye  are  impaired  or  lost,  that  is 
to  say,  ophthalmoplegia  is  developed. 

Ophthalmoplegia  is  of  two  forms:  ophthalmoplegia  externa,  when  the 
paralysis  affects  the  external  muscles  of  the  eyeball  and  the  levator  palpebrse; 
and  ophthalmoplegia  interna,  when 

only  the  pupillary  and  ciliary  muscles  ^^°-  ^^i 

are  involved.  Ophthalmoplegia  in- 
terna is  quite  rare,  although  a  modi- 
fied form  of  it  occurs  in  that  state 
called  the  iVrgyll-Robertson  pupil,  a 
condition  in  which  the  pupil  reacts  to 
accommodation,  but  not  to  light. 
In  this  condition  the  lesion  exists  not 
in  the  nuclei  of  the  nerves,  for  if  it 
did  there  would  be  no  reaction  to  ac- 
commodation, but  in  the  association 
fibres,  whereby  the  reflex  pathway 
is  destroyed.  Ophthalmoplegia  ex- 
terna., on  the  other  hand,  is  by  no 
means  uncommon.  It  is  a  condition 
depending  upon  a  centric  lesion,  and 
occurs  in  an  acute  and  clironic  form 
(see  below).  Because  of  the  fact 
that  the  lesion  is  centric  it  is  usu- 
ally bilateral,  and  if  all  the  muscles 
are  paralyzed  it  is  said  to  be  com- 
plete     external      ophthalmoplegia, 

while,  on  the  other  hand,  if  they  are  simply  impaired  in  function,  or  if  one 
nerve  escapes  while  the  others  are  involved,  it  is  spoken  of  as  partial  (Fig.  131). 


Patient  suffering  from  chronic  ophthalmoplegia 
externa.  The  wrinkling  of  the  forehead  in  the 
eflFort  to  open  the  ej^es  is  noticeable.  The  external 
strabismus  can  be  seen.    (Starr.) 


1024  DISEASES  OF   THE  NERVOUS  SYSTEM 

Etiology  and  Pathology, — Ophthalmoplegia  is  due  to  a  large  number  of 
causes,  such  as  tumors,  areas  of  degeneration,  or  inflammatory  exudations, 
where  the  nerves  take  their  exit  at  the  base  of  the  brain.  (See  Plate  IX.) 
The  additional  causes  are  small  hemorrhagic  extravasations,  arteritis,  throm- 
bosis, or  embolism  of  the  small  vessels  which  supply  the  nuclei  of  these 
nerves.  In  some  cases  the  lesions  resemble  those  of  acute  poliomyelitis,  and 
belong  to  the  affection  called  by  Wernicke  "polioencephalitis  superior." 

Symptoms. — The  symptoms  of  ophthalmoplegia  externa  vary,  of  course, 
with  the  nerves  which  are  affected  and  with  the  severity  of  the  lesions. 
When  the  morbid  process  is  severe,  there  is  not  only  loss  of  power  in  the 
ocular  muscles,  but  in  other  parts  as  well,  so  that  the  symptom-complex  of 
bulbar  paralysis  may  be  present;  or  if  the  tracts  to  and  from  the  higher  areas 
of  the  brain  are  involved,  such  symptoms  as  hemiansesthesia,  hemiplegia,  or 
hemiataxia  may  be  present.  The  pathological  processes  just  described 
are  varied  not  only  as  to  cause  and  situation,  but  as  to  acuteness  as  well. 
The  acute  form  is  ushered  in  by  a  train  of  symptoms  which  necessarily 
arise  when  areas  of  the  nervous  system  so  important  to  life  are  affected. 
Thus,  the  patient  suffers  from  vertigo,  headache,  vomiting,  and  even  coma. 
Unconsciousness  may  last  for  several  days  and  end  in  death,  or,  after  a 
period  of  a  week  or  ten  days,  consciousness  gradually  returns  and  the  symp- 
toms connected  with  the  eyes  alone  remain.  These  consist  in  double  ptosis 
and  various  palsies  of  the  ocular  muscles,  or  total  ophthalmoplegia.  The 
chronic  form  arises  when  the  nervous  lesions  are  gradual  in  onset,  although 
it  may  result  from  the  acute  type  just  discussed.  Here  again  the  degree  of 
the  paralysis  depends  upon  the  severity  of  the  lesions.  In  one  case  a  total 
palsy  may  be  present,  in  another  a  partial  palsy,  and  in  still  a  third  the  palsy 
may  be  progressive,  one  muscle  after  another  failing.  Sometimes  one  mus- 
cle improves  as  another  fails.  Ptosis  and  other  forms  of  ocular  palsy  may 
be  a  part  of  the  transient  and  recurrent  paralysis  in  myasthenia  gravis.  The 
prognosis  depends  upon  the  cause.  If  syphilis  is  a  factor  the  outlook  is 
favorable  as  compared  to  that  type  which  is  due  to  disseminated  sclerosis 
or  bulbar  palsy.  In  no  case  is  the  outlook  anything  but  grave  as  to  recovery, 
although  about  one-half  of  the  mild  cases  recover. 

The  treatment  also  varies  with  the  cause,  and  yet  it  may  be  said  that,  be 
the  cause  what  it  may,  the  only  drugs  which  offer  any  promise  of  relief  in 
the  chronic  form  are  mercury  and  the  iodides.    Hot  baths  may  be  useful. 

In  the  acute  form  freedom  from  any  cause  of  excitement,  the  application 
of  cold  to  the  head,  and  the  use  of  aconite  to  quiet  the  circulation,  if  it  is 
excited,  may  be  of  some  value. 

The  Seventh  or  Facial  Nerve. — The  nucleus  of  the  facial  nerve  is  found 
in  the  lower  part  of  the  pons.  From  this  nucleus  its  fibres  pass  upward  and 
backward  to  the  floor  of  the  fourth  ventricle,  where  they  make  a  sharp  turn 
inward  and  forward  about  the  nucleus  of  the  sixth  nerve,  and  finally 
make  their  exit  between  the  pons  and  the  medulla  (Plate  IX.)  near  the 
eighth  nerve.  After  leaving  the  pons,  the  seventh  nerve  passes  into  the 
internal  auditory  foramen  of  the  petrous  portion  of  the  temporal  bone,  and 
after  passing  through  the  aqueduct  of  Fallopius  emerges  from  the  stylo- 
mastoid foramen  upon  the  surface  near  the  lobe  of  the  ear,     (See  Plate  X.) 


DISEASES  OF  THE  CRANIAL   NERVES  1025 

At  this  point  it  is  divided  into  many  branches  which  supply  the  muscles 
of  the  face  with  motor  impulses.  (See  Plate  X.)  Upon  the  fibres  of  the 
facial  nerve  just  as  it  enters  the  auditory  foramen  a  ganglion  occurs,  com- 
monly called  the  geniculate  ganglion.  This  ganglion  consists  of  an  aggre- 
gation of  cell  bodies  connected  with  sensory  fibres  from  the  chorda  tympani 
nerve,  which  is  a  nerve  of  sensation  and  is  concerned  with  the  special  sense 
of  taste.  The  fibres  of  this  nerve  do  not,  however,  remain  in  contact  with 
those  of  the  facial,  but  leave  it  at  once,  and  by  way  of  the  Vidian,  or  superficial 
petrosal,  nerve  pass  to  the  superior  maxillary  branch  of  the  trifacial.  In 
addition  to  these  sensory  fibres  of  the  chorda  tympani,  the  facial  nerve  also 
has  associated  with  it  the  nerve  of  Wrisberg,  which  is  probably  sensory  in 
function,  and  which  lies  by  the  side  of  the  facial  nerve  as  its  fibres  pass  from 
the  pons  to  the  auditory  foramen,  where  the  ganglion  of  the  chorda  tympani 
just  named  exists.  The  fibres  of  the  nerve  of  Wrisberg  then  pass  to  the 
nucleus  of  the  glossopharyngeal  nerve. 

Etiology. — Interference  with  the  function  of  the  facial  nerve  arises  from 
many  causes,  of  which  the  chief  and  most  frequent  are  injuries  in  its  course 
after  it  leaves  the  pons.  These  may  be  called  peripheral  lesions,  and  when 
the  paralysis  is  peripheral  it  is  called  Bell's  palsy.  Thus,  it  not  infre- 
quently happens  that  a  child  is  born  with  facial  palsy,  which  is  usually  due 
to  injury  to  the  nerve  during  labor  as  by  the  pressure  of  forceps.  So,  too, 
facial  paralysis  is  sometimes  seen  in  children  and  in  adults  as  a  result  of  a 
severe  blow  at  the  lower  part  of  the  ear,  or  of  an  attack  of  mumps  in  which 
the  inflammation  and  swelling  has  been  severe.  Tumors  of  the  neck  and 
inflammation  in  the  middle  ear  also  may  cause  facial  palsy  in  this  manner. 

In  adults  facial  palsy  is  often  due  to  an  inflammation  in  the  stylomastoid 
foramen  as  the  result  of  exposure.  It  is  thought  by  some  that  this  takes  place 
in  certain  individuals  by  reason  of  the  fact  that  this  foramen  is  so  small  that 
very  slight  swelling  causes  pressure  on  the  nerve  and  ablation  of  its  function. 
It  is  this  type  of  paralysis  following  exposure  to  cold  which  has  given  rise 
to  the  belief  among  certain  ignorant  persons  that  it  is  possible  to  be 
*'moon-struck,"  because  a  person  has  slept  out-of-doors  in  the  moonlight 
and  has  developed  facial  palsy  afterward.  The  real  cause  is,  of  course,  the 
exposure  to  cold,  and  not  the  influence  of  the  moon.  That  cold  cannot 
always  be  the  cause  of  this  particular  form  of  facial  palsy  is,  however, 
evident  from  the  fact  that  the  condition  is  no  more  frequent  in  winter  than 
in  summer.     Perhaps  the  condition  is  really  one  of  rheumatic  neuritis. 

More  serious  causes  of  facial  palsy  are  disease  processes  inside  the  skull 
which  press  upon  the  nerve  before  it  passes  through  the  aqueduct  of  Fallo- 
pius.  These  conditions  are  tumor,  inflammatory  processes  at  the  base  of 
the  brain,  most  commonly  arising  from  injury,  syphilis,  or  tuberculosis,  and 
occasionally  one  of  the  acute  infectious  diseases.  So,  too,  a  fracture  of  the 
base  of  the  skull  may  produce  facial  paralysis.  Facial  palsy  due  to  a  lesion 
in  the  pons  is  exceedingly  rare  as  a  single  symptom,  as  is  also  facial  palsy 
due  to  a  lesion  in  the  cortex.  On  the  other  hand,  facial  paralysis  is  usually 
present  in  cases  of  hemiplegia,  but  in  hemiplegia  the  upper  part  of  the  face 
escapes  the  paralysis,  being  innervated  from  both  hemispheres  of  the  brain. 

The  pathological  changes  which  take  place  in  the  facial  nerve  in  cases  of 
65 


1026  DISEASES  OF   THE  NERVOUS  SYSTEM 

facial  paralysis  depend,  of  course,  upon  the  situation  of  the  lesion.  If  the 
lesion  occurs  in  the  nucleus  of  the  nerve,  or  involves  its  fibres  in  such  a  way 
that  it  fails  to  receive  its  normal  trophic  impulses,  degenerative  changes  at 
once  ensue,  the  neuritis  being  of  the  so-called  parenchymatous  type. 

Symptoms. — The  symptoms  of  facial  paralysis  are  very  characteristic.  The 
paralysis  is  nearly  always  unilateral  and  often  total,  in  the  sense  that  all  the 
muscles  upon  one  side  of  the  face  are  impaired  in  function.  It  sometimes 
happens,  however,  that  the  muscles  of  the  forehead  partly  escape.  Because 
of  the  paralysis  of  the  muscles  of  one  side  of  the  face  the  patient  is  unable  to 
wrinkle  the  brow  upon  one  side,  and  is  not  able  to  close  the  lids,  either  as  a 
reflex  act,  as  in  winking,  or  by  volition.  The  corner  of  the  mouth  on  the 
paralyzed  side  is  drooped,  and  if  the  patient  attempts  to  smile  only  one- 
half  of  his  visage  is  wrinkled.  The  nasolabial  fold  is  obliterated  on  the 
paralyzed  side  and  is  usually  accentuated  on  the  normal  side  as  a  result  of 
the  contraction  of  the  muscles  which  are  no  longer  counterbalanced  by 
opposing  muscles.  The  condition  is  not  painful.  If  recovery  does  not 
promptly  ensue  the  reactions  of  degeneration  speedily  develop  in  the 
paralyzed  muscles,  and  there  may  be  contractures  in  them. 

Diagnosis. — ^The  manifest  paralysis  of  the  muscles  of  one  side  of  the  face, 
which  is  particularly  noticeable  when  the  patient  attempts  to  smile  or  frown, 
renders  the  diagnosis  of  facial  palsy  easy  and  the  symptoms  which  the  patient 
presents  can,  moreover,  be  used  very  successfully  in  many  cases  in  determin- 
ing the  site  of  the  lesion.  Thus,  in  some  cases  of  facial  paralysis  the  sense 
of  taste  is  modified  or  lost  upon  the  anterior  two-thirds  of  the  tongue  on  the 
side  affected.  If  this  symptom  is  present,  it  indicates  that  the  lesion  is  one 
which  involves  the  facial  nerve  between  the  geniculate  ganglion  and  the 
point  a  quarter  of  an  inch  above  the  stylomastoid  orifice,  where  the  chorda 
tympani  fibres  leave  it;  or,  to  put  the  proposition  reversely,  if  loss  of  taste 
does  not  accompany  a  facial  palsy  the  lesion  is  either  in  the  stylomastoid 
foramen  within  a  quarter  of  an  inch  of  the  orifice  or  it  may  involve  the  nerve 
before  it  enters  the  bone.  So,  too,  if  there  is  unusual  sharpness  of  hearing 
with  some  buzzing  in  the  ear,  this  also  is  an  indication  of  a  lesion  near  the 
pons  or  in  the  Fallopian  canal,  since  it  is  due  to  paralysis  of  the  stapedius 
muscle  which  is  supplied  by  the  stapedius  nerve.  If  deafness  and  vertigo 
are  present  it  is  probable  that  the  condition  is  due  to  middle-ear  disease  or 
to  some  lesion  which  also  involves  the  auditory  nerve  at  the  base  of  the 
brain.  A  study  of  the  electrical  reaction  of  the  paralyzed  muscles  is  also 
of  great  value  for  the  purpose  of  localizing  the  lesions.  Thus,  if  the  lesion 
exists  in  the  stylomastoid  foramen,  the  muscles  of  the  face  are  cut  off  from 
the  trophic  impulses  which  they  normally  receive  from  their  nuclei  in 
the  pons,  and  as  a  result  the  reaction  of  degeneration  speedily  develops 
and  may  become  complete;  whereas,  on  the  other  hand,  if  the  lesion  which 
causes  paralysis  is  situated  in  the  motor  tract  above  the  nucleus  of  the  facial 
nerve,  or,  in  other  words,  if  it  involves  the  fibres  which  descend  from  the 
motor  area  of  the  cortex,  the  reaction  of  degeneration  does  not  develop 
because  the  muscles  still  receive  trophic  impulses.  Further  than  this,  in 
these  cases  the  paralysis  is  never  so  complete  as  in  the  peripheral  type,  the 
patient  usually  being  able  to  wink  and  to  wrinkle  the  forehead,  the  muscles 


DISEASES  OF   THE  CRANIAL  NERVES  1027 

of  the  forehead  frequently  escaping.  Centric  facial  paralysis  is,  however, 
exceedingly  rare  unless  associated  with  other  symptoms,  as  already  stated. 
In  those  rare  instances  in  which  the  facial  paralysis  arises  from  damage  to  the 
nucleus  of  the  facial  nerve  in  the  pons,  there  are  other  symptoms  of  a  pontile 
lesion  producing,  in  some  instances,  a  crossed  hemiplegia,  as  already 
described,  an  associated  paralysis  of  the  sixth  nerve,  or  the  symptoms  of 
ordinary  bulbar  paralysis.  In  these  cases,  too,  reactions  of  degeneration 
speedily  develop. 

Prognosis  —The  prognosis  in  cases  of  facial  paralysis  varies,  of  course, 
with  the  situation  of  the  lesion  and  with  its  severity.  The  majority  of 
instances  get  well  because  they  have  their  origin  in  an  inflammatory  process 
in  the  stylomastoid  foramen.  The  outlook  when  the  lesions  are  back  of 
the  stylomastoid  foramen  are  not  so  favorable,  and  when  the  nucleus  of 
the  nerve  or  the  motor  area  of  the  cortex  is  diseased,  the  prognosis  is,  of 
course,  very  doubtful  as  to  recovery  of  power  in  the  muscles  of  the  face. 

Treatment. — The  treatment  of  paralysis  of  the  seventh  nerve  depends 
somewhat  upon  the  lesion  which  produces  it.  For  the  relief  of  that  form 
which  is  due  to  inflammation  in  the  stylomastoid  foramen,  it  is  customary  to 
administer  mild  alteratives,  such  as  small  doses  of  the  iodide  of  potassium 
or  sodium,  in  order  to  hurry  the  absorption  of  the  inflammatory  exudate. 
It  is  also  advisable  to  apply  a  small  blister,  about  the  size  of  a  postage 
stamp,  immediately  in  front  of  the  ear  for  its  counterirritant  effect.  In 
those  cases  in  which  there  is  a  gouty  or  rheumatic  diathesis,  the  best 
results  are  often  obtained  by  the  use  of  the  salicylates  in  moderately  large 
doses,  10  to  15  grains  three  or  four  times  a  day,  or  10  drops  of  the  wine  of 
colchicum  root  and  10  grains  of  iodide  of  strontium  may  be  administered 
three  times  a  day.  The  use  of  electricity  for  the  purpose  of  maintaining 
the  nutrition  of  the  facial  muscles  in  any  case  of  peripheral  facial  palsy 
is  not  only  futile,  but  may  be  harmful,  for  the  cause  of  the  muscular  wasting 
is  lack  of  trophic  impulse,  and  as  these  impulses  cannot  reach  the  mus- 
cle, it  is  speedily  exhausted  if  stimulated  by  the  electrical  current,  when 
deprived  of  its  ordinary  means  of  recuperation.  If  middle-ear  disease  is 
present,  it  must,  of  course,  be  treated  by  those  measures  which  are  com- 
monly employed  by  aurists.  In  cases  where  the  lesion  is  centric,  counter- 
irritation  is  useless.  The  only  hope  is  that  nature  aided  by  alterative  drugs, 
such  as  the  iodides,  may  cause  an  absorption  of  the  results  of  the  local  inflam- 
matory process.  Where  the  lesion  is  severe  enough  to  have  destroyed  the 
nerve  cells,  treatment  is  also  useless. 

Facial  Spasm. — Facial  spasm  due  to  irritation  of  the  facial  nerve  is  a 
frequent  affection.  It  may  be  general  or  localized  in  one  or  two  muscles. 
When  the  orbicularis  palpebrarum  is  aftected,  the  condition  is  called  "  ble- 
pharospasm." As  a  rule,  the  muscles  about  the  mouth  are  also  affected. 
When  this  is  the  case,  the  condition  is  called  one  of  "  blepharofacial 
spasm."  To  this  condition  the  French  term  "tic  convulsif "  is  sometimes 
applied.  The  cause  of  facial  spasm  is  unknown.  It  sometimes  develops 
in  nervous  individuals  as  a  result  of  a  severe  nervous  shock.  In  some 
instances  it  seems  to  partake  of  the  nature  of  a  habit  spasm,  and  in  these 
cases  not  infrequently  a  lightning-like  contraction  of  the  muscles  of  the  face 


1028  DISEASES   OF   THE   NERVOUS  SYSTEM 

takes  place.  Sometimes  in  addition  to  facial  spasm  there  is  also  torticollis. 
Very  rarely  facial  spasm  is  due  to  an  irritating  focus  in  the  motor  area  for  the 
face  in  the  cortex,  and  sometimes  it  is  the  early  or  first  symptom  of  an  oncom- 
ing epileptic  seizure.  In  ordinary  facial  spasm  the  muscles  are  not  persist- 
ently contracted,  but  suffer  from  twitchings  which  come  on  in  paroxysms, 
or  which  occur  singly  at  varying  intervals. 

The  prognosis  in  a  case  of  this  kind  is  not  very  favorable,  although,  as  a 
rule,  there  is  no  organic  lesion  to  maintain  it. 

The  treatment  of  facial  spasm  consists  in  a  careful  investigation  to  deter- 
mine if  there  is  any  localized  focus  which  gives  rise  to  reflex  irritation,  as, 
for  example,  disease  of  the  middle  ear.  If  such  an  area  is  found,  it  should 
of  course  be  removed.  In  some  instances  a  hypergesthetic  spot  in  the  nasal 
mucous  membrane  may  be  discovered.  If  no  such  local  area  of  irritation 
can  be  found,  there  is  little  left  for  the  physician  to  do  except  to  administer 
nervous  sedatives,  such  as  the  bromides,  chloral,  and  cannabis  indica,  but 
thes3  in  turn  rarely  do  good  in  this  annoying,  harmless,  but  persistent  con- 
dition. In  young  persons  who  have  a  tendency  to  facial  spasm  as  a  result 
of  habit,  a  powerful  mental  impression  may  aid  in  breaking  up  the  habit, 
particularly  if  there  is  a  tendency  to  hysterical  manifestations. 

The  Eighth  or  Auditory  Nerve. — Disease  of  the  auditory  nerve  may 
result  in  deafness,  tinnitus,  vertigo,  and  loss  of  equilibrium. 

When  deafness  is  due  to  disease  of  this  nerve  it  commonly  arises  from 
some  degenerative  change,  which  in  turn  may  be  due  to  the  effect  of  an 
infectious  disease.  In  other  instances  the  deafness  is  due  to  a  congenital 
defect,  but  in  still  others  it  occurs  as  a  part  of  the  course  of  locomotor  ataxia, 
disseminated  sclerosis,  or  general  paralysis  of  the  insane.  More  rarely  it 
arises  from  a  tumor  of  the  brain  or  from  cerebral  syphilis.  In  deafness  due 
to  these  causes  the  so-called  cochlear  fibres  of  the  auditory  nerve  are  in- 
volved. The  condition  may  be  differentiated  from  that  form  of  deafness 
which  is  due  to  disease  of  the  middle  ear,  the  peripheral  fibres  of  the 
auditory  nerve  not  being  affected,  and  by  the  fact  that  the  latter  class  of 
patients  possess  the  power  of  perceiving  sound  transmitted  through  the 
bones  of  the  head.  Thus,  if  a  tuning  fork  is  placed  against  the  head,  or 
the  teeth,  the  patient  can  perceive  the  sounds  which  it  generates  if  the  deaf- 
ness is  due  to  a  peripheral  cause,  which  produces  interference  with  aerial 
sound  conduction  in  the  external  or  middle  ear,  but  he  cannot  perceive  its 
sound  if  the  deafness  is  due  to  a  centric  cause,  such  as  a  lesion  of  the 
cochlea  of  the  internal  ear,  or  of  the  auditory  nerve  trunk,  or  of  the  auditory 
pathway  to  the  cortex.  Again,  in  those  cases  of  disease  of  the  auditory 
nerve  of  a  centric  character,  the  patient  does  not  find  it  easy  to  hear  in  the 
presence  of  loud  noises,  as  he  often  does  in  cases  of  deafness  due  to  a 
peripheral  lesion. 

The  prognosis  in  deafness  due  to  centric  disease  of  the  auditory  nerve 
is  very  bad. 

When  tinnitus  is  present,  it  arises  as  the  result  of  irritation  of  the  cochlear 
portion  of  the  auditory  nerve  which  supplies  the  organ  of  Corti  in  the  internal 
ear,  or  of  those  fibres  which  pass  from  this  organ  in  the  nerve  trunk  itself. 
The  sound  may  vary  from  a  slight  buzzing  to  a  roaring,  ringing,  or  explo- 


DISEASES  OF   THE   CRANIAL  NERVES  1029 

sive  noise  which  may  be  so  severe  as  to  be  insufferable.  Suicide  is  some- 
times threatened  by  persons  who  are  not  only  persecuted  by  these  noises 
during  the  day,  but  are  unable  to  sleep  by  night  from  the  same  cause.  Little 
can  be  done  for  many  of  these  cases.  In  those  instances  in  which  tinnitus 
arises  from  middle-ear  disease  or  from  anaemia  or  from  the  use  of  drugs, 
such  as  quinine  and  salicylic  acid,  the  condition  can  often  be  relieved,  as  it 
depends  upon  an  irritation  and  not  upon  an  actual  lesion,  as  a  rule. 

The  treatment  depends  upon  the  cause  of  the  tinnitus.  If  it  is  due  to  an 
actual  lesion  of  the  internal  ear  the  prognosis  is  bad  and  treatment  is  futile. 
If  it  is  due  to  gout,  anemia,  or  similar  causes,  the  prognosis  is  fairly  good. 

Vertigo  is  a  condition  in  which  the  patient  loses  the  sense  of  his  normal 
relation  to  surrounding  objects.  In  some  instances  he  seems  to  be  w^hirled 
about  in  space.  In  other  instances  he  seems  to  remain  stationary,  while 
other  objects  are  whirled  about  him.  As  the  patient's  conception  of  his 
relation  to  surrounding  objects  is  disturbed,  he  frequently  falls,  since  this 
conception  has  much  to  do  with  the  motor  impulses  by  which  he  controls 
his  muscles  in  connection  with  the  function  of  muscle  sense.  The  cause  of 
vertigo  may  be  a  functional  disorder  of  the  branches  of  the  auditory  nerve 
which  supply  the  vestibular  portion  of  the  internal  ear,  as  when  it  occurs  in 
the  course  of  indigestion  (autotoxa^mia)  or  under  the  influence  of  a  drug 
such  as  quinine,  or  it  may  be  due  to  actual  lesions  in  connection  with  these 
nerve  fibres  such  as  hemorrhages  into  the  internal  ear,  or  other  damage  to 
the  semi-circular  canals.  Sometimes  also  it  seems  to  be  due  to  reflex  irrita- 
tion produced  by  disease  in  the  middle  ear  or  in  the  external  meatus.  In 
other  instances  the  presence  of  a  foreign  body  in  the  meatus  produces  vertigo. 
When  vertigo  is  severe,  there  may  be  associated  with  it  great  nausea  and 
vomiting,  palpitation  of  the  heart,  profuse  sweating,  a  sense  of  approaching 
syncope,  and  even  collapse.  The  respirations  may  be  rapid.  These  symp- 
toms are  in  part  doubtless  due  to  the  mental  distress  or  fright  from  which 
the  patient  suffers.  There  is  probably  no  symptom  wdiich  causes  so  much 
fright  and  which  is  so  rarely  followed  by  death  as  severe  vertigo.  Nothing 
but  the  awful  apprehension  of  true  angina  pectoris  approaches  the  mental 
distress  of  the  patient  who  suffers  from  this  condition  in  its  well-developed 
form. 

One  form  of  vertigo  arising  as  the  result  of  disease  of  the  internal  ear  is 
called  Meniere's  disease.  It  is  usually  severe  in  its  nature.  Its  onset  is 
sometimes  sudden,  the  patient  being  seized  with  prostration,  pallor,  vomit- 
ing, roaring  in  the  ears,  and  deafness  immediately  after  hearing  a  loud 
report  which  has  not,  of  course,  arisen  from  any  extraneous  source.  This 
form  of  vertigo  is  supposed  to  be  due  to  a  hemorrhage  in  the  semi-circular 
canals,  and  resembles  in  its  onset  an  apoplectic  stroke,  but  it  is  not  charac- 
terized by  paralysis.  In  some  instances  it  seems  to  depend  upon  arterio- 
capillary  fibrosis.  It  may  or  may  not  be  associated  with  absolute  deafness. 
In  the  majority  of  cases  the  patient  suffers  from  recurrent  attacks,  but  as 
the  disease  progresses  the  attacks  last  longer  and  longer,  and  finally  he  not 
uncommonly  has  constant  vertigo. 

The  prognosis  in  cases  of  vertigo  depends  entirely  upon  the  cause  of  the 
disorder.    If  it  is  due  to  an  organic  disease,  unless  that  disease  exists  in  the 


1030  DISEASES  OF   THE  NERVOUS  SYSTEM 

middle  or  external  ear  and  is  removable,  the  outlook  is  serious.  Indeed,  the 
condition  may  be  considered  incurable  if  an  actual  organic  and  centric  lesion 
is  its  cause. 

In  Meniere's  disease  the  treatment  consists  in  rest  in  bed,  the  use  of  an 
ice-bag  on  the  head,  or  blister  behind  the  ear,  and  the  employment  of  large 
doses  of  nervous  sedatives,  such  as  the  bromides  and  chloral.  Certain 
practitioners  claim  to  have  obtained  good  results  from  the  administration 
of  large  doses  of  quinine,  but  it  is  difficult  to  see  how  this  drug  can  do  good 
under  these  circumstances.  Indeed,  one  would  expect  it  to  make  the  con- 
dition much  worse. 

Vertigo  which  is  due  to  autointoxication  arising  from  an  abnormal  state 
of  the  bowels  or  kidneys  should  be  treated  by  the  administration  of  diuretics, 
cholagogues,  purgatives,  and  free  sweatings. 

The  Ninth  or  Glossopharsmgeal  Nerve. — The  ninth  nerve  is  the  nerve 
of  sensation  of  the  pharynx,  the  palate,  and  the  middle  ear.  It  is  also  prob- 
ably connected  with  the  special  sense  of  taste  in  the  posterior  third  of  the 
tongue,  although  it  is  considered  by  some  physiologists  that  those  fibres 
which  are  connected  with  this  function  join  the  glossopharyngeal  fibres 
from  the  fifth  nerve.  Some  of  its  sensory  fibres  enter  the  medulla  oblongata 
near  the  olivary  body  and  terminate  in  the  gray  matter  on  the  floor  of  the 
fourth  ventricle,  while  another  set  of  fibres  ends  in  the  substantia  gelatinosa. 
From  the  latter  point  some  of  its  fibres  ascend  into  the  brain.  In  addition 
to  its  sensory  function  it  also  contains  motor  fibres  which  spring  from  cells 
known  as  the  nucleus  ambiguus.  These  fibres  make  their  exit  from  the  side 
of  the  medulla  back  of  the  olivary  body,  and  escape  from  the  skull  through 
the  jugular  foramen.  The  motor  fibres  supply  the  muscles  of  the  larynx, 
the  oesophagus,  and  pharynx,  and  are  also  connected  with  the  function  of 
respiration,  deglutition,  and  phonation. 

Paralysis  of  the  glossopharyngeal  nerve  is  exceedingly  rare,  and  therefore 
we  possess  but  little  information,  either  clinical  or  pathological,  concerning 
its  condition  in  disease.  Should  the  nerve  itself  be  damaged,  the  symptoms 
consist  in  loss  of  sensation  in  the  upper  half  of  the  pharynx,  loss  of  the  sense 
of  taste  on  the  posterior  half  of  the  tongue,  and  difficulty  in  swallowing 
because  of  paralysis  of  the  pharyngeal  muscles  and  because  of  the  loss  of 
reflex  irritability  of  the  mucous  membrane  of  the  pharynx.  Such  a  con- 
dition sometimes  develops  during  postdiphtheritic  paralysis.  When  lesions 
of  the  nuclei  of  this  nerve  take  place,  the  symptoms  are  practically  those 
of  bulbar  paralysis  (which  see). 

The  Tenth  or  Vagus  Nerve.— This  nerve,  sometimes  called  the  pneumo- 
gastric  nerve,  is  composed  of  both  sensory  and  motor  fibres.  The  sensory 
fibres  pass  upward  from  the  various  portions  of  the  body  which  they  supply 
and  enter  two  ganglia,  one  of  which,  the  upper,  is  large  and  oval,  and  the 
other  is  long  and  irregular  in  outline.  After  leaving  these  ganglia  the  fibres 
pass  to  the  medulla,  some  of  them  terminating  in  the  gray  matter  which 
exists  in  the  floor  of  the  fourth  ventricle,  thereby  forming  the  sensory  centres 
connected  with  respiration  and  the  heart.  Other  of  these  fibres  join  the 
ninth  nerve  and  end  in  the  substantia  gelatinosa  and  from  this  point  new 
fibres  ascend  to  the  brain.     Those  fibres  of  the  pneumogastric  which  are 


PLATE  XI. 


The  Vagus  and  Sympathetic  Fibres  of  the  Right  Side  and  Their 
Anastomoses.     (Modified  from  Rudinger.) 

1,  origin  of  vagus;  2,  anastomosis  with  sympathetic:  3,  superior  laryngeal  and  pharyngeal  plexus- 
4,  the  pulmonary  plexus;  5.  the  inferior  cardiac  fibres,  with  sympathetic  fibres;  6,  the  oesophageal  plexus' 
The  course  of  the  optic  nerve  (7),  the  oculomotor  (8),  the  trochlearis  (9),  the  abducens  (10),  and  the  facial 
(11)  are  also  shown. 


DISEASES  OF   THE  CRANIAL  NERVES  1031 

motor  in  function  take  their  origin  from  the  cells  of  the  nucleus  ambiguus 
and  escape  from  the  side  of  the  medulla,  forming  the  main  trunk  of  the  nerve. 
The  distribution  of  the  afferent  and  efferent  fibres  of  this  nerve  is  well  shown 
in  Plate  XL 

The  tenth  nerve  has  a  far  larger  distribution  than  any  other  cranial  nerve, 
supplying  the  pharynx,  the  larynx,  the  heart,  the  lungs,  oesophagus,  stomach, 
and  intestines,  and  even  the  external  ear  through  an  auricular  branch. 
According  to  some  physiologists  it  is  the  chief  motor  supply  of  the  palate. 
It  joins  the  glossopharyngeal,  or  ninth  nerve,  and  certain  sympathetic 
nerve  fibres,  in  the  formation  of  the  pharyngeal  plexus  which  supplies  the 
pharyngeal  muscles. 

The  superior  laryngeal  branch  supplies  the  cricothyroid  muscle,  the 
thyroepiglottic  and  aryepiglottic  muscles,  and  the  inferior  laryngeal  branch, 
sometimes  called  the  recurrent  laryngeal,  supplies  the  other  laryngeal  mus- 
cles. By  means  of  the  sensory  fibres  which  exist  in  the  superior  laryngeal 
nerve,  the  mucous  membrane  of  the  epiglottis  possesses  sensation,  and  by 
means  of  those  sensory  fibres  which  exist  in  the  recurrent  laryngeal  the 
mucous  membrane  below  the  vocal  cords  is  supplied  with  sensory  filaments. 
If  the  sensory  fibres  in  the  superior  laryngeal  nerve  are  stimulated,  the  respi- 
rations become  slower  and  deeper,  or  they  may  be  arrested  as  the  result  of  a 
reflex  impulse  which  passes  to  the  centre  in  the  medulla.  Closure  of  the 
glottis  may  also  be  produced  in  this  manner. 

The  pulmonary  branches  of  the  vagus  contain  motor  fibres  which  supply 
the  unstriated  muscles  of  the  bronchi,  and  sensory  fibres  for  the  mucous  mem- 
brane of  the  bronchi.  They  apparently  also  contain  fibres  centripetal  in 
character,  which  when  stimulated  diminish  the  inhibitory  action  of  the  pneu- 
mogastric  nerve  upon  the  heart,  thereby  producing  tachycardia.  Those 
branches  of  the  vagus  which  supply  the  oesophagus  innervate  its  muscles, 
on  the  one  hand,  and  supply  its  mucous  membrane  with  sensory  filaments 
on  the  other;  while  those  which  pass  to  the  stomach  contain  not  only  fibres 
which  govern  its  muscles,  but  also  other  fibres  which  control  its  secretion 
and  its  blood  supply.  The  same  facts  hold  true  of  those  fibres  which  pass 
to  the  intestines.  Last,  but  by  no  means  least,  the  pneumogastric  sends  fibres 
to  the  heart,  and  through  these  pathways  an  inhibitory  action  is  exercised 
which  if  stimulated  may  temporarily  arrest  the  heart  in  diastole. 

Not  only  is  the  pneumogastric  nerve  of  very  great  importance  because 
of  the  multiple  functions  which  it  possesses,  but  it  is  also  of  great  importance 
to  the  clinician  because  it  not  infrequently  suffers  from  disease.  Though 
it  is  rarely  the  victim  of  primary  neuritis,  cases  of  rheumatic  neuritis  of  both 
recurrent  laryngeal  nerves  have  been  reported,  and  instances  in  which  this 
nerve  has  been  involved  in  cases  of  multiple  neuritis  due  to  poison,  such  as 
alcohol,  for  example,  are  by  no  means  rare.  So,  too,  it  sometimes  suffers 
in  diphtheritic  paralysis,  and  from  neuritis  arising  from  the  poisons  of 
various  infectious  diseases  such  as  typhoid  fever,  pneumonia,  scarlet  fever, 
malaria,  and  influenza,  from  tumors  and  inflammation  in  the  mediastinum, 
disease  of  the  jugular  vein,  tuberculosis  of  the  mediastinal  glands,  and  from 
pressure  upon  the  nerve  exercised  by  reason  of  dilatation  of  the  left  auricle 
in  cases  of  mitral  stenosis.    In  those  instances  in  which  the  centres  of  the 


1032  DISEASES  OF  THE  NERVOUS  SYSTEM 

pneumogastric  nerve  are  affected  by  disease,  we  find  that  tumors,  hemorrhagic 
extravasations,  the  lesions  of  locomotor  ataxia,  and  disseminated  sclerosis 
are  the  causes.  In  still  other  instances  the  disorder  of  the  function  of  this 
nerve  develops  as  the  result  of  bulbar  paralysis.  Cases  are  also  on  record 
in  which  the  fibres  of  the  nerve  outside  of  the  medulla  have  been  pressed 
upon  by  tumors,  by  the  exudations  due  to  meningitis,  hemorrhages,  and  by 
bone  disease. 

The  symptoms  of  disorder  of  the  function  of  the  vagus  nerve  are,  of 
course,  very  varied.  If  the  lesion  exists  at  the  base  of  the  brain  it  nearly 
always  happens  that  there  is  paralysis  of  the  other  cranial  nerves,  particu- 
larly of  the  ninth,  eleventh,  and  twelfth.  In  such  a  case  if  the  fibres  on  one 
side  alone  are  affected,  there  is  unilateral  paralysis  of  the  fauces,  the  palate, 
and  the  larynx.  The  speech  is  nasal,  and  the  act  of  swallowing  may  be 
impaired.  There  is  also  interference  with  the  action  of  the  vocal  cords.  If 
the  recurrent  laryngeal  branch  is  affected,  there  is  laryngeal  paralysis.  The 
vocal  cord  on  that  side  remains  midway  between  adduction  and  abduction, 
and  fails  to  move  during  phonation.  If  both  of  the  recurrent  laryngeal  nerves 
are  paralyzed,  the  patient  suffers  from  aphonia,  inspiratory  stridor,  and 
dyspnoea.  When  the  pulmonary  fibres  are  affected,  particularly  if  the  lesions 
are  bilateral,  the  respirations  may  become  rapid  and  irregular. 

Irritation  of  the  pulmonary  fibres,  directly  or  indirectly,  may  cause  spasm 
of  the  bronchial  muscles,  and  hypersemia  and  congestion  of  the  bronchial 
mucous  membrane  (asthma). 

If  the  gastric  fibres  are  involved,  there  may  be  vomiting,  pain  in  the 
stomach,  and  loss  of  the  sense  of  hunger  and  thirst.  When  the  cardiac  fibres 
are  severely  affected,  the  pulse  rate  may  be  markedly  accelerated.  If  they  are 
irritated,  an  exceedingly  slow  pulse  may  be  present. 

The  treatment  of  disorders  of  the  vagus  nerve  depends  largely  upon  the 
cause  which  underlies  the  disturbance.  If  there  is  reason  to  believe  that 
there  is  a  syphilitic  exudate  at  the  base  of  the  brain,  or  a  syphilitic  arteritis, 
the  iodides  and  mercury  are,  of  course,  indicated.  So,  too,  in  that  form  of  dis- 
order of  the  vagus  which  results  from  lead  poisoning,  the  iodides,  hot  baths, 
and  purgatives  are  required.  If  it  is  believed  that  a  gummatous  growth 
exists  in  the  thorax  which  irritates  the  vagus  by  pressure,  antisyphilitic 
treatment  is  necessary.  If  there  is  a  distinct  rheumatic  history  leading  one 
to  believe  that  the  recurrent  laryngeal  nerves  are  suffering  from  rheumatic 
paralysis,  already  mentioned,  the  iodides  and  the  salicylates  are  advisable. 
Digitalis  may  also  be  useful  for  the  purpose  of  stimulating  the  pneumogas- 
tric nerve  in  those  cases  in  which  tachycardia  is  present,  and  atropine  may  be 
used  with  the  object  of  diminishing  irritation  in  this  nerve  by  depressing 
its  peripheral  fibres  when  the  pulse  is  unduly  slow. 

Eleventh  or  Spinal  Accessory  Nerve. — ^The  eleventh  or  spinal  accessory 
nerve  is  composed  of  two  parts,  an  accessory  portion,  which  goes  to  the 
pneumogastric,  and  a  spinal  portion.  The  accessory  branch  is  formed 
by  several  fasciculi  which  spring  from  the  medulla  in  series  with  the 
roots  of  the  vagus.  These  fasciculi  form  a  trunk,  and  to  this  trunk  are 
joined  the  fibres  from  the  spinal  portion.  The  nerve  leaves  the  cranium 
with  the  pneumogastric.     In  its  passage  through  the  jugular  foramen  it 


DISEASES  OF   THE  CRANIAL  NERVES  1033 

sends  fibres  to  the  root  ganglion  of  the  vagus,  while  others  pass  over 
the  surface  of  this  ganglion  into  the  pharyngeal,  superior  laryngeal,  and 
recurrent  laryngeal  nerves.  Most  of  the  motor  fibres  of  the  pneumogastric 
are  derived  from  this  accessory  branch.  The  spinal  portion  of  the  nerve 
arises  by  a  series  of  roots  wliich  spring  from  the  lateral  portion  of  the  spinal 
cord,  even  as  low  as  the  sixth  or  seventh  cervical  nerve  roots.  They  spring 
from  the  lateral  column  near  the  origin  of  the  posterior  nerve  roots  and 
form  an  ascending  trunk,  which  enters  the  skull  and  unites  with  the  acces- 
sory portion,  as  already  described.  Before  entering  the  jugular  foramen, 
however,  certain  of  its  fibres  leave  the  accessory  portion,  make  a  sharp 
turn  backward  near  the  internal  jugular  vein,  and  enter  the  deep  surface 
of  the  sternomastoid  muscle,  which  muscle  it  supplies.  Passing  through 
this  muscle,  it  enters  under  the  trapezius,  a  short  distance  above  the  clavicle. 
Here  it  anastomoses  with  fibres  from  the  third  and  fourth  cervical  nerves, 
forming  a  plexus,  which  supplies  the  trapezius  muscle. 

Symptoms. — Disturbances  in  the  function  of  the  accessory  nerve,  so  far 
as  its  spinal  part  is  concerned,  result  in  torticollis,  which  occurs  as  congenital 
wryneck,  as  wryneck  due  to  injury,  and  true  spasmodic  wryneck.  The 
congenital  form  is  due  to  some  defect  in  development  or  to  injury  of  the 
sternomastoid  muscle  at  the  time  of  delivery.  The  right  side  is  afi^ected  in 
the  majority  of  cases.  The  sternomastoid  muscle  is  not  in  the  spasm,  but 
the  head  is  drawn  to  one  side  and  rotated  to  the  opposite  side  as  the  result 
of  shortening  of  the  muscle  upon  the  side  to  which  the  head  is  drawn.  Not 
rarely  there  is  associated  with  this  atrophy  some  wasting  of  the  muscles  of 
the  face  upon  this  side.  Spasmodic  wryneck,  on  the  other  hand,  is  due  to  a 
true  spasm  of  the  muscles  supplied  by  the  spinal  accessory.  It  is  not  met 
with  in  children,  and  very  rarely  in  advanced  life,  but  occurs  most  frequently 
in  middle-aged  persons.  In  a  certain  proportion  of  cases  the  patients  are 
distinctly  hysterical,  and  the  spasm  follows  some  nervous  shock.  In  other 
cases  no  hysterical  stigmata  are  present,  and  it  is  thought  that  the  condition 
is  due  to  that  somewhat  indefinite  state  called  "  rheumatism."  This  form 
of  wryneck  differs  from  the  congenital  variety  in  that  it  is  usually  accom- 
panied by  pain.  The  spasm  may  not  be  constant  but  intermittent.  The 
chin  is  often  protruded  and  raised.  At  times  the  spasm  extends  to  the 
muscles  of  the  face,  and  facial  twitching  may  occur.  Often  the  condition 
becomes  one  of  tonic  spasm  after  having  begun  as  clonic  spasm,  and  if  the 
condition  persists  for  any  length  of  time  the  affected  muscles  may  undergo 
hypertrophy,  and  those  on  the  opposite  side  may  atrophy  from  disuse. 

Those  forms  of  wryneck  in  adults  which  are  characterized  by  intermittent 
or  clonic  spasms  are  rarely  due  to  rheumatism,  so  called,  but  depend  upon 
some  neurosis;  whereas,  the  tonic  spasm  may  be  due  simply  to  muscular 
fixation  through  pain.  In  the  latter  class  of  cases  the  prognosis  is  exceed- 
ingly good,  the  condition  usually  disappearing  under  the  use  of  hot  appli- 
cations or  counterirritant  liniments,  and  the  internal  administration  of  the 
salicylates  and  the  iodides.  Certain  persons  have  advised  the  intramuscular 
injection  of  atropine,  in  the  dose  of  g^o  of  a  grain ,  directly  into  the  belly  of 
the  afflicted  muscle  in  order  that  it  may  depress  the  peripheral  motor  nerve 
endings.     While  this  is  efficacious  in  some  cases,  it  is  prone  to  produce 


1034  DISEASES  OF   THE  NERVOUS  SYSTEM 

moderate  systemic  symptoms,  and  is  not  to  be  resorted  to  unless  the 
condition  fails  to  yield  to  the  plan  of  treatment  already  suggested. 

The  type  depending  upon  a  neurosis  is  much  more  diiEcult  to  treat.  It 
often  remains  unchanged  for  many  months,  and  indeed  may  become  a 
permanent  condition.  Sometimes  a  nervous  shock,  or  some  accident,  may 
suddenly  end  the  spasm. 

Under  the  unfortunate  name  of  "  spurious  wryneck,"  a  condition  of  wry- 
neck develops  as  a  result  of  caries  of  the  spine,  the  spasm  of  the  muscle 
being  due  to  the  lesions  in  the  vertebrae,  or  the  distortion  is  due  to  the  fact 
that  these  bones  do  not  properly  support  the  head. 

Under  the  name  of  "  spasmus  Nutans,"  or  "  nodding  spasm,"  a  condition 
is  met  with  in  which  the  muscles  upon  both  sides  of  the  neck  are  affected  in 
such  a  way  that  there  is  a  nodding  movement.  It  occurs  in  poorly  nourished, 
neurotic  individuals,  and  closely  resembles  habit  chorea.  The  symptoms 
become  most  marked  when  attention  is  called  to  them,  and  are  usually 
absent  during  sleep. 

Paralysis  of  the  spinal  accessory  may  be  due  to  injury,  disease  of  the 
vertebrae,  muscular  atrophy,  or  any  form  of  disease  of  the  spinal  cord  in  the 
cervical  region.  As  the  result  of  the  paralysis  there  may  be  loss  of  power 
to  rotate  the  head  upon  the  vertebral  axis.  The  sternomastoid  muscle  does 
not  stand  out  prominently  as  it  does  when  affected  by  spasm,  and  there  is 
difficulty  in  raising  the  arm  at  a  right  angle  to  the  body.  In  those  com- 
paratively rare  cases  in  which  the  paralysis  is  bilateral,  the  head  may  appear 
to  be  fixed,  as  if  the  fixation  were  due  to  spasm. 

Twelfth  or  Hypoglossal  Nerve. — ^The  twelfth  or  hypoglossal  nerve  arises 
from  a  group  of  cells  in  the  floor  of  the  fourth  ventricle,  at  its  lowest  point. 
Its  fibres  emerge  from  the  medulla,  and  escape  from  the  skull  through  the 
anterior  condyloid  foramen  of  the  atlas,  and  so  pass  to  the  muscles  of  the 
tongue.  Injury  and  disease  of  this  nerve  rarely  take  place  in  its  peripheral 
filaments.  Nearly  always  when  it  is  affected,  the  lesion  is  in  the  bulb  or  in 
the  brain.  Thus,  out  of  79  cases  collected  by  Ascoli,  in  only  one-third  were 
the  peripheral  fibres  affected.  The  causes  of  centric  disease  of  the  hypo- 
glossal nerve  are  an  inflammatory  process  or  growth  at  the  base  of  the  brain, 
or  in  the  medulla  oblongata.  When  the  lesion  is  in  the  medulla,  there  is 
usually  bilateral  paralysis  with  wasting  of  the  tongue,  but  as  the  nuclei  of 
all  the  cranial  nerves  have  their  origin  nearby,  it  nearly  always  happens 
that  there  are  evidences  of  paralysis  of  the  other  cranial  nerves  present. 
Inside  the  bony  casement  the  causes  of  hypoglossal  paralysis  are  inflamma- 
tory exudates,  hemorrhages,  and  disease  of  the  bone.  Very  rarely  the 
peripheral  filaments  of  the  nerve,  after  they  take  their  exit  from  the  atlas, 
suffer  from  neuritis. 

In  some  cases  of  locomotor  ataxia,  syringomyelia,  and  multiple  sclerosis, 
there  is  hemiatrophy  of  the  tongue  with  paralysis.  The  same  symptom 
also  occurs  when  damage  is  done  to  the  peripheral  fibres  of  the  nerve. 
The  tongue  lies  on  the  floor  of  the  mouth,  and  it  is  impossible  for  the 
patient  to  move  the  tongue  upon  the  paralyzed  side.  If  the  tongue  is  pro- 
truded, it  deviates  to  the  paralyzed  side,  but  sometimes  while  the  main 
body  of  the  tongue  may  be  deviated  in  this  manner,  the  tip  points  toward 


MUSCULAR  DYSTROPHIES  1035 

the  sound  side.  Remak  points  out  that  while  the  tongue  lies  on  the 
floor  of  the  mouth  apparently  paralyzed,  it  can  be  easily  pushed  about 
by  the  finger  if  the  paralysis  is  organic;  whereas,  in  hysteria,  all  attempts 
to  move  the  tongue  by  the  finger-tip  cause  efforts  to  resist  these  move- 
ments. The  paralysis  of  the  tongue  impairs  the  speech,  and  also  inter- 
feres with  deglutition  and  mastication  when  the  paralysis  is  bilateral. 

The  prognosis  varies  with  the  cause  of  the  lesion.  In  syphilitic  cases 
recovery  sometimes  occurs  under  active  mercurial  treatment.  In  the  so- 
called  rheumatic  cases,  it  may  take  place  under  the  influence  of  the  iodides 
or  salicylates.  If  an  actual  lesion  at  the  point  of  origin  exists,  the  prog- 
nosis is  bad. 

DISEASES  IN  WHICH  THE   CHIEF   MANIFESTATIONS   ARE 
IN  THE  MUSCLES. 


MUSCULAR  DYSTROPHIES. 

Definition. — Under  this  term  are  described  several  related  maladies, 
characterized  by  alterations  in  the  trophic  state  of  the  muscles,  which  are 
met  with  almost  always  in  early  life  and  which  are  not  due  to  disease  of  the 
nervous  system — that  is  to  say,  they  are  primarily  muscular  in  origin. 
The  alterations  in  the  muscles  cause  loss  of  power  and  the  paralysis  may 
be  thought  to  be  due  to  a  spinal  lesion,  but  this  is  not  the  case. 

Muscular  dystrophy  has  been  divided  by  Erb  into  three  forms,  namely, 
pseudomuscular  hypertrophy,  Erb's  juvenile  dystrophy,  and  the  Landouzy- 
Dejerine  type  of  dystrophy.  Several  other  types  have  been  described  by 
other  writers.     (See  below.) 

Etiology. — ^The  etiology  of  these  dystrophies  is  not  known,  but  they  are 
all  believed  to  be  dependent  upon  faulty  development  of  the  muscles  affected. 
In  other  words,  it  would  seem  as  if  the  vitality  of  certain  muscles  is  of  such 
a  character  that  they  undergo  senile  changes  early  in  life.  When  injuries 
and  the  acute  infectious  diseases  seem  to  be  causative  factors  it  is  probable 
that  they  act  only  indirectly  in  that  they  hasten  the  degenerative  changes 
in  the  feeble  parts. 

Pathology  and  Morbid  Anatomy. — The  changes  in  the  muscles  in  cases 
in  which  atrophy  takes  place  consist  in  a  wasting  and  thinning  of  the  muscle 
fibrils  within  the  sarcolemma.  They  become  shortened  and  pigmented. 
In  other  cases  a  true  degenerative  process  goes  on,  the  fibrils  become  swollen, 
suffer  from  fatty  or  albuminoid  changes,  and  show  fatty  and  granular  masses 
within  the  sarcolemma,  until  finally  the  sarcolemma  may  contain  nothing 
but  fatty  globules.  In  a  third  form  of  dystrophy  there  is,  in  addition  to  fatty 
degeneration  in  the  fibrils,  a  deposit  of  fat  between  the  sheaths  covering  the 
fibrils.  With  these  changes  there  is  also  an  overgrowth  of  connective  tissue, 
and  as  a  consequence  a  muscle  which  is  so  large  as  to  appear  strong  and 
powerful  is  in  reality  feeble  or  powerless. 

Pseudomuscular  Hypertrophy. — This  form  of  muscular  dystrophy  is 
essentially  a  disease  of  early  childhood  beginning  between  the  second  and 


1036  DISEASES  OF   THE  NERVOUS  SYSTEM 

seventh  year.  It  is  characterized  by  enlargement  of  the  muscles  of  the 
calves  of  the  legs,  which  soon  are  seen  to  be  proportionately  too  large  for 
the  rest  of  the  child.  It  is  then  noticed  that  these  muscles  lack  power  and 
this  weakness  causes  the  patient  to  walk  awkwardly,  to  stumble  over  trifling 
obstacles,  to  tire  easily,  and  to  have  difficulty  in  rising  from  the  prone 
to  the  erect  posture,  so  that  the  patient  gets  on  his  feet  very  much  as  a  dog 
does,  largely  by  the  aid  of  the  forelimbs.  But  while  inspection  of  the  mus- 
cles of  the  calves  and  of  the  anterior  portion  of  the  thighs  reveals  that  they 
are  enlarged,  it  will  also  show  that  the  gluteal  muscles  are  atrophied  and 
that  the  muscles  of  the  back  are  weakened,  with  the  result  that  there  is 
developed  anterior  curvature  of  the  spine  and  a  protruding  belly. 

When  the  disease  is  still  further  advanced  alterations  in  the  nutrition  of  the 
muscles  about  the  shoulder-blades  is  usually  present.  The  deltoid  and  the 
supraspinatus,  the  biceps,  and  the  triceps  undergo  atrophy  and  do  not 
appear  to  be  increased  in  size  because  they  seldom  have  the  deposit  of  fat 
which  makes  the  muscles  in  the  legs  seem  unusually  large.  Occasionally, 
however,  such  a  fictitious  hypertrophy  may  be  present  in  these  muscles, 
because  of  loss  of  power  in  the  rhomboidei,  in  the  levatores  anguli  scapulae, 
and  in  the  serrati.  The  shoulder-blades  occupy  a  peculiarly  prominent 
position,  and  because  of  the  wasting  of  the  muscles  already  named  there 
may  be  great  feebleness  in  the  movements  of  the  upper  arm.  The  muscles 
of  the  forearm  and  hand,  however,  usually  escape. 

Contractures  appear,  which,  like  contractures  in  other  forms  of  mus- 
cular atrophy,  result  in  deformities  such  as  club-foot  or  flexion  of  the  legs 
upon  the  thighs  and  the  thighs  upon  the  pelvis.  Contractures  may  also 
take  place  in  the  arms.  It  is  a  fact  worthy  of  note  that,  unlike  other  forms 
of  muscular  atrophy,  this  disease  does  not  show  fibrillary  contractions  in 
the  muscles,  nor  are  the  reactions  of  degeneration  present,  even  when  the 
muscles  are  considerably  atrophied.  Sensation  is  intact,  and  the  reflexes 
are  preserved,  unless  the  muscles  are  so  completely  wasted  that  they  are 
unable  to  contract. 

Prognosis. — ^T'he  prognosis  in  these  cases  is  invariably  unfavorable. 
Periods  of  arrest  in  the  advancement  of  the  disease  may  occur,  but  ulti- 
mately the  patient  is  absolutely  helpless.  Death  never  occurs  from  pseudo- 
muscular  hypertrophy  directly,  being  caused  in  most  cases  by  intercurrent 
diseases  which  attack  the  enfeebled  body. 

Erb's  Juvenile  Muscular  Dystrophy  or  Scapulohumeral  Type.— 
This  form  of  dystrophy  begins  at  about  the  time  of  puberty,  usually  be- 
tween twelve  and  sixteen ;  rarely  as  late  as  the  twentieth  year.  The  pectoral 
muscles,  the  trapezii,  the  latissimus  dorsi,  the  rhomboidei,  and  the  del- 
toids undergo  apparent  hypertrophy  with  progressive  weakening.  This 
results  in  the  falling  forward  of  the  shoulders,  so  that  very  much  the  same 
attitude  is  maintained  as  if  there  was  a  fracture  of  the  clavicles.  The 
scapulae  are  prominent.  In  some  cases  the  disease  ceases  to  develop;  but 
if  it  does  not,  the  loss  of  power  extends  to  the  muscles  of  the  back,  and 
various  forms  of  spinal  curvature  develop.  After  this,  the  gluteal  muscles 
and  those  of  the  thigh  become  enfeebled.  They  may  atrophy  or  may  undergo 
seeming  hypertrophy.    When  the  muscles  of  the  leg  are  enfeebled  club-foot 


MUSCULAR   ATROPHY  OF   THE   PERONEAL   TYPE  1037 

may  be  present.  The  chief  difference,  therefore,  between  pseudomuscular 
hypertrophy  and  Erb's  juvenile  type  of  muscular  dystrophy  is  the  fact  that 
the  latter  disease  develops  later  in  life,  that  it  affects  the  upper  extremities 
before  it  affects  the  lower  extremities,  and  that  atrophy  is  more  marked 
than  hypertrophy. 

Landouzy-Dejerine  Type  of  Muscular  Dystrophy  or  Facioscapulo- 
humeral Type. — This  type  of  muscular  dystrophy  may  appear  in  early 
childhood  or  in  adult  life.  It  is  characterized  by  the  peculiar  fact  that  the 
atrophy  develops  in  the  muscles  of  the  face,  particularly  the  orbicularis  oris, 
and  extends  to  the  muscles  of  the  cheeks  and  those  of  the  forehead,  with 
the  result  that  the  lips  lose  power;  the  mouth  cannot  be  closed,  but  has  a 
peculiar  pouting  expression,  and  speech,  at  least  so  far  as  labial  and  lingual 
sounds  are  concerned,  becomes  very  defective.  So,  too,  the  face  loses  its 
power  of  expression  from  a  similar  cause,  and  there  is  dribbling  of  saliva 
because  the  lower  lip  sags.  Both  sides  of  the  face  are  usually  affected.  The 
orbicularis  palpebrarum  usually  escapes,  as  do  also  the  masseter  muscles. 
Later,  the  muscles  of  the  shoulders  become  affected,  and  finally  those  of  the 
trunk  and  legs  become  involved  until  the  case  closely  resembles  either  one 
of  the  forms  of  muscular  dystrophy  just  described,  save  that  the  facial  symp- 
toms are  prominent. 

In  some  cases  the  symptoms  of  these  three  forms  of  dystrophy  overlap  one 
another  to  such  an  extent  that  it  is  difficult  to  determine  to  which  type  an 
individual  patient  belongs. 

Treatment. — No  form  of  special  treatment  can  produce  advantageous 
results.  The  best  that  can  be  done  is  to  order  for  the  patient  an  out-door 
life,  if  possible  in  the  country,  and  in  a  climate  where  he  can  remain  for  many 
hours  in  sunshine  and  in  a  place  where  he  can  receive  excellent  food.  Gentle 
massage  and  Swedish  movements  may  be  employed,  but  care  must  be  taken 
not  to  tire  the  wasting  muscles.  The  most  that  can  be  expected  from  this 
plan  of  treatment,  however,  is  the  temporary  arrest  of  the  malady.  No  real 
improvement  usually  occurs.  Efforts  to  correct  deformities  produced  by 
contractures  are  generally  useless,  since  the  relief  is  but  temporary. 


MUSCULAR  ATROPHY  OF  THE  PERONEAL  TYPE. 

Definition. — This  is  a  form  of  progressive  muscular  atrophy  which  begins 
in  the  muscles  innervated  by  the  peroneal  nerves,  and  which  does  not  extend 
higher  than  the  knee.  After  the  symptoms  in  the  legs  have  developed,  a 
somewhat  similar  condition  may  affect  the  muscles  of  the  hand  and  fore- 
arms. It  is  sometimes  given  the  name  of  the  "Charcot-Marie-Tooth^'  form 
of  progressive  muscular  atrophy,  or  is  called  the  "  progressive  neural  muscu- 
lar atrophy  of  Hoffman,"  or  primary  neuritic  or  neurotic  atrophy.  It  is 
an  uncommon  disease,  but  not  so  rare  as  was  formerly  believed. 

Etiology. — ^There  seems  to  be  a  distinct  hereditary  predisposition,  since 
it  frequently  affects  several  members  of  a  family,  and  can  be  traced  through 
several  generations.  It  usually  develops  during  the  first  two  decades  of 
life. 


1038  DISEASES  OF   THE   NERVOUS  SYSTEM 

Pathology  and  Morbid  Anatomy. — The  condition  depends  upon  degen- 
erative changes  in  the  muscles,  in  the  nerves,  and  sometimes  in  the  pos- 
terior columns  of  the  spinal  cord.  There  is  also  sometimes  a  circumscribed 
atrophy  in  the  anterior  horns  of  the  gray  matter,  and  perhaps  degeneration  of 
the  lateral  columns  of  the  cord.  Whether  the  disease  arises  in  the  peroneal 
nerves  primarily,  or  whether  the  lesion  begins  in  the  posterior  horns  of  the 
gray  matter  in  the  spinal  cord,  is  unknown. 

Symptoms. — The  symptoms  of  this  form  of  muscular  atrophy  consist  in 
weakness  of  the  muscles  of  the  foot  and  of  the  'peroneal  muscles  of  the  leg, 
followed  by  atrophy  in  the  anterior  and  posterior  tibial  muscles,  with  the 
production  of  drop-foot,  which  makes  it  impossible  for  the  patient  to  walk. 
Unlike  the  two  forms  of  muscular  dystrophy  just  described,  fibrillary  con- 
tractions are  present  in  the  affected  muscles,  and  there  is  a  loss  of  reflex 
activity  and  of  electric  excitability,  so  that  the  last  stage  of  the  reaction 
of  degenera.tion  may  finally  be  present.  The  various  forms  of  club-foot  may 
come  on  as  secondary  conditions.  When  the  upper  extremities  are  affected, 
fibrillary  contractions  can  be  seen  in  the  muscles  of  the  hand,  and  after  loss 
of  power  has  been  present  for  some  time,  deformities  of  the  hand  may  arise 
from  contractures.  In  some  cases  the  progress  of  the  disease  is  exceedingly 
rapid,  but  in  others  it  is  equally  slow.  In  still  others  the  wasting  extends 
so  that  all  the  muscles  of  the  extremities  and  trunk,  and  even  those  of  the 
face,  may  undergo  atrophy. 

Prognosis. — -The  prognosis  as  to  recovery  is  hopeless,  but  patients  ma}' 
live  for  many  years  unless  destroyed  by  some  intercurrent  disease. 

Treatment. — Aside  from  hygienic  measures,  no  method  of  treatment  can 
arrest  the  progress  of  the  malady. 


FUNCTIONAL  NERVOUS  DISEASES  AND  DISEASES  OF 
DISPUTED  PATHOLOGY. 

MYOTONIA  CONGENITA. 

Definition. — Myotonia  congenita,  commonly  called  Thomsen's  disease, 
is  an  exceedingly  rare  affection  not  dependent  upon  disease  of  the  ner- 
vous system,  and  characterized  by  hypertrophy  of  the  muscular  fibres 
with  the  proliferation  of  their  nuclei.  These  changes  result  in  loss  of 
power. 

Symptoms. — ^The  chief  symptom  of  Thomsen's  disease  is  a  rigidity  of  the 
muscles,  which  develops  after  they  have  been  quiescent.  This  spasm  of  the 
muscles  comes  on  when  the  patient  attempts  to  move,  and  may  be  so  severe 
as  to  make  walking  practically  impossible.  Because  of  the  inability  of  the 
patient  to  balance  opposing  muscles  in  different  portions  of  his  body,  he 
may  fall.  After  a  time,  if  the  patient  persists  in  his  endeavor  to  walk  or  to 
make  other  movements,  the  spasm  passes  off,  and  the  muscles  respond  as  in 
the  normal  individual  so  that  ordinary  movements  can  be  carried  on  with 
ease;  but  if  the  muscles  are  irritated  bv  percussion  or  are  allowed  to  rest  and 


PARAMYOCLONUS  MULTIPLEX  1039 

another  attempt  is  made  to  move,  they  instantly  pass  into  spasm.  The 
affected  muscles  develop  electrical  reactions  of  a  peculiar  type,  namely, 
a  tonic  contraction  under  the  galvanic  current,  which  comes  on  sluggishly 
and  lasts  longer  than  in  health.  If  the  electrical  application  is  continued 
contraction  waves  pass  over  the  muscles,  but  there  is  no  marked  atrophy 
or  great  loss  of  power  except  in  so  far  as  the  spasm  interferes  with  ordinary 
muscular  movement.  The  disease  is  so  exceedingly  rare  that  less  than  40 
cases  have  been  reported.  A  physician  named  Thomsen,  himself  a  sufferer 
from  the  disease,  first  described  it. 


PARAMYOCLONUS  MULTIPLEX. 

Definition. — Paramyoclonus  multiplex  is  a  condition  of  the  motor  nervous 
system  in  which  sudden  contractions  of  the  muscles  take  place,  the  con- 
tractions resembling  those  produced  by  the  use  of  a  slowly  interrupted 
faradic  current.  It  is  sometimes  called  myoclonus,  multiple  myoclonus, 
myoclonus  epilepticus,  spinal  epilepsy,  and  Friedreich's  disease,  but  it  is 
not  to  be  confused  in  the  mind  of  the  student  with  Friedreich's  ataxia,  a 
very  different  malady.    It  is  a  rare  affection. 

Etiology. — ^The  cause  is  unknown.  In  a  very  few  instances  it  has  been 
thought  to  be  hereditary,  but  in  all  probability  this  is  the  case  only  in  the 
sense  that  the  parents  or  grandparents  have  suffered  from  neurotic  states. 
It  is  not  rarely  associated  with  epilepsy,  and  it  may  develop  when  a  nervous 
system  naturally  unstable  is  sapped  by  excessive  mental  overwork  or  other 
stress. 

The  contractions  may  simultaneously  affect  similar  muscles  in  both 
limbs,  or  may  occur  in  series  involving  first  one  side  and  then  the  other,  or 
pass  from  muscle  to  muscle.  Very  rarely  only  one  side  is  affected.  In  most 
instances  the  face  and  trunk  muscles  escape  as  in  Friedreich's  original  case. 
The  ocular  muscles  are  never  affected.  The  arms  are  more  commonly 
affected  than  the  legs  and  the  muscles  about  the  arm  and  shoulder  and 
those  of  the  thigh  are  more  frequently  and  severely  affected  than  those  of 
the  forearm  or  leg.  The  muscles  of  the  hands  and  those  of  the  feet  escape. 
The  severity  of  the  contractions  varies  greatly.  In  some  instances  they  are  so 
moderate  as  to  be  noticeable  only  when  the  patient  is  stripped  of  his  clothing. 
In  others  they  are  severe  enough  to  throw  him  off  his  feet.  The  motions 
or  attitudes  of  the  patient  vary,  of  course,  with  the  muscles  affected  and  the 
degree  of  their  contractions.  The  effect  of  voluntary  movements  upon  the 
contractions  is  also  varied.  In  some  instances,  as  in  Friedreich's  first  case, 
a  voluntary  movement  inhibits  or  diminishes  the  contractions,  but  in  other 
cases  voluntary  movement  seems  to  exaggerate  it.  Mental  excitement 
increases  them.  They  cease  during  sleep  and  are  usually  less  severe  when 
the  patient  is  standing  than  when  he  is  sitting  or  lying  down.  If  the  affected 
muscles  are  irritated  by  tapping  them  a  spasm  is  induced.  The  deep  reflexes 
may  be  increased  or  diminished,  but  electrical  irritability  is  not  altered  nor 
do  any  trophic  changes  occur.  Some  superficial  vasomotor  palsy  may  be 
present  in  the  extremities. 


1040  DISEASES  OF   THE  NERVOUS  SYSTEM 

Diagnosis. — Paramyoclonus  multiplex  is  separated  from  chorea  by  the 
fact  that  the  movements  of  chorea  resemble  those  of  the  will  in  that  cer- 
tain groups  of  muscles  act  together  and  do  not  contract  suddenly  as  from 
an  electrical  shock.  Voluntary  movements  are  prone  to  decrease  those  of 
myoclonus  and  to  increase  those  of  chorea.  Chorea  is  usually  a  unilateral 
affection,  while  myoclonus  is  usually  bilateral.  The  facial  muscles,  which 
are  so  commonly  affected  in  chorea,  are  rarely  affected  in  the  malady 
under  discussion.  Electrical  chorea,  or  Dubini's  disease,  is  separated  from 
paramyoclonus  multiplex  by  the  fact  that  it  is  accompanied  by  pyrexia, 
progressive  muscular  atrophy,  and  paralysis,  and  by  loss  of  response  on  the 
part  of  the  muscles  to  faradic  electricity.  From  hysterical  spasm  para- 
myoclonus is  separated  by  the  presence  in  hysterical  cases  of  the  stigmata 
of  that  state,  such  as  disorder  of  the  color  fields  and  areas  of  hypersesthesia 
or  anaesthesia.  In  those  cases  of  hysteria  in  which  these  stigmata  are  absent 
the  differential  diagnosis  may  be  impossible. 

Paramyoclonus  multiplex  may  be  separated  from  the  "maladie  des  tics 
convulsifs,"  described  by  French  neurologists,  by  the  fact  that  in  that  affec- 
tion the  movements  are  more  like  gestures  and  not  infrequently  echolalia 
is  present. 

Prognosis. — ^The  prognosis  as  to  complete  and  permanent  recovery  is  not 
good.  Rarely  death  ensuesin  a  few  months.  More  commonly  the  condition 
persists  in  varying  severity  for  years. 

Treatment. — ^The  treatment  consists  in  measures  devoted  to  the  improve- 
ment of  the  general  health  by  out-door  life,  good  food,  and  avoidance  of  all 
causes  of  nervous  irritation  and  exhaustion.  Remedies  like  arsenic,  phos- 
phorus, iron,  and  similar  roborants  are  useful  to  this  end,  but  are  not  cura- 
tive. Occasionally  a  carefully  regulated  course  of  hydrotherapy  at  some 
well-equipped  and  well-managed  sanatorium  is  servicable. 


PARALYSIS  AGITANS. 

Definition. — Paralysis  agitans,  sometimes  called  "shaking  palsy,"  or 
"Parkinson's  disease,"  is  a  condition  in  which  different  parts  of  the  body, 
especially  the  forearms  and  hands,  are  affected  by  a  continuous  tremor. 
When  the  disease  is  well  advanced,  the  patient  leans  forward,  assuming  a 
peculiar  attitude,  and  may  suffer  from  festination. 

Etiology. — ^The  precise  cause  of  paralysis  agitans  is  not  known.  It  has 
been  thought  to  follow  severe  nervous  shock  and  injuries  to  the  central  ner- 
vous system.  In  other  instances  it  has  followed  excessive  nervous  strain. 
Thus,  in  one  case  under  the  writer's  care,  the  treasurer  of  a  very  large 
corporation,  after  many  years  of  hard  work,  developed  a  well-marked  degree 
of  paralysis  agitans.  He  was  quite  certain  that  the  tremor  first  began  in 
those  muscles  which  were  employed  in  the  signing  of  several  hundred  papers 
a  day. 

Paralysis  agitans  develops  most  frequently  between  the  ages  of  fifty  and 
fifty-five.  Gowers  analyzed  80  cases  and  found  the  average  age  incidence 
to  be  fifty-two  years,  and  Wollenberg  found  that  10  out  of  20  cases  occurred 


PARALYSIS  AGITANS  1041 

at  ages  varying  from  fifty  to  fifty-five.  The  disease  also  not  infrequently 
develops  during  the  fifth  and  seventh  decades  of  life.  A  few  cases  occur- 
ring in  early  adult  life  and  in  childhood  have  been  reported.  Hadden, 
Gowers,  Berger,  and  others  have  seen  the  disease  in  individuals  whose  ages 
ranged  from  twenty  to  thirty,  and  Weil  and  Rouvillois  have  reported  a  case 
occurring  in  a  child  of  ten.  Lannois  also  mentions  a  case  occurring  in  a 
child  aged  twelve. 

Men  are  more  frequently  affected  than  women.  Thus,  of  67  cases  col- 
lected from  the  reports  of  St.  Thomas'  and  St.  Bartholomew's  Hospitals, 
London,  47  occurred  in  men  and  20  in  women.  In  78  American  cases  Dana 
found  the  proportion  of  men  to  women  to  be  as  5  to  3. 

The  neuropathic  constitution  may  be  considered  as  a  predisposing  cause, 
but  direct  inheritance  of  the  disease  is  rare.  A  few  instances  of  apparent 
direct  transmission  from  parent  to  offspring  have  been  reported,  and  Berger 
cites  one  in  which  the  disease  appeared  in  three  successive  generations. 
Borgherini  reported  7  cases  occurring  in  a  family  of  9  brothers  and  sisters. 
Three  children  of  these  individuals  developed  paralysis  agitans  between  their 
fortieth  and  fiftieth  years. 

Pathology — Nothing  is  known  of  the  pathology  of  this  affection  which 
throws  any  light  on  the  cause  of  the  symptoms. 

Symptoms. — The  symptoms  of  paralysis  agitans  are  tremor,  muscular 
rigidity,  a  retardation  of  ordinary  voluntary  movements,  and  a  change  in  the 
gait.  The  tremors  are  rhythmical  in  character,  amount  to  four  or  five  per 
second,  and  move  the  part  in  various  directions.  Thus,  when  the  hand  is 
affected,  the  fingers  may  be  flexed  and  extended,  abducted  and  adducted. 
The  most  common  movement  is  a  rubbing  of  the  thumb  against  the  index 
finger,  in  much  the  same  way  that  a  pill  might  be  made  by  such  a  rolling 
movement.  In  some  instances,  particularly  if  the  patient  becomes  excited, 
the  amplitude  of  the  movements  becomes  greatly  increased,  so  that  the  hand 
or  the  head  shakes  as  it  does  in  a  severe  rigor.  Unlike  the  intention  tremors 
of  certain  forms  of  organic  nervous  disease,  the  tremor  of  paralysis  agitans 
is  passive.  Be  the  position  of  the  body  and  arms  what  it  may,  the  trembling 
continues,  and  while  certain  attitudes  may  diminish  the  amplitude  of  the 
tremor,  it  is  always  present  except  when  some  definite  and  active  movement 
is  attempted,  when  the  tremor  diminishes  or  even  ceases.  Thus,  if  the  fist 
is  clenched,  or  the  patient  shakes  hands  with  a  friend,  the  movement  may 
stop  momentarily.  On  the  other  hand,  nicely  adjusted  muscular  move- 
ments such  as  are  involved  in  writing  do  not  stop  the  tremor,  and  for  this 
reason  handwriting  is  usually  impossible  when  the  disease  is  well  developed. 

The  tremor  not  only  involves  the  head  and  arms  but  extends  to  the  legs 
as  well,  and  it  may  affect  the  muscles  of  the  thigh.  Rarely  the  muscles  of 
the  jaw  are  affected.  The  tremor  continues  only  during  the  waking  hours, 
and  usually  ceases  in  sleep.  Not  rarely  paralysis  agitans  is  associated  with 
insomnia  because  the  twitching  movements  keep  the  patient  awake,  or  the 
aching  in  the  affected  muscles  makes  the  patient  so  uncomfortable  that 
sleep  is  postponed  until  the  patient  is  exhausted.  As  the  patient  stands  in 
front  of  the  physician,  the  chin  is  usually  pushed  forward  and  the  body  bent 
forward.  The  arms  and  the  elbows  are  slightly  flexed. 
66 


1Q42  DISEASES  OF   THE  XERVOUS   SYSTEM 

After  the  disease  is  well  developed,  chronic  muscular  rigidity  becomes  a 
SATnptom  which  is  even  more  constant  than  tremor.  It  not  only  involves  the 
parts  that  we  have  spoken  of,  but  also  the  muscles  of  the  neck  and  back,  and 
even  those  of  the  face.  As  the  patient  walks,  his  gait  usually  increases  in  speed 
and  the  attitude  is  that  of  a  person  who  is  attempting  to  progress  rapidly. 
It  is  unfortunate  that  the  term  "paralysis  agitans"  is  applied  to  the  early 
stages  of  this  disease,  for  paralysis,  in  the  sense  of  great  loss  of  power,  only 
occurs  in  its  very  last  stages,  and  not  infrequently  the  patient  will  suffer 
from  the  malady  for  years  without  developing  paral}iic  symptoms.  The 
skin  covering  the  parts  affected  is  not  infrequently  unduly  moist  by  reason 
of  profuse  perspiration.  There  are  no  disturbances  of  sensation,  and  the 
mind  is  unaffected  save  by  the  mental  depression  which  is  produced  by  the 
annoyance  of  the  disease. 

Diagnosis. — Paralysis  agitans  is  to  be  separated  from  multiple  sclerosis 
by  its  onset  late  in  life,  by  the  fineness  of  the  tremor,  by  the  fact  that  it 
is  present  when  no  voluntary  movement  is  made,  and  by  the  presence  of 
rigidity.  An  examination  of  the  eyes  fails  to  reveal  the  nystagmus  or  the 
changes  in  the  optic  nerve  which  are  characteristic  of  multiple  sclerosis.  In 
paretic  dementia  the  tremor  is  not  rh>i;hmical,  occurs  when  the  patient 
makes  a  movement  and  not  when  at  rest,  and  there  is  associated  "^ith  the 
tremor  the  mental  disturbance,  the  scanning  speech,  and  evidences  of 
paralysis. 

Sometimes  in  old  persons  a  senile  tremor  develops.  This  chiefly  affects 
the  head,  and  is  increased  rather  than  decreased  by  active  movements;  but 
in  some  instances  senile  tremor  bears  a  close  resemblance  to  paralysis 
agitans.  Indeed,  it  has  been  suggested  that  the  latter  disease  is  essentially 
a  premature  nervous  senility. 

Prognosis. — Paralysis  agitans  does  not  materially  shorten  life.  It  fre- 
quently lasts  for  twenty  years.  Recovery  practically  never  occurs.  Tem- 
porary remissions  in  the  severity  of  the  symptoms  may  take  place. 

Treatment. — As  in  many  diseases  which  apparently  depend  upon  func- 
tional derangement,  treatment  is  not  followed  by  very  satisfactory  results. 
The  patient  should  be  forbidden  to  subject  himself  to  nervous  stress  and 
worry,  which  materially  increase  the  severity  of  the  malady.  Everything 
should  be  done  to  reinstate  his  nervous  balance  by  a  healthy  out-door  life 
and  freedom  from  care.  Massage  and  electricity,  as  a  rule,  do  little  good. 
In  some  cases  they  do  harm  by  increasing  the  exhaustion  of  the  affected 
muscles. 

A  very  large  number  of  drugs  have  been  employed  with  asserted  good 
results,  but  none  have  the  confidence  of  those  members  of  the  profession 
who  have  had  large  experience.  Of  all  the  remedies  which  have  been 
recommended,  hyoscine  seems  to  have  received  the  greatest  amount  of 
praise.  It  should  be  given  in  the  dose  of  jto"  ^^  ^  grain  once,  t^^'ice,  or 
thrice  a  day;  the  size  of  the  dose  and  the  frequency  of  its  administration 
being  governed  by  the  severity  of  the  tremor  and  by  the  susceptibility  of 
the  patient  to  drugs  of  this  character.  Duboisine  may  also  be  given  in 
similar  doses.  Where  there  is  much  aching  of  the  affected  muscles,  hot 
compresses  give  relief,  and  if  the  patient  is  in  a  condition  of  nervous  irri- 


CHOREA   MINOR  1043 

tation,  the  bromides  and  chloral  are  advantageous.  The  employment  of 
such  powerful  nervous  and  vascular  sedatives  as  veratrum  viride  and  gel- 
semium  must  be  resorted  to  with  great  caution.  In  doses  large  enough  to 
quiet  the  tremor  they  are  prone  to  produce  too  much  circulatory  depression. 


CHOREA  MINOR. 

Definition. — Chorea  minor,  or  acute  chorea,  sometimes  called  "Syden- 
ham's chorea,"  or  "St.  Vitus'  dance,"  is  a  nervous  disease  characterized 
by  irregular,  purposeless  movements,  sometimes  limited  to  certain  muscles, 
but  at  others  involving  all  the  muscles  of  the  limbs,  face,  and  trunk.  It 
affects,  in  the  great  majority  of  instances,  children  between  the  fifth  and 
fifteenth  years  of  life. 

Etiology. — That  sex  acts  as  a  predisposing  cause  of  chorea  is  shown  by 
the  fact  that  girls  are  affected  three  times  as  often  as  boys,  and  in  the  period 
of  life  from  the  fifteenth  to  the  twenty-fifth  year  males  escape  almost  entirely. 
The  age  which  predisposes  to  its  development,  or  is  most  susceptible, 
is  from  the  fifth  to  the  fifteenth  year.  After  the  fifteenth  year  it  steadily 
decreases  in  frequency  until  the  twenty-fifth  year  is  reached,  after  which 
it  is  very  rarely  met  with.  The  disease  may,  however,  occur  at  all  ages. 
Nervous,  high-strung  children  suffer  from  it  more  frequently  than  those 
of  a  more  phlegmatic  temperament,  particularly  if,  in  addition,  they  are 
anaemic,  and  have  a  family  history  indicating  that  they  are  prone  to  attacks 
of  acute  rheumatism. 

Of  the  exciting  causes  may  be  named  sudden  shock  or  acute  mental 
excitement,  but  in  all  such  cases  these  causes  are  indirect,  that  is,  they 
serve  to  disturb  the  nervous  equilibrium,  already  unstable  from  other 
causes.  In  some  cases  the  disease  seems  to  be  acquired  by  association  with 
a  choreic  child,  and  in  this  way  a  large  number  of  children  in  homes  and 
asylums  may  become  affected.  Whether  many  of  these  cases  are  true  chorea 
or  merely  imitations  of  it,  or  due  to  hysteria,  is  difficult  to  determine. 

That  there  is  a  very  close  relationship  between  acute  articular  rheu- 
matism and  true  chorea  is  certain.  Even  those  physicians  who  deny 
that  the  rheumatism  produces  chorea  are  forced  to  admit  that  the  occur- 
rence of  chorea  after  attacks  of  acute  rheumatic  infection  is  remarkably 
frequent.  Not  rarely  chorea  complicates  the  development  and  progress  of 
the  acute  endocarditis  produced  by  this  infection.  Whether  the  poison  of 
rheumatism  affects  the  nerve  cells  of  the  brain,  or  whether  the  disease  is 
due  to  changes  in  the  finer  capillaries  supplying  the  brain,  or  to  minute 
emboli,  is  unknown.  Certain  clinicians  have  endeavored  to  show  that 
chorea  is  due  to  a  specific  infection,  and  Pianese  isolated  a  diplococcus 
which  was  capable  of  producing  an  experimental  chorea.  There  is  no 
proof,  however,  that  such  a  specific  agent  exists. 

Under  the  name  of  chorea  gravidarum,  a  form  of  the  disease  is  met  with 
in  pregnant  women,  usually  only  in  primiparse.  In  these  cases  the  gravid 
state  seems  to  develop  a  condition  of  lack  of  nervous  equilibrium,  for  the 
condition  ceases,  as  a  rule,  with  the  termination  of  pregnancy.    Occasionally 


1044  DISEASES  OF   THE  NERVOUS  SYSTEM 

in  old  age  a  senile  chorea  develops,  but  it  is  a  distinct  entity  from  the 
chorea  of  childhood. 

Frequency. — Chorea  is  much  more  frequently  met  with  in  England  than 
in  the  United  States.  Morris  Lewis  has  shown  that  its  period  of  greatest 
frequency  is  March. 

Pathology  and  Morbid  Anatomy. — Cases  of  chorea  come  to  autopsy  infre- 
quently, and  therefore  we  have  not  as  much  information  in  regard  to  post- 
mortem findings  in  this  disease  as  is  desirable.  In  most  of  those  instances 
in  which  death  occurs  during  an  attack  of  chorea,  the  autopsy  reveals  acute 
endocarditis,  or  chronic  endocarditis  with  an  acute  exacerbation,  and  not 
rarely  some  degeneration  of  the  myocardium.  In  the  great  majority  of 
instances  the  results  of  examining  the  brain  have  been  negative,  and  if  the 
positive  results  which  have  been  obtained  are  compared,  they  are  found  to 
be  most  variable.  In  some  instances  an  intense  hyperemia  has  been 
present;  in  others  minute  hemorrhages;  in  still  others  there  have  been 
small  areas  of  inflammation  and  softening;  while  other  cases  have  shown 
signs  of  meningitis,  or  thrombosis  of  the  smaller  bloodvessels  supplying 
the  brain.  So,  too,  the  changes  which  have  been  found  in  the  spinal  cord 
have  been  too  varied  to  lead  one  to  believe  that  they  are  in  any  way  closely 
connected  with  the  disease.  Some  observers  have  considered  that  they  were 
the  result  rather  than  the  cause  of  the  condition.  Choreiform  movements 
sometimes  develop  in  persons  who  have  suffered  from  an  organic  brain 
lesion,  but  there  is  no  reason  to  believe  that  this  form  of  chorea  and  chorea 
minor  have  any  close  anatomical  relationship. 

Symptoms. — The  onset  of  chorea  may  be  either  sudden  or  gradual.  In 
those  cases  in  which  it  is  gradual,  it  is  first  noted  that  the  child  is  restless, 
and  seems  unable  to  keep  still.  Not  rarely  it  is  awkward  in  its  movements, 
and  falls  over,  or  bumps  into  articles  of  furniture.  When  the  disease  is 
developed  the  child  is  continually  restless,  the  arm  or  arms  being  moved 
in  every  possible  direction.  Sometimes  the  muscles  of  the  shoulders  are 
worked  as  if  the  child  was  uncomfortable  by  reason  of  ill-fitting  clothes. 
The  body  is  roiated  from  one  side  to  the  other,  and  the  chin  drawn  first  to 
one  shoulder  then  to  the  other,  then  elevated,  then  depressed.  When  the 
movements  are  marked,  walking  is  interfered  with  and  it  may  be  difficult 
for  the  patient  to  stand.  Unlike  most  involuntary  movements,  the  move- 
ments of  chorea  are  not  confined  to  one  group  of  muscles,  but  usually 
attack  different  groups  alternately.  Neither  is  the  movement  in  the  nature 
of  a  tremor.  It  is  like  a  voluntary  movement,  but  is  purposeless  and  incom- 
plete. Not  infrequently  the  child  laughs  and  cries  without  adequate  cause. 
The  movements  affect  the  upper  extremities  more  than  the  lower  extremi- 
ties. The  tongue  is  sometimes  involved,  and  for  this  reason  the  speech  may 
be  disturbed.  The  child  also  frequently  gives  vent  to  curious  guttural  or 
smacking  sounds,  due  to  the  action  of  the  muscles  of  the  mouth,  pharynx, 
and  tongue.  These  sounds  may  also  be  increased  by  spasm  of  the  diaphragm. 
Occasionally,  chorea  may  be  limited  to  one  limb,  when  it  is  called  mono- 
chorea, or  when  it  is  confined  to  one  side  of  the  body  it  is  called  hemichorea. 
These  motions  distinctly  interfere  with  ordinary  voluntary  movement, 
and  it  becomes  almost  impossible  for  the  child  to  perform  an  ordinary  act 


CHOREA    MINOR  1045 

slowly;  if  it  is  to  be  successfully  carried  out,  it  must  be  done  with  great 
rapidity.  Any  cause  which  produces  mental  excitement  in  the  patient 
greatly  increases  the  severity  of  the  jerking.  Some  clinicians  have 
recorded  an  exceedingly  severe  form  of  chorea  in  which  the  patient  has  such 
violent  muscular  movements  that  he  bites  his  tongue,  can  not  eat,  and  is 
thrown  about  from  side  to  side  as  if  he  were  in  a  violent  convulsion.  The 
twitchings  of  chorea  may  or  may  not  stop  with  sleep.  In  those  cases  in 
which  the  movements  continue  at  night,  the  disease  is  usually  severe,  and 
it  is  in  this  type  of  cases  that  death  sometimes  occurs  from  exhaustion. 

The  mental  state  of  the  patient  is  one  of  irritability  and  peevishness.  In 
adults  there  may  be  hallucinations,  and  even  a  violent  delirium.  Some 
have  thought  that  those  cases  in  which  insanity  develops,  and  to  which 
the  name  chorea  insaniens  is  applied,  do  not  belong  to  ordinary  chorea 
minor.  These  mental  disturbances  not  rarely  complicate  the  chorea  of 
pregnancy. 

Except  for  the  exhaustion  of  the  general  system  which  is  produced  by 
the  movements,  there  is  no  impairment  of  strength,  nor  is  the  electric 
reaction  of  the  muscles  altered.  In  some  cases  of  a  severe  type,  leading  to  a 
fatal  issue,  hyperpyrexia  has  been  noted,  which  is  probably  due  to  endo- 
carditis. Many  years  ago  I  reported  a  case  of  monochorea  in  which  the 
temperature  of  the  affected  part  was  raised.  In  some  instances  weakness 
or  even  marked  paralysis  occurs  in  one  or  more  of  the  affected  limbs,  and  to 
this  type  of  cases  is  applied  the  term  "  paralytic  chorea." 

Complications. — As  already  stated,  chorea  is  a  disease  which  is  associated 
with  a  lack  of  nervous  stability.  It  is  manifest,  therefore,  that  it  may  often 
be  complicated  by  symptoms  of  hysteria.  Indeed,  it  may  be  difficult  to 
determine  whether  the  patient  is  hysterical  or  choreic.  That  endocarditis 
frequently  precedes,  or  accompanies,  or  complicates  chorea,  has  also  been 
stated,  but  every  case  of  chorea  that  presents  a  cardiac  murmur  is  not  neces- 
sarily suffering  from  endocarditis,  since  the  murmur  is  not  infrequently 
due  to  anaemia,  or  to  relaxation  of  the  fibres  surrounding  the  mitral  orifice. 

Diagnosis. — Ordinary  cases  of  chorea  in  childhood  are  easily  diagnosed, 
particularly  if  the  history  of  the  patient  is  borne  in  mind.  Between  the  ages 
of  fifteen  or  twenty-five  care  must  be  taken  that  it  is  not  confused  with 
hysteria.  Sometimes,  too,  choreiform  movements  develop  in  those  parts 
which  are  affected  by  infantile  cerebral  palsy,  but  in  such  cases  paralysis 
is  present  and  muscular  rigidity  is  noticeable,  while  the  movements  are 
really  different  (athetosis). 

Duration  and  Prognosis. — Chorea  minor  usually  lasts  from  two  to  three 
months,  and  sometimes  extends  over  a  year.  Mild  cases  may  continue 
for  only  a  few  weeks.  The  prognosis  as  to  recovery  is  good,  the  mortality 
being  about  3  per  cent.,  if  all  cases  are  included,  death  being  due  to  com- 
plications rather  than  to  the  disease  itself.  Relapses  are  not  infrequent  in 
chorea.  Unfavorable  symptoms  are  rapid  loss  of  flesh,  fever,  and  delirium. 
The  prognosis  is  worse  as  to  duration  in  adults  than  in  children.  In  the 
chorea  of  pregnancy  the  prognosis  is  very  much  more  grave  than  any  other 
form  of  the  disease,  the  mortality  varying  from  20  to  25  per  cent.  Senile 
chorea  is  often  a  permanent  affection  and  is  rarely  fatal. 


1046  DISEASES  OF   THE  NERVOUS  SYSTEM 

Treatment. — From  what  has  been  said  in  regard  to  the  general  condition 
of  the  patient  who  suffers  from  chorea,  it  is  evident  that  mental  and  nervous 
quiet  are  absolutely  essential.  The  child  should  not  be  exposed  to  the 
excitement  or  mental  stress  of  school-work,  neither  should  it  be  subjected 
to  punishment  or  to  criticism  because  of  its  movements.  On  the  contrary, 
the  fact  that  it  is  suffering  from  choreic  movements  should  be  ignored  unless 
the  physician  is  convinced  that  the  case  is  one  of  hysteria  and  not  of  chorea. 
Iron  and  arsenic  are  to  be  given  if  ansemia  is  present,  and  the  salicylates  are 
useful  if  there  is  a  rheumatic  history.  If  the  movements  are  severe  enough 
to  exhaust  the  child,  it  should  be  kept  in  bed  and  sleep  should  be  obtained 
by  the  use  of  hypnotics.  These  drugs,  however,  must  be  used  cautiously 
lest  they  produce  general  depression,  and  it  should  always  be  remembered 
that  a  hot  pack  will  often  put  a  choreic  child  to  sleep  and  temporarily  or 
permanently  arrest  the  choreic  movements.  I  have  seen  life  saved  in  at 
least  two  instances  by  the  hot  pack. 

Although  there  is  no  specific  remedy  for  chorea,  arsenic  nearly  approaches 
the  position  of  a  specific.  How  it  acts  is  not  known.  The  best  way  to 
administer  it  is  in  the  form  of  Fowler's  solution,  starting  with  2  drops  three 
times  a  day  for  a  child  of  ten,  and  increasing  it  a  drop  a  day  until  some 
puffiness  about  the  eyes  and  nose  or  gastrointestinal  irritation  indicates  that 
the  full  physiological  effect  of  the  drug  is  present,  when  it  should  be  stopped 
or  cut  down  to  one-half  the  quantity.  If  this  is  not  done  an  arsenical 
neuritis  may  develop. 

Next  to  arsenic  in  value  is  cimicifuga,  given  in  the  dose  of  ^  drachm  of 
the  fluid  extract  twice  or  thrice  a  day.  Antipyrin  and  acetanilid  have  also 
been  employed  with  success.  Bromides  should  be  tried  after  the  other 
drugs  have  failed. 

If  the  chorea  of  pregnancy  becomes  severe  it  may  be  necessary  to  induce 
labor. 

Other  Forms  of  Chorea. 

Huntington's  Disease. — ^Under  the  name  of  "  hereditary  chorea,"  or 
Huntington's  disease,  an  affection  is  met  with  which  must  be  clearly  differen- 
tiated from  chorea  minor.  It  is  a  rare  condition  which,  as  its  name  indicates, 
is  hereditary,  although  it  does  not  always  affect  consecutive  generations, 
sometimes  passing  from  the  grandparent  to  the  child,  although  in  such  cases 
the  parent  is  usually  excessively  neurotic.  Both  sexes  suffer  from  it  equally. 
The  disease  begins  between  the  thirtieth  and  fortieth  year  of  life  in  most 
instances,  and  no  exciting  cause  can  usually  be  discovered. 

Its  early  symptoms  consist  in  twitchings  of  the  muscles  of  the  face  and 
upper  extremities,  which  gradually  increase  in  severity  and  in  the  area 
which  they  involve,  until  the  entire  muscular  system  may  be  affected.  The 
patient,  under  these  circumstances,  carries  on  a  series  of  grimaces  and  ges- 
ticulations, but  it  is  a  noteworthy  fact  that  he,  or  she,  can  inhibit  these 
movements  at  least  for  a  period  long  enough  to  permit  the  voluntary 
movement  which  it  is  desired  to  make.  When  the  muscles  of  the  trunk 
and  legs  are  involved  the  body  is  tossed  hither  and  thither  with  rapid 


HYSTERIA  1047 

movements.  Sensation  is  not  involved.  Paralysis  of  a  hemiplegic  type 
develops  very  rarely.  The  mind  gradually  fails,  the  mental  failure  being 
preceded  by  depression  and  irritability. 

Huntington's  chorea  is  an  incurable  disease.  It  usually  ends  in  the 
patient  becoming  bedridden  and  dying  from  some  intercurrent  malady. 
It  may,  however,  last  for  many  years.  Cases  are  on  record  in  which  the 
patient  has  lived  thirty  years  after  the  disease  began  to  manifest  itself.  The 
progressive  character  of  the  malady,  the  period  of  life  at  which  it  develops, 
the  progressive  dementia,  and  the  history  of  heredity  all  aid  in  separating 
it  from  chorea  minor. 

The  morbid  anatomy  is  not  understood.  In  some  cases  the  lesions  of 
the  brain  have  resembled  those  of  paretic  dementia. 

The  treatment  consists  in  a  healthy  out-door  life,  and  the  use  of  nervous 
sedatives,  and  tonics,  with  the  object  of  maintaining  the  patient's  general 
health.  Cases  apparently  identical  with  Huntington's  chorea,  but  occur- 
ring singly,  are  spoken  of  as  chronic  chorea. 

Dubini's  Disease. — Under  the  name  of  "  electrical  chorea,"  or"Dubini's 
disease,"  a  form  of  chorea  characterized  by  severe  muscular  contractions 
resembling  those  produced  by  electricity  has  been  described  by  Dubini  as 
affecting  peasants  in  Northern  Italy.  Occasionally,  the  movements  may  be 
epileptiform  in  character.  Paralysis  soon  develops;  pain  is  suffered  in  the 
head,  neck,  and  back,  and  death  results,  as  a  rule,  from  exhaustion.  A  few 
cases  have  been  reported  as  having  recovered. 

Another  form  of  electrical  chorea  seen  in  children  has  been  described  by 
Bergeron.  Such  cases  usually  recover.  I  showed  such  a  case  before  the 
Neurological  Society  of  Philadelphia  many  years  ago.  The  patient,  a  boy, 
a  little  past  puberty,  suffered  from  violent  contractions  which  were  electrical 
in  character. 


HYSTERIA. 

Definition. — Hysteria  is  a  chronic  functional  disturbance  of  the  nervous 
system  in  which  the  motor  nervous  system  may  manifest  its  disorder  by 
convulsions,  palsies,  or  contractures,  the  psychical  nervous  apparatus  by 
emotional  disturbances,  and  the  sensory  apparatus  by  lost,  diminished,  or 
increased  sensibility.  It  is  manifest,  therefore,  that  the  disease  involves 
both  the  central  and  peripheral  portions  of  the  nervous  system,  but  there  can 
be  no  doubt  that  the  dominating  condition  is  a  psychosis.  Hysteria 
undoubtedly  depends  upon  a  condition  of  disturbed  nervous  equilibrium. 

Etiology. — ^There  can  be  no  doubt  that  this  affection  is,  to  some  extent, 
hereditary;  that  is,  a  parent  or  parents  who  possess  an  unstable  nervous 
system  naturally  transmit  a  similar  condition  to  their  offspring,  and  in  a  very 
large  proportion  of  cases  it  will  be  found  that  the  patient  is  a  child  of  parents 
who  have  at  various  times  manifested  neurotic  or  hysterical  disorders. 
Age  has  a  distinct  influence  upon  the  disease.  Its  most  frequent  period  of 
occurrence  is  from  fifteen  to  twenty-five  years  of  age  in  women,  although 
in  males  it  usually  appears  at  from  twenty  to  thirty.     Occasionally,  how- 


1048  DISEASES  OF   THE  NERVOUS  SYSTEM 

ever,  children  suffer  from  it,  particularly  before  puberty,  and  sometimes 
much  earlier  than  this.  The  condition  is  met  with  far  more  frequently  in 
females  than  in  males,  but  statistics  vary  from  40  to  1  to  4  to  1  or  even  2 
to  1,  according  to  different  writers.  It  is  much  more  common  in  the  very  poor 
and  in  the  rich  than  in  the  middle  classes,  and  in  the  Latin  races  than  in  the 
Anglo-Saxon  race.  In  x\merica  it  is  most  frequently  met  with  in  the  poorer 
class  of  Jews,  who  are  often  underfed,  poorly  housed,  much  confined,  and 
under  great  nervous  excitation  and  stress.  It  is  much  more  common  in 
France  and  Italy  than  in  Germany  and  England. 

If  it  be  true  that  the  underlying  cause  of  hysteria  is  a  lack  of  nervous 
control  or  balance,  it  is  evident  that  a  number  of  conditions  may  be  con- 
sidered as  direct  causes  of  the  malady.  In  other  words,  any  condition  which 
upsets  the  nervous  balance  may  provoke  the  disease.  It  is,  therefore,  fre- 
quently found  that  some  great  grief  or  intense  joy  has  been  productive 
of  the  first  manifestation  of  the  disease,  or,  again,  that  some  injury  or 
fright  has  acted  in  a  similar  manner.  Great  worry  in  business,  or  over  a 
love  affair,  may  produce  a  similar  result.  None  of  these  causes  would  pro- 
foundly affect  a  healthy  nervous  system.  All  of  them  are  sufficient  to 
disturb  the  balance  of  a  nervous  organization  already  abnormal. 

Pathology. — As  already  stated,  hysteria  is  a  purely  functional  disease, 
and  the  central  and  peripheral  nervous  systems  show  no  alterations  which 
can  be  considred  as  responsible  for  the  malady. 

Symptoms. — Hysterical  individuals  usually  present  evidences  of  nervous 
irritability  which  may  manifest  itself  in  great  excitement,  in  violent  anger, 
in  undue  anxiety,  or  in  great  mental  depression.  All  of  these  manifesta- 
tions may  follow  one  another  with  extraordinary  rapidity.  The  patient  also 
manifests  distinct  lack  of  self-control,  both  in  regard  to  her  emotions  and 
her  impulses.  At  times  she  may  seem  utterly  incapable  of  accomplishing 
anything  which  ought  to  be  done.  At  another  time  she  can  develop  an 
amount  of  energy  and  persistence  which  is  surprising,  provided  that  she 
conceives  it  to  be  her  duty  or  her  wish  to  accomplish  such  an  end.  The 
power  of  thought  is  in  no  way  impaired,  but  judgment  is  warped  and  uncer- 
tain. Not  infrequently  the  patient  has  perverse  ideas  which  may  seem  to 
amount  to  delusions,  but  which  do  not  remain  constant  as  in  cases  of  insanity. 

In  some  instances  the  first  symptoms  of  the  malady  are  manifested  by  a 
hypersensitiveness,  so  that  the  girl  cries  easily,  and  perhaps  laughs  more 
readily  and  for  a  longer  time  than  is  necessary  in  the  appreciation  of  a 
remark  which  is  amusing.  Restless  sleeping  also  may  be  present.  As  the 
condition  develops,  attacks  of  headache  and  vomiting  may  come  on,  and  she 
may  suffer  from  somnambulism. 

When  the  condition  becomes  still  more  severe,  so  that  it  amounts  to 
that  state  which  is  sometimes  called  "hysteria  major,"  the  disturbances  of 
sensation  and  motion  become  intense.  In  addition  to  attacks  of  crying 
and  laughter,  the  patient  may  pass  into  a  trance  or  into  a  condition  of 
catalepsy.  Or,  again,  the  patient  may  suddenly  fall  and  be  seized  by  a 
convulsion  which  is  distinctly  epileptiform  in  character.  Often,  however, 
the  convulsion  is  more  largely  tonic  than  clonic,  the  hands  and  fingers 
being  flexed  and  the  forearm  flexed  on  the  arm,  while  the  legs  and  feet  are 


HYSTERIA  1049 

extended  and  the  eyes  closed.  If  the  eyelids  are  lifted,  the  eyeballs  are  often 
found  to  be  fixed  in  convergence  or  undergo  irregularmovements.  The  pupils 
are  dilated.  The  surface  of  the  body  is  more  or  less  anaesthetic.  As  a  rule, 
the  patient  does  not  froth  at  the  mouth  as  much  as  in  true  epilepsy,  nor  does 
she  bite  her  tongue  as  is  done  in  epilepsy.  So,  too,  she  rarely  hurts  herself 
when  in  the  convulsive  seizure.  The  attack  may  last  from  a  few  minutes 
to  several  hours,  or  even  longer  than  this,  and  may  vary  in  its  intensity 
from  semi-consciousness  with  slight  twitchings  of  the  muscles  to  apparent 
total  unconsciousness  and  severe  convulsive  seizure.  The  expression  of 
the  face  is  often  quite  characteristic.  In  some  instances  it  is  remark- 
ably peaceful  after  the  convulsion  passes  by.  In  others  it  is  ecstatic  or 
terror-stricken.  In  very  young  patients  curious  guttural  and  other  sounds 
may  be  made,  and  the  patient  may  bark  like  a  dog  or  mew  like  a 
cat. 

It  is  noteworthy  that  many  of  these  patients  are  conscious  of  what  is  going 
on  around  them  during  the  attack,  although  at  the  time  they  may  manifest  no 
evidence  of  this.  Not  rarely  a  sharply  spoken  word  of  command  may  bring 
the  attack  to  a  close,  or  the  threat  of  applying  some  instrument  which  is  capa- 
ble of  causing  pain  may  do  likewise.  When  the  patient  returns  to  conscious- 
ness, it  may  be  found  that  there  is  loss  of  power  in  an  arm  or  leg,  or  upon  one 
side  of  the  body,  with  or  without  loss  of  sensation.  Frequently  the  so-called 
hysterogenic  zones  may  be  discovered,  pressure  upon  which  causes  pain  and 
may  provoke  an  hysterical  attack,  or  if  pressure  on  these  parts  is  used  during 
the  attack  it  may  arrest  it. 

The  sensory  symptoms  of  hysteria,  in  distinction  from  those  just  described 
in  connection  with  a  critical  period,  consist  in  ancBsthesia  in  all  its  forms,  par- 
ticularly analgesia  of  the  cutaneous  and  mucous  surfaces  and  disturbances 
in  the  special  senses.  The  most  common  form  of  cutaneous  ancesthesia  is 
hemiancesthesia  involving  exactly  one-half  the  body.  After  this,  the  most 
common  type  is  segmental  anaesthesia,  in  which  an  arm,  or  leg,  or  part  of  the 
face  is  anaesthetic,  the  margin  of  the  anaesthetic  area  being  sharply  defined, 
while  the  disturbance  of  sensation  does  not  correspond  to  the  distribution 
of  any  one  nerve  trunk.  Much  more  rarely  patches  of  anaesthesia  occur 
in  different  portions  of  the  body.  In  these  anaesthetic  areas  the  senses  of 
touch  and  of  heat  and  cold  are  usually  preserved  to  some  slight  extent. 
Occasionally,  the  affected  part  has  a  subnormal  temperature.  When  the 
anaesthesia  is  limited  to  one  side  it  affects  the  left  far  more  frequently  than 
the  right  half  of  the  body.  If  the  anaesthesia  is  of  the  hemianaesthetic,  or 
segmental,  type  there  is  usually  more  or  less  complete  loss  of  motor  power 
in  the  same  limb. 

The  disturbances  of  special  sense  consist  in  an  anaesthetic  condition  of 
the  retina  whereby  the  visual  field  is  greatly  narrowed,  particularly  for  cer- 
tain colors  and  often  for  those  colors  which  normally  have  the  widest  field, 
and  the  color  sense  is  disturbed  or  reversed.  These  disturbances  may  or 
may  not  complicate  those  just  named.  When  hemianaesthesia  is  present, 
the  eye  upon  the  affected  side  is  sometimes  partly  or  even  totally  blind,  not  as 
in  organic  hemianopic  hemianaesthesia.  So,  too,  the  acuity  of  the  auditory 
nerve  may  be  diminished,  particularly  upon  that  side  of  the  body  which  is 


1050  DISEASES  OF   THE  NERVOUS  SYSTEM 

most  affected.  The  sense  of  taste  may  also  be  perverted  and  the  sense  of 
smell  may  be  lost. 

Neuralgic  pains  are  not  common  in  hysteria  except  when  there  is  present 
grave  anaemia  and  other  common  causes  of  neuralgia.  In  certain  portions 
of  the  body,  however,  hypersesthesia  of  the  skin  may  be  present  as  in  the 
hysterogenic  zones  described.  These  zones  are  most  frequently  found  in 
females  in  the  groin,  whence  the  name  "ovarian"  tenderness,  and  under 
the  mammary  glands,  and  in  males  on  the  scrotum,  also  along  the  spine, 
but  they  may  be  found  in  any  part.  Paralysis  of  the  extraocular  muscles 
is  sometimes  met  with.  Usually  the  internal  rectus  is  affected,  and  some- 
times the  external  rectus.  Speech  may  be  impaired  by  paralysis  of  the 
adductors  of  the  vocal  cords.  The  development  of  this  condition  is  called 
"  hysterical  aphonia,"  the  patient  being  speechless,  or  able  to  converse  only 
in  a  whisper.    The  onset  of  this  condition  is  usually  sudden. 

The  paralysis  of  motion  already  referred  to  often  persists  for  a  long  period 
of  time,  and  in  association  with  this  paralysis  it  not  rarely  happens  that 
other  muscles,  often  those  which  are  antagonistic  to  the  ones  which  are 
paralyzed,  suffer  from  contractures.  At  first  these  muscles  may  be  simply 
abnormally  irritable  and  the  contractures  may  be  jSeeting,  or  they  may  last 
as  long  as  the  paralysis  of  motion  and  sensation,  and  in  this  way  resemble 
the  contractures  which  are  sometimes  met  with  in  cerebral  diplegia.  Tremors 
may  also  affect  the  muscles  of  an  arm,  of  the  face,  or  of  a  leg,  and  these 
tremors  may  resemble  those  of  paralysis  agitans  or  other  diseases  charac- 
terized by  tremor,  particularly  if  the  patient  has  been  associated  with  such 
a  case.  The  amount  of  atrophy  or  wasting  which  occurs  in  a  paralyzed 
part  is  usually  very  slight,  and  depends  almost  entirely  upon  lack  of  use. 

Of  the  internal  viscera  it  may  be  said  that  the  functions  are  not  gravely 
impaired  in  most  instances,  unless  perchance  these  viscera  suffer  from  the 
chief  manifestations  of  the  disease.  A  very  common  symptom  of  hysteria, 
present  in  the  majority  of  cases  is  the  sensation  as  if  a  ball  or  small  orange 
rose  into  the  pharynx.  This  is  called  "globus."  In  other  instances  violent 
attacks  of  vomiting  develop.  In  still  others,  the  "rifting"  of  large  quantities 
of  gas,  or  of  air  which  has  been  swallowed,  takes  place,  accompanied  by 
much  rumbling  in  the  abdomen.  In  still  other  instances  rumination,  or,  as 
it  is  sometimes  called,  "merycismus,"  occurs;  that  is,  the  patient  regur- 
gitates food,  which  has  been  swallowed,  into  the  mouth  for  a  second  chewing. 
At  other  times  intestinal  disorders  are  present.  I  have  seen  a  large  phantom 
tumor  of  the  intestine,  in  a  patient  who  had  constantly  refused  food  until  she 
was  emaciated  to  the  last  degree,  give  rise  to  the  belief  that  a  malignant 
growth  was  present.  At  times  these  patients  have  a  perverse  appetite,  eat- 
ing chalk  or  other  materials  not  commonly  swallowed.  The  urine  is  some- 
times very  limpid  and  free.  At  other  times  it  is  scanty  and  high  colored. 
After  an  acute  attack  of  hysteria  it  is  usually  limpid. 

Of  the  circulatory  disorders  attacks  of  tachycardia  are  by  no  means 
uncommon.  Sometimes  the  patient  will  complain  of  severe  pain  in  the 
neighborhood  of  the  heart.  This  pseudoangina  is  characterized  by  a  sensa- 
tion of  distention  of  the  heart  in  distinction  from  the  pain  of  true  angina, 
which  is  usually  described  as  if  the  heart  were  being  tightly  compressed. 


HYSTERIA  1051 

The  peripheral  vascular  system  may  also  be  disturbed.  Abnormal  flushing 
or  blushing  or  local  anaemia  and  pallor  may  be  present.  At  times  even 
oedema  may  develop.  In  other  instances  the  part  becomes  so  pallid  or  slate- 
like in  color  that  it  resembles  Raynaud's  disease,  but  true  gangrene  does  not 
develop.  Very  rarely,  indeed,  a  sharp  febrile  movement  may  take  place. 
Sometimes  hysterical  patients  sufi^er  from  attacks  of  hiccough  or  of  sneezing, 
or  of  rapid  breathing,  cough,  or  difficulty  in  swallowing. 

Under  the  name  of  "  hysteroepilepsy,"  a  form  of  hysteria  characterized 
by  violent  convulsions  closely  resembling  those  of  true  epilepsy  is  described 
by  many  foreign  authors.  It  is  rare  in  this  country.  In  some  instances 
the  convulsive  seizure  is  not  epileptoid,  but  cataleptoid  or  tonic.  The 
patient  may  lie  in  bed  with  the  arms  extended,  as  in  ecstasy,  or  with  the 
hands  tightly  clinched,  as  in  terror  or  anger,  or  the  state  may  resemble 
simple  stupor  or  even  coma.  At  other  times  a  psychical  disturbance  is  mani- 
fested so  that  the  patient  develops  a  delirium.  Often  several  of  these  processes 
are  combmed.  At  first  the  patient  experiences  an  aura  as  in  epilepsy.  This 
is  followed  by  the  epileptoid  form  of  convulsion,  and  this  again  by  the  con- 
tortions and  emotional  attitudes  just  described.  An  emotional  confusion 
is  not  rare;  hallucinations  and  delusions  may  occur  and  confinement  in  an 
asylum  may  be  necessary.    Finally  a  stage  of  delirium  may  develop. 

Diagnosis. — Under  some  circumstances  there  is  no  more  difficult  diagnosis 
than  the  differentiation  of  hysteria  from  organic  nervous  disease,  particularly 
if  the  patient  has  had  an  opportunity  of  studying  the  symptoms  presented 
by  patients  with  organic  nervous  lesions.  The  important  points  in  differ- 
entiation are  the  contraction  of  the  visual  fields  and  the  alterations  in  the 
color  fields,  the  fact  that  the  areas  of  anaesthesia  are  not  confined  to  any 
given  distribution  of  sensory  nerves,  the  presence  of  hysterogenic  or  hyper- 
sesthetic  spots,  the  fact  that  wasting  does  not  develop  to  any  degree  in  the 
paralyzed  muscles,  the  absence  of  the  reaction  of  degeneration,  the 
maintenance  or  persistence  of  the  deep  reflexes,  and  the  peculiar  emotional 
state.  Again,  the  anaesthetic  area  may  be  moved  from  the  first  place  affected 
by  the  mere  placing  of  a  coin  or  a  magnet  over  the  affected  part.  Hysterical 
contractures  also  usually  disappear  in  sleep  or  when  the  patient  is  under 
the  influence  of  an  anaesthetic.  In  the  epileptoid  form  of  attack  the  tongue 
is  never  bitten  nor  the  limbs  injured. 

Prognosis. — ^The  prognosis  as  to  life  is  good.  The  attacks  usually  diminish 
in  frequency  and  severity  with  advancing  years,  but  the  question  of  prognosis 
is  also  governed  by  the  degree  of  nervous  instability  in  the  patient  and  in 
her  parents.  When  the  hereditary  influence  is  bad  and  the  surroundings 
of  the  patient  are  unfavorable  the  malady  may  last  a  lifetime.  In  those 
who  are  well-to-do  and  who  can  afford  to  take  the  treatment  required  by 
such  cases,  the  outlook  is  better  than  in  those  who  are  continually  exposed 
to  bad  surroundings,  with  nervous  stress  and  strain. 

Treatment.: — ^The  treatment  consists  in  the  removal  of  the  patient  from 
those  causes  which  tend  to  produce  nervous  irritability  and  stress.  If  the 
home  surroundings  of  the  patient  are  such  as  to  increase  nervous  irritation, 
the  patient  must  be  removed  from  those  surroundings.  Such  a  patient 
should  always  be  taken  from  school  and  given  lessons  under  a  private  instruc- 


1052  DISEASES  OF   THE  NERVOUS  SYSTEM 

tor.  If  the  symptoms  are  severe  the  Weir-Mitchell  rest  cure  is  essential. 
If  they  are  not  severe  enough  for  this,  an  out-door  life  with  a  moderate 
amount  of  healthy  exercise  carried  to  the  point  of  fatigue,  but  not  of  exhaus- 
tion, is  needful.  If  anaemia  is  present  it  must  be  overcome  by  proper  tonics. 
Insomnia  and  peripheral  nervous  irritation  should  be  treated  by  hot  and 
cold  packs  and  the  various  forms  of  hydrotherapy.  Sedatives  may  be  needed, 
but  it  must  be  remembered  that  the  administration  of  hypnotics  to  neurotic 
patients  frequently  produces  a  drug  habit.  Local  anaesthesia,  in  addition 
to  being  treated  by  hydrotherapy,  will  also  be  benefited  by  the  use  of  the 
rapidly  interrupted  faradic  current  administered  by  means  of  the  ordinary 
wet  sponge,  or,  if  the  anaesthesia  is  marked,  through  the  dry  wire  brush. 
The  physician  must  exercise  a  dominant  influence  over  the  patient,  and  she 
must  be  put  under  the  charge  of  a  trained  nurse  of  strong  character,  who,  on 
the  one  hand,  will  not  be  irritated  by  peculiarities,  but  will  tactfully  dis- 
courage them.  This  mental  side  of  the  treatment  is  too  frequently 
overlooked. 

The  treatment  of  the  hysterical  attack  itself  consists  in  the  administration 
of  nitrite  of  amyl.  There  are  few  cases  of  true  hysteria  that  will  not  be  at 
once  relaxed  if  convulsed,  and  the  attack  stopped  by  this  drug,  which,  on 
the  one  hand,  is  perfectly  safe,  and,  on  the  other,  produces  so  powerful  a 
mental  impression  that  its  use  is  appreciated  by  the  patient.  If  nitrite  of 
amyl  cannot  be  employed,  ether  may  be  used  and  pushed  freely,  but  chloro- 
form is  usually  too  agreeable  to  the  patient  to  be  advantageous.  Not  rarely 
the  use  of  the  dry  electric  brush  or  even  of  the  actual  cautery,  which  may 
be  touched  at  various  points  on  either  side  of  the  spine,  is  advantageous 
through  the  powerful  mental  impression  it  produces. 


EPILEPSY. 

Definition. — Epilepsy  is  a  disease  characterized  by  attacks  of  unconscious- 
ness, which,  in  the  well-developed  form  of  the  malady,  are  accompanied  or 
followed  by  convulsions.  The  convulsions  at  the  moment  of  onset  are 
usually  tetanic  or  tonic  in  type,  but  almost  immediately  become  clonic. 
Indeed,  so  typical  of  epilepsy  are  clonic  convulsions  that  all  convulsions 
of  this  class  are  called  "epileptiform."  Epilepsy  separates  itself  from  other 
convulsive  conditions  associated  with  unconsciousness  by  the  fact  that  it  is 
a  chronic  malady,  whereas  epileptiform  convulsions  arising  from  other 
causes  occur  but  a  few  times  in  the  lifetime  of  the  individual,  as,  for  example, 
in  puerperal  eclampsia  or  ursemic  poisoning.  Hysterical  convulsions,  how- 
ever, closely  resemble  it. 

Etiology. — ^The  etiology  of  epilepsy  is  unknown,  although  in  a  certain 
proportion  of  cases  injuries  to  the  brain  substance  arising  from  external  or 
internal  causes  undoubtedly  predispose  to  or  produce  the  disease.  In  some 
instances  it  has  been  thought  that  the  condition  is  hereditary,  and  this  is  cer- 
tainly true  in  the  sense  that  epileptic  parents  often  have  epileptic  children. 
By  far  the  largest  number  of  cases  collected  by  any  one  writer,  so  far  as 
the  author  is  aware,  are  those  of  Gowers,  who  analyzed  no  less  than  1450 


EPILEPSY  1053 

cases  of  epilepsy,  finding  that  an  inherited  tendency  was  indicated  by  the 
presence  of  insanity  or  epilepsy  in  ancestors  or  collateral  relations  in  rather 
more  than  one-third  of  the  cases  (35  percent.),  and  rather  less  frequently  in 
males  than  in  females,  for  there  was  this  history  in  33  per  cent,  of  the  males 
and  37  per  cent,  of  the  females.  There  was  a  family  history  of  epilepsy  in 
two-thirds  of  the  inherited  cases,  of  insanity  in  one-third,  and  of  both  dis- 
orders in  one-tenth  of  the  cases.  In  the  56  cases  recorded  by  Sieveking 
heredity  was  the  cause  in  11.  Reynolds,  in  his  collection  of  cases,  found 
the  proportion  to  be  31  per  cent.  Hasse  has  collected  1000  cases,  and  has 
found  heredity  the  cause  in  no  less  numbers  than  the  others.  If  we  take 
the  average  result  of  the  conclusions  reached  by  the  clinicians  just  named, 
who  give  exact  figures,  we  find  that  we  have  to  deal  with  4300  cases  of 
epilepsy,  of  which  a  little  over  26  per  cent,  were  due  to  heredity.  Whether 
epilepsy  can  be  induced  in  a  child  by  hereditary  influences  arising  from 
chronic  alcoholism  or  chronic  lead  poisoning  is  open  to  debate.  Certain 
neurologists  are  firmly  convinced  that  these  factors  are  active. 

In  other  instances,  apparently  healthy  children  develop  epilepsy  after 
suffering  from  some  of  the  infectious  diseases  such  as  scarlet  fever.  In  these 
cases  the  infection  has  either  produced  some  definite  lesion  in  the  brain 
or  has  so  impaired  the  normal  growth  of  certain  cells  in  the  cerebral  cortex 
that  their  natural  balance  is  destroyed,  with  the  result  that  periodic  explo- 
sions of  nervous  energy  take  place. 

Syphilis  acts  as  a  cause  of  epilepsy  in  two  ways.  When  the  parent  is 
syphilitic,  the  child  may  sufl^er  from  hereditary  syphilis  or  from  a  para- 
syphilitic  disease  of  the  nervous  system,  with  imperfect  cerebral  develop- 
ment. In  other  cases  acquired  syphilis  produces  epilepsy  in  adults.  Indeed, 
more  than  one  writer  has  expressed  the  belief  that  an  epilepsy  beginning 
after  the  twenty-fifth  year  is  syphilitic  in  origin.  This  is  rather  an  exag- 
gerated statement,  but  it  is  nevertheless  true  that  more  than  three-fourths 
of  all  cases  of  epilepsy  begin  before  the  twentieth  year.  About  half  of 
them  begin  in  the  second  decade  of  life.  Quite  a  large  proportion  begin 
between  the  seventh  and  tenth  years. 

In  some  instances  the  epilepsy  dates  from  the  reception  of  some  severe 
injury  to  the  head.  Cases  that  have  a  traumatic  origin,  those  which  are 
due  to  syphilitic  gumma  or  other  form  of  brain  tumor,  usually  belong  to 
that  type  which  is  called  "Jacksonian"  or  "localized"  epilepsy,  although 
they  may  ultimately  develop  all  the  characteristics  of  the  so-called  idio- 
pathic form. 

For  many  years  it  was  considered  that  a  host  of  conditions  tended 
to  produce  epilepsy  by  reflex  irritation.  Such  causes  as  foreign  bodies 
in  the  ear  or  in  the  nose,  intestinal  worms,  and  uterine  disorders  have  been 
considered  as  causative  factors,  but  in  all  such  cases  it  cannot  be  denied  that 
these  agents  act  indirectly  in  the  sense  that  they  provoke  an  irritation  which 
reflexly  unsets  the  nerve  balance  or  equilibrium  of  an  unstable  motor  area 
of  the  brain.  In  other  words,  in  any  case  of  epilepsy  it  is  to  be  understood 
that  the  underlying  factor  is  a  lack  of  stability  or  nervous  balance. 

The  influence  of  sex  is  not  very  great,  but  males  are  affected  somewhat 
more    frequently    than    females.     Althaus    has    examined    an   enormous 


1054  DISEASES  OF   THE  NERVOUS   SYSTEM 

amount  of  statistics  to  obtain  results  bearing  on  this  point.  He  found  that 
in  54,442  cases  there  were  28,960  males  and  25,482  females. 

Posthemiplegic  epilepsy  due  to  cerebral  injury  may  occur  at  any  age,  but 
there  can  be  no  doubt  that  it  far  more  commonly  occurs  in  infants  than  in 
adults.  In  at  least  two-thirds  of  the  cases  the  onset  is  before  the  fifth  year 
of  age,  and  in  nearly  one-half  it  is  during  the  first  two  years  of  life.  It  is  not 
uncommon  for  the  paralysis  to  occur  in  infancy  and  the  epilepsy  to  begin 
at  puberty.  This  prolonged  interval  is  rare  in  adults,  in  whom  the  epileptic 
seizures  usually  begin  in  less  than  one  year. 

The  frequency  with  which  epilepsy  comes  on  after  the  hemiplegia  of 
childhood  has  been  very  exhaustively  studied.  Thus,  in  Osier's  cases, 
20  children  out  of  97  suffered  from  it.  In  the  80  cases  collected  by 
Gaudard  11  children  had  hemiepilepsy,  and  66  children  out  of  160  cases 
collected  by  Wallenburg  were  epileptic  after  hemiplegia.  In  another  series 
of  cases  collected  by  Osier  15  children  out  of  23  were  thus  affected. 

Pathology. — The  pathology  of  epilepsy  is  not  known.  It  is  true  that  at 
autopsy  many  cases  of  epilepsy  show  atrophic  or  degenerative  changes  in  the 
cerebrum,  but  this  holds  true  of  only  a  certain  proportion,  and  not  of  those 
instances  of  so-called  idiopathic  epilepsy  in  which  there  is  no  history  of 
syphilis,  or  of  injury,  or  of  damage  to  the  brain  through  disease  of  its  blood- 
vessels. In  this  idiopathic  form  the  most  careful  macroscopic  and  micro- 
scopic examinations  of  hundreds  of  cases  have  failed  to  reveal  any  alteration 
which  can  be  considered  as  responsible  for  the  malady.  Some  of  the  micro- 
scopic lesions  which  have  been  described  by  certain  investigators  are  with- 
out doubt  present,  but  in  these  cases  the  question  arises  whether  they  are 
not  the  result  rather  than  the  cause  of  the  affection. 

That  epilepsy  is  a  result  of  an  explosive  discharge  of  nervous  energy  from 
the  motor  areas  of  the  cortex  is  proved  by  the  fact  that  similar  convulsions 
can  be  produced  in  man  and  in  the  lower  animals  by  irritating  these  areas, 
and  that  growths  and  injuries  which  irritate  them  produce  similar  symptoms. 
The  somewhat  ancient  theory  that  the  convulsive  disturbance  is  the  result 
of  lesions  in  the  medulla  and  the  pons  is  no  longer  accepted. 

Symptoms. — One  of  the  first  and  most  marked  symptoms  of  an  oncoming 
attack  of  epilepsy  is  a  peculiar  sensation  felt  in  some  portions  of  the  body, 
generally  below  the  head,  which  gradually  rises  up  over  the  patient,  either 
rapidly  or  slowly,  like  an  oncoming  cloud,  until,  the  head  having  been  reached, 
the  patient  is  immediately  convulsed  and  unconscious,  and  almost  instantly 
is  seen  to  be  in  the  very  acme  of  the  nervous  storm,  Simultaneously  with  the 
arrival  of  this  aura  in  the  cervical  region  the  person  utters  a  peculiar  cry  or 
scream,  so  characteristic  that  it  has  been  called  the  "epileptic  cry,"  being 
probably  due  not  so  much  to  a  voluntary  impulse  as  to  a  sudden  expulsion 
of  the  air  from  the  thorax  by  the  convulsive  contraction  of  the  abdominal 
muscles,  as  well  as  those  of  the  thorax,  and  its  rapid  passage  through  the 
glottis  narrowed  by  rigid  spasm  of  the  muscles  governing  this  opening. 
Synchronously  with  this  cry  the  muscles  of  the  whole  body,  in  a  widespread 
attack,  become  strongly  contracted  until  they  are  in  a  tonic  spasm,  and  then, 
having  momentarily  relaxed,  pass  into  alternating  relaxations  and  contrac- 
tions, which  throw  the  patient  now  to  this  side,  now  to  that. 


EPILEPSY  1055 

During  the  tonic  spasm  the  muscles  of  the  face  often  produce  marked 
distortions  of  the  features,  in  some  cases  bringing  about  the  so-calUd  risus 
sardonicus;  the  head  may  be  drawn  to  one  side,  and  under  thes^ircum- 
stances  the  eyes  are  generally  turned  in  the  same  direction;  the  jaws  are 
locked  one  against  the  other,  and  the  lower  jaw  may  also  be  drawn  away 
from  the  median  line  of  the  face  in  the  same  direction  as  the  eyeballs.  Some- 
times the  whole  body  is  rotated.  In  970  cases  analyzed  by  the  writer,  com- 
plete rotation  to  the  right  is  mentioned  as  being  present  in  49  persons,  and 
to  the  left  in  52  cases.  There  is,  therefore,  no  difference  worthy  of  note 
in  these  numbers. 

The  arms  are  strongly  flexed  at  the  elbows,  while  the  hand  is  still 
more  strongly  flexed  at  the  wrist;  the  fingers  are  also  so  bent  into  the 
palm  of  the  hand  that  not  unfrequently  the  skin  in  this  region  is  found 
indented  by  the  nails.  The  arms,  legs,  and  body  are  drawn  and  jerked  in 
the  direction  of  the  most  powerful  muscles,  and,  as  a  consequence  of  this, 
opisthotonos,  during  the  tonic  stage,  is  by  no  means  uncommon.  Excep- 
tions to  this  rule  do,  however,  frequently  occur,  and  when  present  show  that 
the  paroxysm  is  exerting  its  chief  influence  on  the  weaker  muscles,  while  the 
stronger  ones  are  affected  at  least  to  a  less  degree.  As  a  general  rule,  too, 
the  muscles  of  one  side  suffer  more  than  those  of  the  other.  Unfortunately, 
in  the  cases  collected  by  me,  in  only  158  instances  were  any  remarks 
on  this  point  made.  In  these  158  the  right  side  was  most  affected  in  77  cases, 
and  the  left  side  in  81  cases.  It  is  evident,  therefore,  that  both  sides  suffer 
about  equally.  The  legs  may  be  firmly  flexed  on  the  abdomen,  while  the 
fingers  are  rigidly  extended. 

The  change  in  the  color  of  the  face  is  very  marked  and  almost  typical  of 
the  disease,  being  at  first  pale,  then  flushed,  the  flushing  deepening  often  into 
a  livid  purple,  owing  to  the  asphyxia  produced  by  the  convulsive  contraction 
of  the  thorax.  In  some  cases  the  eyelids  are  widely  drawn  apart  so  that  the 
eyes,  owing  to  their  fixation,  have  a  staring  appearance;  in  others  they  are  so 
tightly  closed  that  the  fingers  of  the  onlooker  can  scarcely  force  the  lids 
apart.  The  staring,  but  blank,  expression  of  the  eyes  is  also  increased  by 
the  slow  dilatation  of  the  pupils  which  always  accompanies  the  asphyxia. 

The  duration  of  the  tonic  contractions  rarely  exceeds  two  minutes,  and  in 
most  cases  is  limited  to  but  a  few  seconds.  It  is  followed  by  the  clonic  spasms, 
already  described,  which  are  ushered  in  by  more  or  less  violent  tossings,  but 
whose  onset  is  forewarned  by  peculiar  vibratory  thrills,  which  run  through 
all  the  affected  muscles.  The  eyelids  tremble,  the  body  changes  its  position 
never  so  slightly,  and  then,  as  if  the  vibrations  gained  greater  and  greater 
power  with  each  moment,  the  fibriUary  tremors  give  way  to  muscular  con- 
tractions. The  expression  of  the  face,  which  in  the  preceding  stage  was  set 
and  firm,  is  now  constantly  changed  by  the  movements  of  the  facial  muscles; 
the  jaws,  no  longer  locked  together,  are  gnashed  and  crunched  one  upon 
the  other;  the  tongue  is  alternately  protruded  and  drawn  back,  and,  as  a 
consequence,  is  often  caught  between  the  teeth  and  bitten  and  lacerated. 
The  excessive  movements  of  the  muscles  of  mastication  force  the  increased 
quantities  of  liquid  secreted  by  the  salivary  glands  from  the  mouth  in  the 
form  of  froth,  which  is  often  stained  with  blood  by  reason  of  the  injuries  to 


1056  DISEASES  OF   THE  NERVOUS  SYSTEM 

the  tongue.  The  constancy  of  the  convulsive  movements  now  becomes  less 
and  less  marked;  well-developed  remissions  occur  between  each  toss  of  the 
body,  until  the  movements  cease  entirely;  but  it  should  be  constantly  borne 
in  mind  that  the  prolongation  of  the  remissions  does  not  produce  any  decrease 
in  the  severity  of  the  intervening  spasm,  the  final  spasm  often  being  even 
more  violent  than  the  first. 

The  intense  discoloration  of  the  face  begins  to  pass  away  as  soon  as  the 
remissions,  by  their  length,  permit  the  blood  to  be  oxygenated,  its  disap- 
pearance being  temporarily  arrested  by  each  paroxysm.  Finally,  the  spasms 
having  ceased,  the  patient  lies  before  us  relaxed,  unconscious,  and  exhausted, 
and  passes  into  a  deep  sleep  or  coma,  which  lasts  a  variable  length  of  time, 
and  from  which  he  cannot  be  aroused  except  very  rarely,  and  then  with 
great  difficulty. 

One  of  the  most  interesting  and  important  of  all  the  symptoms  is  the 
so-called  aura.  Difference  of  opinion  has  arisen  as  to  the  frequency  of  its 
occurrence,  some  authors  stating  it  to  be  very  rare,  while  others  see  it  very 
constantly.  There  can  be  little  doubt  that  in  many  cases  it  is  as  constantly 
present  as  in  others  it  is  absent,  and  it  would  appear  that  the  nationality  of 
the  patient  has  something  to  do  with  the  occurrence  of  this  signal  of  the 
attack;  at  least,  if  we  may  judge  by  the  statements  of  the  chief  authors  of 
each  nation.  Thus,  in  America,  Wood  states  that  "the  aura  is  wanting  in  a 
very  large  proportion  of  the  cases  of  true  epilepsy,"  and  Hammond  agrees 
with  him.  In  England,  Gowers  stated  it  to  occur  in  about  one-half  of  the 
cases,  and  Bristowe  states  it  to  be  not  uncommon.  In  France  and  Belgium 
the  aura  appears  to  be  present  in  more  than  half  the  cases,  in  one  form  or 
another,  as  it  is  also  in  Germany,  according  to  Nothnagel.  In  970  cases 
collected  by  the  writer  it  was  found  that  the  aura  was  recorded  as  present  in 
362  cases  and  absent  in  138  cases. 

The  aura,  or  warning,  while  possessing  general  characteristics  common 
to  all  cases,  is  by  no  means  identical  in  each  individual.  By  far  the  largest 
number  of  cases,  where  it  is  present,  have  it  in  an  extremity,  and  if  it  be 
not  there,  then  it  is  often  in  the  stomach;  and  it  is  not  uncommon  to  see 
persons  suffering  from  epilepsy  who  have  as  an  aura  a  general,  indefinable 
sensation  all  over  the  body.  In  much  more  rare  instances  the  aurse  are 
situated  in  the  organs  of  special  sense,  and  are  evidenced  by  sudden  attacks 
of  blindness  or  deafness.  It  is  worthy  of  note,  however,  that  whereas  the 
aura  may  differ  in  every  case  in  origin,  seat,  and  limitation,  they  are  remark- 
ably constant  in  the  same  individual,  rarely,  if  ever,  changing  in  kind,  although 
they  may  vary  in  degree.  A  careful  analysis  of  an  enormous  number  of 
cases  by  hundreds  of  observers  shows  that  the  aura  most  commonly  met 
with  is  that  beginning  in  the  hand;  next,  that  beginning  in  the  leg  or  foot; 
next  most  common,  that  arising  in  some  of  the  viscera,  and,  after  these,  those 
which  arise  in  the  face  and  tongue.  The  rarest  form  of  aura  is  that  which 
arises  in  the  sides  of  the  trunk. 

Not  only  may  the  seat  of  the  aura  be  varied,  but  its  sensations  may  be 
even  more  aberrant.  Undoubtedly  the  most  common  sensation  is  the  inde- 
scribable sensation  of  a  vapor  or  cloud,  already  spoken  of;  but  in  a  large 
number  of  cases  the  sensations  are  described  as  being  quite  painful,  or 


EPILEPSY  1057 

perhaps  as  partaking  of  the  feehng  that  the  part  is  in  active  movement 
when  in  reaUty  it  is  still  quiet.  Others  speak  of  it  as  a  sensation  of  cold, 
others  of  heating  and  burning,  and  still  others  of  trembling  and  indescribable 
distress.  In  certain  cases  the  sensation  is  confined  to  the  spot  where  it  is 
first  noticed,  and  fails  to  travel  upward  or  toward  the  central  nervous  system. 

Status  efilepticus  is  a  condition  in  which  convulsion  follows  convulsion 
so  rapidly  that  consciousness  is  not  regained.  In  some  instances  the  patient 
dies  within  a  few  hours  as  a  result  of  exhaustion  or  asphyxia.  As  the  case 
goes  on  the  convulsions  are  replaced  entirely  by  coma,  or,  in  rare  cases, 
violent  attacks  of  mania"  may  develop.  In  this  state  the  body  rapidly 
emaciates,  bed-sores  develop,  and  death  ensues  from  exhaustion. 

An  extraordinary  number  of  fits  may  occur  in  a  brief  space  of  time 
without  causing  death,  or  even  very  great  exhaustion.  A  very  good  ex- 
ample of  this  fact  is  that  of  a  case  reported  by  Newington,  which  is  as 
follows:  On  the  twentieth  day  of  the  month,  at  5  a.m.,  the  fits  began  in 
the  woman  under  his  care.  By  5  p.m.  the  same  day  she  had  had  274  fits, 
and  by  5  a.m.  on  the  21st  she  had  384  more,  or  622  fits  in  twenty-four 
hours.  This  makes  a  rate  of  one  nearly  every  minute.  By  5  a.m.  on  the 
22d  she  had  400  more;  by  5  a.m.  on  the  23d,  525;  by  5  a.m.  on  the  24th, 
355,  and  from  5  a.m.  on  this  day  to  5  a.m.  on  the  25th  she  had  214  fits.  Alto- 
gether she  had  2156  fits  in  five  days,  and  yet  survived,  being  fed  by  the 
rectum. 

Motor  paralysis  may  succeed  epileptic  paroxysms,  and  this  is  particularly 
the  case  in  those  instances  where  the  convulsive  movements  are  largely 
unilateral  in  character. 

A  very  important  question,  connected  not  only  with  the  prognosis  of 
epilepsy,  but  also  with  its  relation  to  medical  jurisprudence,  lies  in  the  influ- 
ence which  the  disease  may  exercise  on  the  mental  condition  of  the  sufferer. 
Russell  Reynolds  has  arrived  at  the  following  conclusions  in  regard  to  the 
effects  of  the  disease  on  the  intellect: 

1.  That  epilepsy  does  not  necessarily  involve  any  mental  change. 

2.  That  great  mental  impairment  exists  in  some  cases,  but  this  is  the 
exception  rather  than  the  rule. 

3.  That  females  suffer  (in  mental  vigor)  more  frequently  than  males,  and 
also  more  severely. 

4.  That  the  commonest  failure  is  loss  of  memory,  and  that  this,  if  regarded 
in  all  degrees,  is  more  frequent  than  integrity  of  that  faculty. 

5.  That  apprehension  is  more  frequently  preserved  than  lost. 

6.  That  ulterior  mental  changes  are  rare. 

7.  That  depression  of  spirits  is  common  in  males,  rare  in  females,  but 
that  excitability  of  temper  is  found  in  both  sexes. 

Complications. — Naturally  enough,  a  very  common  variety  of  complication 
is  some  traumatism,  severe  or  mild,  which  is  suffered  as  the  result  of  the  fall 
accompanying  the  fit,  whereby  the  head  is  struck  against  some  hard  or 
sharp  object.  The  severity  of  the  injury  may  be  anything  from  fracture  to 
a  slight  abrasion  or  bruise.  When  such  an  accident  happens  it  should  not 
be  forgotten  that  the  coma  of  the  fit  may  be  dangerously  deepened  by  the 
concussion,  and  also  that  the  coma  may  mislead  the  physician  so  that  it  is 
67 


1058  DISEASES  OF   THE  NERVOUS  SYSTEM 

regarded  as  the  natural  sequence  of  the  attack  rather  than  the  result  of  the 
injury.  Fractures  of  the  clavicle  are  very  common.  In  the  same  manner 
various  dislocations  may  ensue.  The  presence  of  a  fracture  in  an  epileptic 
is  a  very  much  more  serious  matter  than  would  appear  at  first  glance,  for 
even  if  the  fits  are  not  very  frequent  they  are  almost  sure  to  cause  a  fresh 
solution  of  continuity,  or  even  to  convert  a  simple  into  a  compound  fracture 
by  the  jerkings  of  the  muscles.  Splints  are,  of  course,  of  value,  and  the 
limb  may  be  v^rapped  in  a  pillow.  Careful  watching  with  quiet  rest  in  bed 
must  always  be  insisted  upon,  since  under  these  circumstances  a  second 
fall  is  avoided  on  the  advent  of  a  new  attack. 

In  other  cases  apoplexy  may  occur,  due  to  the  sudden  strain  upon  the 
cerebral  bloodvessels  during  the  fit,  and  if  the  coma  following  an  attack 
is  prolonged  or  peculiar,  this  fact  should  be  called  to  mind.  The  inequality 
of  the  pupils,  the  stertorous  respiration,  the  fact  that  the  tongue  cannot  be 
protruded  straight  from  the  mouth,  all  point  to  a  cerebral  lesion;  but  the  rise 
of  temperature,  the  coma,  and,  last  of  all,  the  hemiplegia  are  characteristic 
of  both  states,  and  cannot  be  used  for  differential  diagnosis. 

Diagnosis. — Undoubtedly,  the  most  similar  convulsive  condition  that  we 
have  is  that  due  to  hysteria,  and  the  diagnosis  of  one  from  the  other  is 
as  difficult  in  some  cases  as  it  is  essential  and  necessary  for  treatment  and 
cure.  The  other  conditions,  with  which  it  might  be  confused,  are  uraemia, 
alcoholic  epilepsy,  tetanus,  and  syncope.  In  the  accompanying  table  are 
arranged  all  these  disorders,  which  briefly  and  succinctly  shows  the  different 
points  between  them,  although  of  necessity  it  is  somewhat  arbitrary  on 
account  of  the  lack  of  space. 

The  very  irregularity  of  true  epilepsy  makes  it  extremely  difficult  to 
give  clear  and  well-defined  outlines  of  it  against  another  disease,  par- 
ticularly when  we  remember  that  epilepsy  and  hysteria  often  go  hand  in 
hand. 

By  far  the  most  important  differential  point  between  the  two  disorders 
just  named,  when  not  complicated  with  still  another  disease,  is  the  character 
of  the  movements.  As  already  pointed  out,  in  epilepsy  they  are  typically 
at  variance  with  those  of  daily  life,  while  in  hysteria  they  are  often  equally 
typical  of  ordinary  muscular  contractions,  or,  in  other  words,  are  more 
purposive  in  character;  and  frequently  there  is  prolonged  tonic  contraction 
of  the  muscles,  giving  rise  to  the  assumption  of  positions  which  bear  more  or 
less  resemblance  to  normal  attitudes.  In  hysteria,  also,  consciousness  is 
impaired  sometimes,  but  never  so  completely  as  in  true  epilepsy.  Indeed, 
most  commonly  the  individual  knows  all  that  goes  on  around  her,  for,  while 
she  may  give  no  sign  of  consciousness  by  words  or  looks  during  the  attack, 
she  may  afterward  be  able  to  narrate  all  that  has  occurred.  Less  commonly, 
however,  a  condition  known  as  automatic  consciousness  exists,  in  which, 
during  the  paroxysm,  the  patient  understands  all  that  is  said,  but  forgets 
everything  on  the  return  to  quietness. 

The  fact  that  the  patient  is  a  female  cannot  be  regarded  as  affirmative 
evidence  of  hysteria  in  the  least,  but  if  the  fit  occurs  in  a  male  it  may  be 
taken  as  fairly  positive  evidence  of  epilepsy;  and  yet  it  should  always  be 
remembered  that  males  may  suffer  from  hysteroid  attacks. 


EPILEPSY 


1059 


Table  of  Differential  Diagnosis  of  Epilepsy  from  Hysteria,  etc. 


Signs. 

Epilepsy. 

Hysteria. 

Uraemia. 

Petit  mal. 

Alcoholic 
epilepsy. 

Tetanus. 

Syncope. 

Apparent 
cause. 

None. 

Emotion. 

None. 

None. 

None. 

None. 

Mental 
shock. 

Aura  or 
prodro- 
mata. 

Generally 
present, 
but  short. 

Globus 
hystericus, 
palpitation, 
choking. 

Headache, 
vomiting, 
and  dys- 
pepsia. 

Faintness 
and  dim- 
ness of 
vision. 

Tremors. 

Nervous- 
ness. 

Not  so  well 
defined  as 
in  epilepsy. 

Onset. 

Sudden. 

Often  grad- 
ual. 

Often  grad- 
ual. 

Sudden. 

Sudden  or 
gradual. 

Gradual, 
begins  in 
jaw. 

Sudden  or 
gradual. 

Scream. 

At  onset 
and  sud- 
den. 

During 
attack. 

Frequently 
none. 

Frequently 
none. 

May  or  may 
not  be 
present. 

None. 

None. 

Convul- 
sion. 

First  tonic, 
then  clonic. 

Rigidity 
more  pro- 
nounced 
with  more 
aching. 

Rigidity 
generally 
absent. 

No  rigidity. 

Movements 
more  clonic 
than  tonic. 

Always 
tonic. 

None. 

Biting. 

Tongue. 

Tongue, 
lips,  and 
hands. 

Tongue. 

None. 

Rarely. 

None. 

None. 

Micturi- 
tion. 

Frequent. 

Never. 

Never. 

Rarely,  ex- 
cept when 
bladder  is 
affected. 

Rarely. 

Sometimes 

Never. 

Defecation 

Occasion- 
ally. 

Never. 

Never. 

Never. 

Rarely. 

Rarely. 

Never. 

Talking. 

Never. 

Frequent. 

Muttering. 

Never. 

Never. 

Never. 

None. 

Duration. 

A  few 
minutes. 

Generally 
many 
minutes. 

From  a 
minute  to 
hours. 

Momentary. 

May  be  pro- 
longed. 

Hours. 

Indefinite 
time. 

Conscious- 
ness. 

Lost. 

Generally 
preserved. 

Lost. 

Not  lost 
always,  but 
clouded. 

Lost. 

Preserved. 

Lost. 

Termina- 
tion. 

Spontane- 
ous. 

Maybe 
induced 
by  shock. 

Spontaneous 

Spontaneouf 

Spontaneous 

Spontane- 
ous. 

Gradual, 
with  no 
somno- 
lence. 

The  movements  of  the  hysterical  patient  after  the  tonic  condition  has 
passed  away  are  as  clonic  as  those  of  epilepsy,  but  still  possess  some  purposive 
characteristics,  and  are  not  so  bizarre  as  are  those  of  the  true  disease.  Thus, 
the  head,  arms,  and  legs  are  struck  with  evident  endeavor  against  the  floor 
or  surrounding  furniture.  Another  point,  which,  when  it  occurs,  is  very 
distinctive,  is  the  onset,  toward  the  close  of  a  hysterical  convulsion  of  a 
second  stage  of  tonic  spasm  such  as  occurred  at  the  beginning.  It  will  be 
remembered  that  this  does  not  occur  in  epilepsy;  although  it  must  be  borne 
in  mind  that  in  cases  of  the  "status  epilepticus"  the  rapid  onset  of  another 
attack  may  show  a  second  tonic  stage.  This  can  be  separated,  however, 
by  the  fact  that  it  is  followed  by  clonic  movements,  whereas  the  secondary 
tonic  stage  of  hysteria  is  usually  followed  by  relaxation  and  temporary 
recovery. 

Finally,  too,  in  hysteria,  some  pecuhar  emotional  position  is  often  assumed, 


1060  DISEASES   OF   THE  NERVOUS   SYSTEM 

as  of  the  crucifix,  or  of  intense  grief,  or,  perhaps,  immoderate  laughter,  with 
corresponding  movements  of  the  trunk.  If  the  patient  is  quiet  at  this  time, 
a  smile  may  float  across  the  face,  while  the  eyes,  with  a  look  of  pleasure, 
pain,  or  entreaty,  may  seem  to  be  gazing  at  some  object  very  far  off.  In 
some  very  well  developed  cases  the  expression  of  pleasure  is  followed  by  a 
look  of  pain,  with  painful  movements,  or  an  appearance  of  voluptuous 
entreaty,  with  sensual  and  venereal  desire  evidenced  by  gestures.  Very 
commonly  areas  of  anaesthesia  and  hypersesthesia  occur  in  these  patients 
and  are  of  all  degrees  of  intensity  and  limitation.  Search  for  them  gen- 
erally shows  their  presence  after  attacks  of  convulsions,  but  they  may  persist 
from  one  attack  to  the  other,  or  develop  spontaneously.  In  nearly  all  cases 
these  areas  are  unilateral,  and  may  extend  over  one-half  of  the  body,  the 
line  of  demarcation  of  the  anaesthesia  or  hyperaesthcsia,  from  the  sound 
area,  being  clearly  and  abruptly  defined,  generally  at  the  median  line  of  the 
front  and  back  of  the  trunk.  It  will  be  called  to  mind  that  such  conditions 
are  absent  in  true  epilepsy.  Hallucinations  are  far  more  common  after 
the  fit  in  hysteria  than  in  epilepsy,  and  sometimes  they  even  occur  during 
the  attacks. 

A  very  useful  differential  point,  strongly  insisted  upon  by  Charcot  and 
Bourneville,  is  that  in  true  epilepsy  there  is  generally  a  very  considerable 
rise  of  temperature  during  an  attack,  while  in  hysteroepilepsy  the  tempera- 
ture remains  normal  or  only  slightly  raised.  Not  rarely  malingerers  simulate 
attacks  of  epilepsy,  and  very  serious  injuries  are  sometimes  submitted  to 
by  these  persons  to  carry  out  their  designs.  The  points  to  be  looked  into 
are:  the  condition  of  the  pupils,  which,  in  the  simulated  attack,  always  react 
normally;  nor  can  the  corneal  reflexes  be  held  back;  the  color  of  the  face  is 
rarely  changed,  and  the  thumbs  are  rarely  flexed  as  they  should  be.  Marc 
has  pointed  out  that  in  malingerers  the  bystander  can  readily  straighten 
out  the  thumbs,  and  that  they  remain  so;  whereas  in  epilepsy  they  instantly 
become  flexed  again. 

Suggestions  as  to  movements  are  sometimes  followed  by  malingerers, 
and  the  movements  generally  lack  the  bizarre  character  so  typical  of  epilepsy. 

If  tobacco  smoke  or  ammonia  be  held  to  the  nose  of  the  fraud,  he  gener- 
ally is  forced  to  disclos3  his  true  condition.  The  fact  that  in  malingerers 
there  is  no  rise  of  temperature  is  a  differential  point. 

Prognosis. — The  physician  can  always  assure  the  patient  and  friends  that, 
so  far  as  the  disease  itself  in  its  ordinary  form  is  concerned,  there  is  little 
danger  of  death,  since,  as  a  general  rule,  unless  the  attacks  are  very  severe, 
death  rarely  occurs,  unless  indirectly  by  the  fall  of  the  body  into  a  stream 
or  well,  or  when  in  some  position  where  a  steady  head  is  necessary  for  safety. 
Accidental  asphyxia,  due  to  the  burying  of  the  face  in  the  pillow  at  night, 
or  to  the  impaction  of  food  in  the  larynx,  may  occur,  but  even  this  accident 
is  uncommon. 

The  question  which  the  friends  will  always  ask  is:  What  is  the  prospect 
of  ultimate  recovery,  or,  at  the  least,  will  there  be  any  progress  toward  an 
improvement?  Unfortunately,  the  reply  ought  not  in  any  case  to  be  favor- 
able, even  for  ultimate  improvement,  for  the  experience  in  the  past  of  every 
practitioner  has  been  that  cures  rarely  occur. 


EPILEPSY  1061 

Jacksonian  Epilepsy. — By  the  term  Jacksonian  epilepsy  we  mean  an 
affection  which  separates  itself  from  true  or  ordinary  idiopathic  epilepsy 
by  several  peculiarities.  By  far  the  most  important  of  the  peculiar  signs 
is  the  character  of  the  onset,  which  always  begins,  in  the  typical  Jacksonian 
disease,  in  some  peripheral  portion  of  the  body,  and  most  frequently  in  the 
muscles  of  the  thumb  or  hand,  so  that  for  the  moment  the  movements 
are  localized  and  may  remain  localized  at  the  point  of  origin,  or  imme- 
diately diffuse  themselves  over  muscle  after  muscle  until  all  the  arm,  leg, 
or  other  groups  of  muscles  are  involved.  It  is  of  the  greatest  importance, 
however,  that  the  reader  should  keep  the  aura  of  an  attack  separated  in  his 
mind  from  the  onset,  remembering  that  the  term  onset  is  here  used  by  the 
writer  to  designate  the  beginning  of  the  period  following  the  aura,  if  there 
be  one.  Jacksonian  epilepsy  may  be  of  almost  any  degree  of  severity,  for 
in  rare  cases  but  one  muscle  may  suffer  throughout  an  entire  attack,  or  in 
others  the  entire  body  may  be  finally  convulsed.  There  may  or  may  not  be 
loss  of  consciousness,  its  presence  or  absence  being  dependent  upon  the 
severity  of  the  attack.  In  those  instances  in  which  only  a  few  localized 
muscles  are  involved,  consciousness  is  more  commonly  preserved  than 
lost. 

Petit  Mai  or  Minor  Epilepsy. — Petit  mal  differs  in  no  way  in  its  essential 
characters  from  epilepsy  of  a  much  more  highly  developed  form,  but  in  its 
minor  characteristics  it  is  sufficiently  at  variance  with  haul  mal,  or  grand 
mal,  to  separate  it  in  the  minds  of  clinicians.  In  its  most  common  form 
petit  mal  consists  of  a  momentary  less  of  consciousness,  accompanied  by 
pallor,  or,  more  rarely,  flushing  of  the  face.  The  man  who  is  subject  to  the 
disease  suddenly  stops  what  he  is  doing  for  a  moment  or  two,  and  then  takes 
up  his  work  or  subject  as  soon  as  he  recovers,  and  at  the  point  where  he 
ceased,  being  often  unconscious  of  the  break  in  his  conversation  or  labor. 
Reynolds  has  divided  this  minor  form  of  the  affection  into  two  divisions. 
In  the  first  he  places  those  who  are  attacked  and  have  no  evident  spasm, 
and  in  the  second  group  are  those  who  have  evident  spasm.  The  seizures 
are  characteristically  fugacious,  and  if  any  spasm  is  present  it  is  nearly, 
always  of  the  tonic  variety.  Sometimes  the  disorder  of  motility  lies 
chiefly  in  an  inhibition  of  an  act  about  to  be  performed.  The  fork  in 
a  man's  hand  at  a  dinner-table  may  be  raised  half-way  to  the  mouth,  then 
held  in  mid-air  for  a  moment,  and  then,  as  the  attack  passes  away,  continue 
on  its  journey  to  the  mouth;  or,  a  woman  playing  the  piano  may  suddenly 
pause  with  her  fingers  raised  from  the  keys,  miss  the  time  of  three  or  four 
bars,  and  then  go  on  exactly  where  she  left  off,  as  if  no  interruption  had 
occurred. 

Treatment. — By  far  the  most  valuable  drug  in  use  to-day  for  the  relief  of 
epilepsy  is  bromide  of  strontium.  In  many  cases  the  remedy  undoubtedly 
gives  relief  when  it  is  pushed  in  a  suitable  manner,  and,  in  the  majority 
of  instances,  the  seizures  are  so  decreased  both  in  violence  and  frequency 
that  its  use  may  be  said  to  be  indicated  in  nearly  every  case  of  the  dis- 
ease.    In  a  very  small  minority,  however,  it  signally  fails. 

A  very  important  point  to  be  borne  in  mind  is  that  the  drug  often  seems 
to  have  produced  a  complete  cure,  and  this  results  in  carelessness  in  the 


1062  DISEASES   OF    THE   NERVOUS  SYSTEM 

regularity  of  administration.  The  patient  should  be  impressed  by  the  fact 
that  every  day  passed  without  a  fit  is  a  step  forward,  and  that  every  fit  carries 
him  many  steps  backward.  He  should  also  be  made  to  use  the  drug  in 
moderation  for  at  least  three  years  after  all  fits  have  ceased,  and  to  watch, 
after  that  time,  for  the  slightest  sign  of  their  return.  The  quantity  taken 
each  day  should  be  gradually  decreased,  not  suddenly  stopped. 

The  iodide  of  potassium  is  entirely  useless  in  epilepsy,  unless  it  is  due  to 
syphilis,  when  it  is  of  the  greatest  service.  Under  this  condition  the  bro- 
mides and  all  other  drugs  should  be  set  aside  while  it  is  pushed  to  the 
utmost.  As  is  well  known,  syphilitics  usually  bear  the  drug  extremely  well, 
and  the  writer  knows  of  one  instance  where  no  less  than  800  grains  were 
taken  every  twenty-four  hours,  with  rapid  improvement  as  a  result. 

When  the  convulsions  are  due  to  a  gumma  the  iodide  of  potassium  is, 
however,  too  slow  in  its  action,  and  should  be  replaced  by  mercury  in  order 
to  break  down  the  growth  without  delay,  lest  a  seizure  end  the  scene  by 
asphyxia  or  some  similar  accident. 

In  every  case  the  physician  should  make  careful  inquiry  as  to  the  pres- 
ence of  an  aura,  and,  if  it  is  present,  he  should  order  that  the  patient  be 
provided  with  pearls  of  amyl  nitrite,  one  of  which  is  to  be  broken  and  its 
contents  inhaled  the  moment  the  warning  of  an  approaching  fit  develops. 
By  this  means  attacks  can  often  be  abortive. 


ECLAMPSIA. 

The  term  "eclampsia"  is  applied  to  convulsions  affecting  children  and 
pregnant  women,  or  women  who  have  just  been  delivered. 

Infantile  Eclampsia. — In  infantile  eclampsia  the  attacks  are  epileptiform 
in  character  and  seem  to  depend  upon  a  condition  of  undue  irritability  of 
the  nervous  system,  which  is  still  further  disturbed  by  some  reflex  cause. 
Thus,  it  is  commonly  supposed  that  gastric  and  intestinal  indigestion  may 
produce  infantile  eclampsia,  and  certainly  the  presence  of  foreign  bodies 
in  the  stomach  and  intestines  may  act  in  this  manner.  Again,  many 
physicians  believe  that  the  first  dentition,  by  reason  of  the  irritation  in  the 
gums,  may  result  in  such  a  seizure.  A  host  of  other  causes  of  peripheral 
irritation  have  also  been  held  responsible.  Not  rarely  the  underlying  cause 
is  rickets.  It  is  often  stated,  in  text-books  on  medicine,  that  the  acute 
infectious  fevers  are  frequently  initiated  by  a  convulsive  seizure.  As  a 
matter  of  fact  this  rarely  occurs  in  an  ordinary  child  when  infected  in  this 
manner. 

The  convulsive  attack  varies  in  severity  from  a  mere  clinching  of  the 
fingers  and  the  drawing  of  the  thumb  into  the  palm  of  the  hand  to  a  severe 
clonic  or  tonic  convulsion  closely  resembling  epilepsy  or  hysteroepilepsy. 
In  many  instances  the  child  has  a  single  attack  and  no  more.  In  other  cases 
several  attacks  occur  within  a  few  days.  In  still  others  the  occurrence  of 
one  or  more  attacks  of  convulsions  seems  to  develop  a  convulsive  habit,  and 
in  these  instances  the  child  may  become  a  confirmed  epileptic.  In  such 
cases,  however,  it  is  probable  that  the  condition  of  indigestion,  or  other 


ECLAMPSIA  1063 

direct  cause,  simply  induces  a  nervous  explosion  on  the  part  of  a  brain,  which 
has  an  impaired  stability. 

Diagnosis. — The  condition  must  be  separated  from  the  convulsions  pro- 
duced by  organic  cerebral  disease  (which  see). 

Prognosis. — The  prognosis  in  infantile  eclampsia  is  good  for  single  attacks, 
and  becomes  grave  in  direct  proportion  to  their  severity  and  repetition.  Such 
attacks  occurring  in  feeble,  poorly  nourished  children  are  more  grave  than 
in  those  who  are  better  able  to  withstand  an  illness. 

Treatment. — This  consists  in  removing  the  cause  of  local  irritation,  if  it 
can  be  found.  If  it  exists  in  the  stomach  or  the  bowels,  it  should  be  removed 
by  an  emetic  or  a  purge.  If  the  gums  are  inflamed  they  should  be  lanced. 
If  rickets  is  the  cause  it  must  be  cured  if  possible. 

The  treatment  of  the  attack  itself  consists  in  the  administration  by  the 
mouth,  if  swallowing  is  possible,  of  5  or  10  grains  of  bromide  with  from 
2  to  4  grains  of  chloral,  or  by  the  use  of  20  grains  of  sodium  bromide  with 
5  grains  of  choral  in  starch-water,  by  the  rectum.  If  laryngeal  spasm  is 
marked,  and  is  a  dangerous  symptom  an  inhalation  of  nitrite  of  amyl  may 
be  used,  or  chloroform  may  be  employed  if  the  heart  is  not  weak. 

Puerperal  Eclampsia  usually  occurs  in  young  primiparse.  The  convul- 
sions are  tonic  and  clonic.  The  pathology  of  the  condition  is  not  under- 
stood. Without  doubt  the  condition  is  toxic.  In  some  instances  it  is  probably 
due  to  perverted  functional  activity,  or  actual  disease,  of  the  kidneys. 
In  other  instances  it  seems  to  be  dependent  upon  perverted  metabolism. 
Not  infrequently,  in  association  with  the  albuminuria  of  pregnancy,  there 
is  albuminuric  retinitis,  and  even  blindness  with  general  anasarca.  That 
the  presence  of  Jcetus  in  utero  exercises  some  influence  is  shown  by  the 
fact  that  not  infrequently  the  convulsions  cease  as  soon  as  the  uterus  is 
emptied. 

Puerperal  eclampsia  is  an  exceedingly  dangerous  condition.  The  mor- 
tality varies  from  20  to  30  per  cent.,  or  even  more  than  this.  In  a  certain 
proportion  of  cases  it  can  be  prevented,  and  for  this  reason  the  physician 
should  repeatedly  examine  the  urine  of  the  pregnant  woman  for  several 
months  before  the  termination  of  pregnancy  to  determine  that  the  kidneys 
are  carrying  out  their  eliminative  function  properly. 

Treatment. — -The  uterus  must  be  emptied,  the  poisons  must  be  eliminated, 
and  the  nervous  system  must  be  quieted.  For  the  best  method  of  emptying 
the  uterus,  the  reader  is  referred  to  books  upon  obstetrics.  If  arterial  tension 
is  high  and  there  is  much  cyanosis,  the  patient  should  be  freely  bled  and 
the  intravenous  injection  of  normal  saline  solution  employed,  unless  there 
is  a  tendency  to  pulmonary  oedema,  when  the  intravenous  injections  should 
not  be  used.  Copious  irrigation  of  the  large  bowel  or  the  injection  of  an 
ounce  of  magnesium  sulphate  dissolved  in  a  half-pint  of  water  and  2 
ounces  of  glycerin  are  also  useful.  If  the  convulsions  are  severe  in  these 
cases  many  physicians  treat  the  condition  by  the  use  of  large  doses  of  20  to 
30  minims  of  the  tincture,  or  even  of  the  fluid  extract,  of  veratrum  viride, 
giving  it  in  some  cases  hypodermically.  This  drug  lowers  arterial  tension, 
quiets  the  spinal  cord,  and  produces  sweating.  Pilocarpine  is  never  to  be 
employed,  as  it  almost  invariably  causes  pulmonary  oedema. 


1064  DISEASES  OF   THE  NERVOUS  SYSTEM 


TETANY. 

Tetany  is  a  condition  in  which  intermittent  unilateral  or  bilateral  tonic 
and  painful  spasm  affects  certain  muscle  groups,  usually  of  the  upper  limbs, 
although  occasionally  it  involves  the  legs  as  well.  It  is  sometimes  called 
"tetanilla, "  or  "idiopathic  muscular  spasm."  The  disease  is  exceedingly 
rare  in  America,  but  comparatively  common  in  certain  European  countries, 
notably  Sweden  and  Austria.  It  is  probable  that  tetany  is  merely  a  symptom 
of  several  different  conditions.  One  type  of  it  occurs  in  epidemic  form  in 
Austria,  particularly  during  the  months  of  March  and  April,  affecting 
chiefly  youths  between  fifteen  and  twenty-five  years  of  age.  These  persons 
usually  belong  to  the  lower  walks  of  life.  Occasionally  it  develops  in  women, 
particularly  at  the  time  of  pregnancy  or  during  nursing.  A  very  few  cases 
have  been  reported  in  children  below  puberty  and  in  persons  of  advanced 
years. 

Etiology. — In  the  opinion  of  many  persons  tetany  is  due  to  autointoxica- 
tion or  to  intoxication  due  to  some  infectious  agent.  Thus,  it  has  been 
frequently  reported  as  occurring  in  persons  who  are  suffering  from  chronic 
gastrointestinal  disorders,  particularly  cases  of  gastric  dilatation,  and  it  has 
occurred  in  such  cases  after  the  gastric  contents  have  been  removed  by 
lavage.  It  seems  to  be  more  frequent  in  persons  who  follow  certain  occu- 
pations than  in  others.  Thus,  out  of  314  male  patients  mentioned  by  Frankl- 
Hochwart  no  less  than  141  were  shoemakers  and  41  were  tailors.  This 
has  caused  certain  persons  to  believe  that  certain  types  of  tetany  were  of  the 
nature  of  an  occupation  neurosis.  Tetany  sometimes  develops  in  those 
who  have  suffered  partial  or  total  extirpation  of  the  thyroid  gland.  It  is  also 
met  with  in  children  who  are  suffering  from  rickets.  In  some  cases  tetany  is 
a  manifestation  of  hysteria. 

Pathology  and  Morbid  Anatomy. — As  the  condition  is  a  functional  one, 
and  as  few  of  these  cases  come  to  autopsy,  we  know  little  concerning  their 
morbid  anatomy.  In  a  few  instances  autopsy  has  revealed  hypersemia  and 
minute  hemorrhages  in  the  anterior  cornua  of  the  spinal  cord,  but  it  is  very 
doubtful  if  these  are  characteristic  of  the  malady. 

Symptoms. — ^The  prodromal  symptoms  of  tetany  are  usually  those  indica- 
tive of  a  toxaemia.  The  patient  first  suffers  from  some  aching  or  pain  in  the 
extremities,  and  may  have  headache  and  dizziness,  and  feel  heavy  and  stupid. 
As  already  stated,  the  disorder  usually  affects  one  or  both  arms  and  involves 
in  particular  the  muscles  of  the  forearms  and  hand,  causing  the  palm  of 
the  hand  to  be  flexed  upon  the  wrist  while  the  fingers  are  extended.  Some- 
times the  forearm  is  flexed  at  the  elbow.  In  other  instances  the  phalanges 
are  flexed  and  the  distal  phalanges  extended.  When  the  lower  extremities 
are  affected,  the  feet  and  toes  show  somewhat  similar  contractures.  The 
toes  may  overlap  one  another  and  be  forcibly  flexed,  and  the  foot  may  be  bent 
at  the  ankle  in  the  position  of  clubfoot.  Occasionally,  in  very  severe  cases, 
some  of  the  muscles  of  the  trunk  and  those  of  the  neck  and  throat  may  be 
involved,  and  even  the  ocular  muscles  may  contract,  so  that  a  form  of  nys- 
tagmus is  present.     It  is  a  noteworthy  fact,  first  enunciated  by  Trousseau, 


TETANY  1065 

that  pressure  exercised  upon  the  affected  limb  will  generate  an  attack,  pro- 
vided that  the  nerve  trunks  or  the  bloodvessels  are  affected  by  the  pressure. 
This  is  known  as  "Trousseau's  symptom."  The  pressure  must  be  continued 
from  thirty  seconds  to  five  minutes  to  produce  an  effect.  While  the  presence 
of  Trousseau's  symptom  is  pathognomonic  of  tetany,  its  absence  does  not 
disprove  the  presence  of  the  disease. 

Under  the  name  of  "  Trousseau's  sign  "  tapping  of  the  nerves  of  the  arms, 
or  legs,  when  surrounded  by  an  elastic  band,  may  induce  the  spasm. 
Spasm  may  also  be  induced  if  the  facial  nerve  is  irritated  in  this  manner 
(Chvostek's  sign).  Under  the  name  of  "Erb's  sign"  lies  the  fact  that  the 
motor  nerves  manifest  a  marked  increase  in  electrical  irritability,  particularly 
with  the  galvanic  current.  Hoffmann  has  pointed  out  that  the  superficial 
sensory  nerves  are  also  exceedingly  sensitive,  and  that  moderate  pressure  upon 
them,  which  ordinarily  would  not  be  felt,  may  cause  a  severe  pain  similar  to 
that  produced  by  striking  the  ulnar  nerve  at  the  elbow  ("Hoffmann's  sign"). 
If  the  irritation  of  the  motor  nerve  is  repeatedly  produced,  a  marked  increase 
in  the  excitability  of  the  tributary  muscles  follows.  Occasionally,  nervous 
lesions  appear  in  the  skin  such  as  urticaria  or  herpes,  pigmentation,  and  loss 
of  the  hair  and  nails.  An  attack  of  tetany  may  last  from  a  few  minutes  to 
several  days.  It  may  be  so  moderate  that  it  can  be  overcome  by  the  will  of 
the  patient,  or  so  severe  that  the  limb  is  entirely  beyond  control.  If  an 
attempt  is  made  to  reduce  the  spasm  by  force  it  causes  great  pain,  and  if  the 
contractions  of  the  muscles  are  marked  and  cramp-like  the  pain  is  also 
severe.  The  attack  passes  off  gradually  and  is  often  followed  by  impaired 
sensation  and  loss  of  power  in  the  affected  parts.  There  is  no  loss  of  con- 
sciousness in  the  great  majority  of  cases. 

Diagnosis. — The  development  of  comparatively  localized  tonic  spasms 
in  association  with  the  other  symptoms  already  described  renders  the  diag- 
nosis of  tetany  quite  easy.  The  disease  must  be  separated  from  Jacksonian 
epilepsy  and  hysteria.  This  can  be  done  by  the  development  of  Trousseau's, 
Chvostek's,  and  the  other  signs  just  named,  by  the  absence  in  tetany  of  the 
various  stigmata,  including  the  reversal  of  the  color  fields,  found  in  hysteria. 
It  is  differentiated  from  Jacksonian  epilepsy  by  the  prolonged  character  of 
the  attack  and  the  fact  that  it  can  be  produced  at  the  will  of  the  physician. 
Hysterical  contractures  sometimes  assume  the  form  of  tetany,  and  cases  of 
apparently  true  tetany  may  have  hysterical  features. 

Prognosis. — The  prognosis  as  to  life  is  good  unless  the  provoking  cause 
is  in  itself  serious,  as,  for  example,  when  the  thyroid  gland  has  been  removed. 
In  other  words,  in  no  instance  does  tetany  itself  threaten  vitality,  although 
the  underlying  cause  of  the  tetany  may.  Most  cases  recover.  Some 
suffer  from  only  one  attack.  In  others  the  symptoms  disappear  after  many 
attacks  as  soon  as  the  cause  is  removed. 

Treatment. — This  deals  largely  with  the  removal  of  the  exciting  cause.  If 
gastric  dilatation  is  present  and  if  its  nature  is  such  that  it  can  be  benefited 
by  lavage  or  operation,  these  measures  must  be  instituted.  In  some  instances 
where  there  is  reason  to  believe  that  the  condition  results  from  autointoxi- 
cation, mild  saline  purgatives,  diuretics,  and  moderate  doses  of  calomel  or 
blue  mass  are  advisable,  and,  in  addition,  hot  packs  may  be  given  to  aid  in 


1066  DISEASES  OF   THE  NERVOUS  SYSTEM 

the  elimination  of  poisons  by  the  skin  and  to  act  as  nervous  sedatives. 
When  disease  of  the  thyraid  gland  is  present,  the  administration  of  thyroid 
extract  is  indicated.  If  there  is  present  a  general  condition  of  debility, 
ansemia,  iron,  arsenic,  and  similar  tonics  combined  with  an  out-door  life  and 
avoidance  of  nerve  irritation  are  essential. 


LATAH. 

Latah  is  a  state  very  closely  allied  to  the  saltatory  spasm  described  by 
Bamberger,  and  the  patients  described  by  Beard  as  "jumpers."  The  chief 
symptom  of  latah  is  involuntary  and  uncontrollable  mimicry  by  the  patient 
of  everything  she  sees  or  hears.  There  is  also  frequent  coprolalia  or  the 
spasmodic  ejaculation  of  filthy  words.  The  disease  is  common  among  the 
Malay  races,  and  its  geographical  distribution  corresponds  with  the  countries 
inhabited  by  these  people.  It  occurs  commonly  enough  among  the  Filipinos 
and  is  known  by  the  Tagalogs  as  "  mali-mali."  It  is  seen  in  Ceylon  and 
Burmah,  and  the  disease  known  in  Siberia  as  "  myriachit "  is  probably 
identical  with  it.     Kraepelin  allies  latah  with  hysteria. 

The  subjects  of  latah  are  almost  invariably  women  in  early  adult  life. 
Men  rarely,  if  ever,  suffer  from  the  disease.  There  is  a  distinct  hereditary 
tendency,  but  the  cases  show  no  evidence  either  of  hysteria  or  epilepsy.  It 
is  a  very  common  spectacle  indeed,  in  Malay  villages,  to  see  one  of  these 
unfortunate  women  pursued  by  a  crowd  of  tormenting  boys.  They  dance 
in  front  of  her,  going  through  all  sorts  of  grotesque  and  obscene  movements, 
and  the  unfortunate  victim,  apparently  struggling  to  the  utmost  to  resist 
the  impulse,  exactly  imitates  all  their  actions  to  her  own  great  rage  and 
mortification.  Besides  such  examples  of  complete  echochinesia,  or  mimicry 
of  motion,  there  frequently  is  echolalia,  or  mimicry  of  speech.  When  startled 
or  frightened  these  patients  utter  irrelevant  words  or  incoherent  noises 
and  make  involuntary  movements.  Consciousness  is  never  lost  during 
these  attacks.  This  latter  type  closely  resembles  the  "jumping  Frenchmen" 
of  Maine  and  Canada,  who  jump  violently  and  suddenly  with  a  loud  cry  when 
startled  or  when  under  strong  emotion.  Jumpers,  and  latah  patients  as  well, 
will  frequently  obey  any  sharp,  sudden  command  given  them.  Undoubtedly, 
this  represents  some  form  of  psychic  suggestion  acting  on  a  weak  and  unstable 
will.  The  Malay  is  notoriously  unstable  in  his  mental  makeup,  and  the 
patients  are  markedly  neurotic.  They  are  pusillanimous  and  easily  startled. 
As  a  rule,  both  the  superficial  and  deep  reflexes  are  increased.  Many  of 
these  patients  suffer  later  from  serious  mental  disorders.  Among  the  Philip- 
pine natives " mali-mali"  patients  are  believed  to  be  particularly  prone  to  the 
outbreaks  of  maniacal  furor  known  as  amok. 


AMOK  (RUNNING  AMOK). 

This  term  is  used,  in  Malayan  countries,  to  designate  cases  of  maniacal  furor 
in  which  a  native  rushes  out  in  the  streets  of  his  village  with  kris  or  barong, 
cutting  down  every  one  in  his  path,  until  he  himself  is  dispatched  or  com- 
mits suicide.    It  is  a  question  whether  these  outbreaks  should  be  considered  as 


ASTASIA-ABASIA  1067 

evidences  of  a  specific  disease.  Preceding  the  attack  the  patient  is  in  a 
stupid,  morose,  or  melanchoHc  condition  for  several  days.  During  this 
period  there  frequently  is  amnesia,  and  during  the  attack  itself  complete 
amnesia  is  the  rule.  The  exciting  causes  of  the  outbreak  are  usually 
psychical;  grievance  over  some  real  or  fancied  wrong,  over  financial  losses, 
marital  difficulties,  fear  of  disgrace  or  punishment,  and  the  sight  or  smell 
of  blood.  The  disease  almost  always  attacks  young  adult  males.  Vari- 
ous causes  have  been  advanced  for  this  condition.  Alcoholism  may  be 
excluded,  as  the  Malay,  although  not  a  total  abstainer,  is  very  frugal  in  the  use 
of  liquors.  So,  too,  opium  smoking  cannot  be  considered  the  cause  of  the  dis- 
ease. Bevan  Lewis  believes  it  to  be  a  psychical  epilepsy,  and,  indeed,  transi- 
tory furor  very  much  resembling  the  attacks  of  amok  are  frequently  seen  in 
epileptics.  Earlier  travellers  and  writers  ascribed  these  attacks  to  religious 
mania.  Schuebe  discredits  this  idea  on  the  ground  that  the  Koran  does  not 
justify  the  killing  of  unbelievers,  and  he  quotes  Ellis  to  the  effect  that  amok- 
running  occurred  among  Malays  before  they  were  converted  to  Mohamme- 
danism. The  Malayan  races  chiefly  subject  to  amok  are  the  Bugis,  Illanums, 
and  the  Sulus,  or  Joloanos,  in  the  Southern  Philippines.  In  many  instances 
among  this  last  tribe  the  motive  is  undoubtedly  religious.  During  the  service 
of  the  United  States  army  in  the  Philippines  a  most  melancholy  case  occurred 
in  an  officer,  corresponding  exactly  to  the  typical  amok  cases.  This  man, 
an  excellent  soldier,  and  a  man  of  exemplary  personal  habits,  after  a  few 
days  of  brooding  and  melancholy,  suddenly  appeared  on  the  veranda  of 
his  quarters  with  a  rifle  and  began  to  shoot  into  his  company  formed  up  in 
close  proximity.  He  could  not  be  secured,  and  after  wounding  a  number 
of  his  men  he  was  shot  and  killed  by  one  of  his  own  sergeants.  With  regard 
to  the  responsibility  of  these  cases  no  general  rule  can  be  laid  down.  The 
responsibility  cannot  be  affirmed  in  all  cases,  nor  can  it  be  denied.  Most  of 
the  cases  of  amok  are  clearly  irresponsible.  Mention  has  been  made,  under 
Latah,  of  the  occasional  outbreaks  of  furor  resembling  amok  that  take  place 
in  that  disease. 

According  to  Kraepelin,  who  has  studied  this  condition  in  Java  very 
recently,  amok  is  not  an  entity,  but  embraces  a  variety  of  conditions  in 
which  sudden,  violent,  impulsive  acts  are  committed  while  consciousness 
is  clouded.  Some  cases  belong  to  the  class  of  the  "insanity  of  adolescence," 
some  are  epileptics,  a  few  may  be  instances  of  "malarial  psychosis,"  but  there 
are  rare  cases  of  amok  that  Kraepelin  cannot  explain.  Latah  is  distin- 
guished from  it  by  the  complete  preservation  of  consciousness  in  that  state. 


ASTASIA-ABASIA. 

Definition. — Astasia-abasia  is  a  symptom  of  hysteria.  It  occasionally 
follows  disturbance  of  the  nervous  system  produced  by  injury,  and  in  that 
sense  might  be  considered  a  traumatic  neurosis.  Occasionally  it  has  fol- 
lowed the  acute  infectious  diseases. 

Symptoms. — The  symptoms  consist  in  a  partial  or  complete  inahiUty  to  vse 
the  lower  limbs  in  standing  or  in  walking,  although  if  the  patient  lies  upon 


1068  DISEASES  OF   THE  NERVOUS  SYSTEM 

her  back  in  bed  she  can  move  her  legs  perfectly.  Examination  fails  to  reveal 
any  alteration  from  the  normal  as  to  motion,  co-ordination,  or  sensation. 
When  the  condition  simply  interferes  with  walking,  it  is  called  "dysbasia." 
Patients  who  may  be  quite  unable  to  walk  can,  nevertheless,  swim  perfectly. 
The  prognosis  is  as  favorable  as  that  of  ordinary  hysteria,  and  the 
treatment  is  the  same  as  that  which  is  employed  for  patients  who  are 
suffering  from  hysteria  or  neurasthenia. 


NEURASTHENIA. 

Definition. — Neurasthenia  is  a  condition  in  which  the  nervous  system 
suffers  from  various  functional  disorders  due  to  excessive  mental  and  ner- 
vous stress  and  strain  whereby  the  energies  of  the  patient  are  exhausted. 
For  this  reason  it  is  often  called  nervous  exhaustion. 

Etiology. — The  most  common  cause  of  neurasthenia  in  men  is  pro- 
longed mental  strain  produced  by  business  reverses  or  the  carrying  through 
of  some  important  and  difficult  enterprise.  The  severity  of  this  strain  is 
by  no  means  always  in  direct  proportion  to  the  size  of  the  undertaking. 
The  condition  is  not  met  with  in  the  lower  classes  except  occasionally,  and 
is  largely  dependent  upon  the  nervous  temperament  of  the  individual  and 
the  condition  of  his  general  health  and  surroundings.  In  women  the  condi- 
tion is  commonly  met  with  as  a  result  of  excessive  social  duties,  as  after  a 
winter  season  devoted  to  late  balls  and  receptions,  or  it  occurs  in  those  who 
have  passed  through  a  long  period  of  nervous  strain  resulting  from  the 
nursing  of  a  sick  husband,  child,  or  some  near  relative,  whereby  there  is  not 
only  physical  exhaustion  but  mental  anxiety  to  exhaust  reserve  energy.  It 
is  evident,  therefore,  that  many  causes  may  produce  this  condition  pro- 
vided they  result  in  a  great  expenditure  of  nervous  energy  with  so  little  sleep 
that  rest  cannot  be  obtained. 

Every  individual  may  be  said  to  possess  two  funds,  or  sources,  of  nervous 
energy.  From  one  of  these  he  takes  daily  that  force  which  is  necessary  for 
the  performance  of  his  physiological  functions  and  labor.  The  second  fund 
is  kept  in  reserve  to  meet  the  demands  of  extraordinary  occasions  and  is 
maintained,  as  is  the  reserve  fund  of  a  bank,  to  meet  conditions  which  are 
abnormal.  The  patient  who  suffers  from  neurasthenia  is  one  who  has  not 
only  expended  his  ordinary  fund,  but  drawn  so  largely  upon  his  reserve  fund 
that  he  is, a  nervous  bankrupt,  and  he  suffers  from  a  large  number  of  more 
or  less  serious  symptoms  because  the  various  parts  of  his  body  do  not 
receive  enough  nervous  energy  to  cause  them  to  perfectly  perform  their 
normal  functions.  If  the  strain  has  been  very  profound  and  severe,  and 
the  patient  is  one  whose  nervous  balance  is  not  very  stable,  it  can  be 
readily  understood  that  a  very  serious  state  may  develop,  and  that  the  life 
of  the  patient  may  be  jeopardized  if  any  intercurrent  disease  develops. 

Symptoms. — The  symptoms  of  neurasthenia  are  exceedingly  varied, 
depending  in  many  instances  upon  the  organ,  or  organs,  which  are  chiefly- 
affected  by  the  state  of  nervous  exhaustion.  In  some  cases  the  mental  con- 
dition of  the  patient  suffers  chiefly  and  the  symptoms  may  vary  from  mere 


NEURASTHENIA  1069 

irritability  of  temper  to  great  mental  depression  and  even  to  mental  aberra- 
tion, in  the  form  of  melancholia  or  even  actual  insanity.  Sometimes  per- 
sistent insomnia  develops.  In  other  instances  the  functions  of  the  digestive 
tract  suffer  chiefly,  and  in  others  the  heart  displays  the  greatest  evidence 
of  disturbed  nerve  supply,  so  that  attacks  of  palpitation  ensue,  or  instead 
a  lack  of  vasomotor  control  results  in  attacks  of  vertigo  or  syncope.  In 
addition  to  these  definite  and  specific  symptoms  the  patient  often  com- 
plains of  a  host  of  subjective  symptoms  which  are  quite  extraordinary  in 
character.  In  spite  of  the  variability  of  symptoms  the  following  are  con- 
stantly met  with:  sense  of  chronic  fatigue,  of  exhaustion,  and  irritability. 
Hysteria  is  not  infrequently  associated  with  neurasthenia. 

Diagnosis. — The  physician  should  never  reach  a  diagnosis  of  neurasthenia 
until  by  repeated  examinations  and  study  of  the  patient,  and  his  secretions, 
he  is  convinced  that  no  grave  organic  disease  exists  which  may  be  responsi- 
ble for  the  symptoms  presented.  If  cardiac  and  renal  disease  are  excluded, 
and  no  other  organic  malady  can  be  found  of  sufficient  gravity  to  produce 
the  illness,  and  if  the  history  of  the  patient  reveals  the  existence  of  some 
cause  capable  of  producing  nervous  exhaustion,  the  diagnosis  of  neuras- 
thenia may  be  reached. 

,  Prognosis. — The  prognosis  of  neurasthenia  depends  upon  the  ability  of 
the  physician  to  remove  the  patient  from  exposure  to  the  causes  which  have 
produced  the  condition,  upon  the  ability  or  willingness  of  the  patient  to 
follow  those  methods  of  life  which  are  conducive  to  the  re-establishment 
of  nervous  balance  and  reserve  energy,  and  upon  the  age  and  general  physical 
state,  for  if  the  patient  be  one  who  is  far  advanced  in  years,  or  who  by  reason 
of  disease  or  heredity  is  possessed  of  low  recuperative  power,  it  is  manifest 
that  complete  recovery  may  be  impossible.  Given  a  case  of  neurasthenia 
in  which  all  the  conditions  which  are  unfavorable  may  be  excluded  the 
prognosis  is  favorable,  but  the  physician  must  be  cautious  in  stating  the 
duration  of  the  period  of  recovery,  for  the  progress  toward  health  is 
governed  not  alone  by  the  skill  displayed  in  treatment,  but  by  the  recuper- 
ative power  of  the  individual,  a  power  which  every  physician  of  experience 
recognizes  as  a  very  variable  quantity.  Not  rarely  a  seemingly  frail 
person  recovers  speedily,  whereas  another  patient  of  a  more  powerful 
build  and  physique  makes  progress  so  slowly  as  to  cause  great  discourage- 
ment. 

Treatment.— From  what  has  been  said  of  the  causes  of  this  condition  it 
is  manifest  that  the  chief  aim  of  the  physician  must  be  the  re-establishment 
of  the  normal  nervous  energy  or  power.  As  first  pointed  out  by  Weir  Mitchell, 
this  can  only  be  obtained  by  the  accumulation  of  energy,  and  this  accumula- 
tion of  energy  is  to  be  had  only  by  absolute  mental  and  physical  rest  on  the 
one  hand  and  proper  feeding  on  the  other,  the  circulatory  and  other  vital 
functions  being  maintained  by  passive  exercises  and  electricity.  The  patient 
must  so  arrange  his  or  her  affairs  that  no  business  worries  or  family  cares 
will  be  experienced.  For  this  it  is  essential  that  the  treatment  shall  be 
carried  out  in  a  health  resort  far  removed  from  the  home  and  office,  or  in  a 
hospital  or  "rest-cure  house,"  where  the  patient  will  be  absolutely  isolated 
from  ordinary  surroundings.    An  attempt  to  carry  out  the  "cure"  at  home 


1070  DISEASES  OF   THE  NERVOUS  SYSTEM 

nearly  always  ends  in  failure,  because  the  needed  degree  of  mental  discipline 
is  not  obtainable  and  the  sounds  made  by  the  rest  of  the  family  annoy  the 
patient  or  develop  curiosity  or  worry  as  to  their  cause.  It  is  also  essential 
that  a  skilled  trained  nurse  shall  be  in  absolute  control  of  the  patient  without 
any  interference  by  members  of  the  family.  The  patient  is  not  allowed  to 
sit  up,  but  is  required  to  remain  in  bed  at  perfect  rest.  The  action  of  the 
kidneys,  bowels,  and  skin  is  carefully  looked  after  by  suitable  remedies, 
and  once  every  day  massage  is  given  over  the  entire  body  to  give  the  effects 
of  passive  exercise.  In  many  cases  it  is  well  to  give  massage  in  the  afternoon 
and  faradic  electricity  in  the  morning,  the  slowly  interrupted  current  being 
employed  to  exercise  the  muscles,  and  this  in  turn  followed  by  a  general 
application  of  the  rapidly  interrupted  current  from  the  head  to  the  feet  for 
fifteen  minutes.  These  measures  combined  with  a  cool  sponging  in  the 
early  morning  and  an  alcohol  rub  at  bedtime,  with  the  administration  of 
small  quantities  of  food  every  three  hours,  will  usually  cause  the  patient  to 
complain  of  being  "too  busy"  instead  of  feeling,  as  they  state  they  will 
feel  at  the  beginning  of  the  "cure,"  that  time  hangs  heavily  on  their  hands. 
The  patient  must  not  receive  or  write  letters  nor  must  she  read,  since 
this  requires  not  only  nervous  but  muscular  strain.  In  some  cases  the 
nurse  is  permitted  to  read  aloud  to  the  patient  for  an  hour  a  day.  Under 
such  a  plan  of  treatment,  in  which  all  the  nervous  energy  which  it  is  possible 
to  conserve  is  secured,  and  in  which  every  opportunity  is  offered  for  the 
addition  of  units  of  force  by  proper  feeding,  lasting  and  complete  recovery 
is  usually  obtained. 

TRAUMATIC  NEUROSES. 

Definition. — Under  the  term  traumatic  neuroses  there  is  described  a  con- 
dition in  which  an  individual,  after  exposure  to  some  severe  mental  shock 
or  physical  injury,  develops  a  train  of  symptoms  which  do  not  depend 
upon  any  demonstrable  lesion  of  the  nervous  system.  As  the  result  of 
functional  disorder  of  the  nervous  system  in  various  parts  of  the  body,  fol- 
lowing the  accident,  the  patient  presents  symptoms  which  are  chiefly  sub- 
jective, though  they  may  be  somewhat  objective,  and  he  may  be  actually 
and  completely  incapacitated  from  performing  the  ordinary  acts  of  life  for 
a  long  period  of  time.  Rarely  the  disability  may  be  permanent,  but  in 
these  cases  the  question  always  arises  as  to  whether  there  has  not  been  in 
addition  to  the  functional  disturbance  an  actual  organic  lesion.  It  is  evident, 
therefore,  that  cases  of  this  character  may,  and  do,  present  to  the  physician 
very  difficult  problems  in  differential  diagnosis,  for  not  only  may  functional 
disorders  exist  side  by  side  with  those  due  to  true  organic  change,  but  in 
addition  the  functional  disturbances  may  simulate  organic  disease  so  closely 
as  to  cause  great  confusion  in  symptomatology.  When  to  these  natural 
difficulties  are  added  the  desire  of  the  patient  to  obtain  heavy  damages 
from  the  individual  or  corporation  responsible  for  the  injury,  it  at  once 
becomes  evident  that  malingering  or  unintentional  and  subconscious  pro- 
duction of  symptoms  may  be  commonly  met  with. 


TRAUMATIC  NEUROSES  1071 

Etiology. — The  most  common  cause  of  traumatic  neuroses  are  railroad 
accidents,  trolley-car  accidents,  falls,  and  injuries  received  from  falling 
bodies.  As  a  result  of  exposure  to  one  of  these  causes,  with  associated  mental 
shock  due  to  terror  or  horror,  the  nervous  system  develops  the  perversions 
about  to  be  described. 

Symptoms. — It  is  manifest  from  what  has  already  been  said  that  the  symp- 
toms may  be  most  varied  as  to  severity,  distribution,  and  duration.  Prob- 
ably the  most  common  statement  of  the  patient  is  that  he  has  lost  power 
in  one  or  more  parts  of  his  body,  or  he  may  suffer  from  disturbances  of 
sensation,  with  or  without  loss  of  power.  In  males  it  is  not  infrequently 
claimed  that  the  injury  has  resulted  in  a  loss  of  sexual  power,  particularly 
if  the  back  has  received  a  blow  or  strain,  even  if  the  genital  apparatus 
is  itself  entirely  unaffected.  In  women  the  most  common  complaint  is  of 
pain  or  weakness  in  the  back,  of  pelvic  pain  or  displacement  of  the  pelvic 
organs,  and  of  vesical  disorders.  In  other  cases  the  chief  claim  is  that  more 
or  less  violent  pain  or  tingling  in  the  limbs  is  suffered.  When  loss  of  power 
is  suffered  from  it  appears  usually  as  a  hemiplegia  or  a  brachial  monoplegia, 
but  if  it  be  a  hemiplegia  the  face  nearly  always  escapes.  Paraplegia  is  very 
rare  and  the  sphincters  of  the  bladder  and  rectum  always  escape. 

Those  paralyses  which  are  not  truly  organic  can  be  separated  from  those 
that  are  such  by  the  facts  that  the  reactions  of  degeneration  do  not  develop 
in  the  paralyzed  parts  and  the  deep  reflexes  are  usually  preserved.  Anaes- 
thesia is  practically  always  present  if  the  paralysis  of  motion  is  complete, 
and  it  is  of  the  type  of  hysterical  paralysis  in  that  it  has  often  a  sharp  line 
of  degeneration  which  is  not  coincident  with  the  distribution  of  the  sensory 
nerves  of  the  part.  Paraplegic  cases  do  not  suffer  from  anaesthesia  of  the 
genital  organs.  Again,  it  sometimes  occurs  that  the  symptoms  complained 
of  are  not  constantly  in  the  same  part  or  that  positive  suggestions  may 
cause  their  development  elsewhere.  Not  rarely  an  examination  of  the 
color  fields  of  such  a  patient  will  reveal  the  reversals  commonly  found  in 
hysteria.  Disorders  of  all  the  special  senses  may  also  occur  and  total  dis- 
appearance of  these  functions  may  take  place^ — as  complete  deafness,  blind- 
ness, or  loss  of  taste  or  smell.  Occasionally  the  patient  may  develop  attacks 
which  resemble  to  some  degree  ordinary  epilepsy  or  catalepsy,  but  these 
attacks  are  separated  from  true  epilepsy  by  the  points  already  named  when 
discussing  that  disease. 

If  we  carefully  exclude  from  any  case  of  nervous  disorder  following  an 
injury  the  presence  of  an  actual  organic  lesion,  we  may  unhesitatingly  state 
that  the  patient  is  sufl'ering  from  hysteria  or  neurasthenia  due  to  injury, 
and  we  can  treat  him  accordingly.  On  the  other  hand,  it  is  not  to  be  for- 
gotten that  the  patient  who  suffers  from  the  symptoms  he  describes  is  often 
a  most  miserable  and  unfortunate  individual,  as  deserving  of  our  pity  as  if 
we  found  him  the  victim  of  an  incurable  malady  due  to  destruction  of  a 
part  of  his  body.  His  functional  disorders  are  as  real  to  him  and  cause  him 
as  much  suffering  as  if  they  depended  upon  organic  causes,  and  a  nervous 
system  functionally  perverted  may  be  as  useless  as  one  actually  grossly 
diseased,  just  as  a  watch  which  needs  regulating  may  be  as  useless  to  its 
owner  as  one  in  which  a  spring  is  broken.    While,  therefore,  it  is  our  duty 


1072  DISEASES   OF    THE  NERVOUS  SYSTEM 

to  relieve  such  patients  by  every  means  in  our  power,  and  to  bear  in  mind 
that  their  sufferings  are  often  very  real,  we  are  forced  to  recollect  that  the 
condition  may  not  be  permanent,  as  it  would  be  after  a  destructive  injury, 
and  so  when  the  case  has  become  one  of  medicolegal  importance  it  may 
not  be  possible  to  testify  that  the  patient  is  incurable  and  permanently 
disabled.  Not  only  is  tliis  true,  but  it  is  also  a  fact  that  the  very  continuance 
of  litigation,  and  the  frequent  appearance  of  the  patient  before  attorneys 
and  experts  for  both  sides  and  before  a  crowded  court-room,  may  make 
recovery  impossible  by  still  further  exciting  and  disturbing  nervous  balance, 
for  aside  from  this  form  of  excitement  the  description  of  the  scene  of  the 
accident  impresses  its  terrors,  over  and  over  again,  upon  a  mind  already 
horror-stricken  by  the  original  occurrence.  Perfectly  sincere  persons  often 
suffer  all  the  symptoms  they  describe  up  to  the  period  when  the  trial  of  the 
case  is  finished  and  then  speedily  improve. 

Treatment. — The  treatment  varies,  of  course,  with  the  character  of  the 
symptoms,  but  it  may  be  said  to  be  practically  identical  with  that  already 
advised  in  cases  of  hysteria  and  neurasthenia. 


OCCUPATION  NEUROSES 

An  occupation  neurosis  is  a  state  in  which  the  innervation  of  a  part 
becomes  functionally  disturbed  by  the  exhaustion  of  the  nervous  centres 
supplying  it,  and  in  all  probability  by  exhaustion  of  the  nerve  endings  as 
well.  The  causes  of  this  exhaustion  are  exceedingly  numerous.  Almost 
every  pursuit  in  life  which  involves  the  continuous  use  of  muscles  of  the 
hand  and  wrist  may  produce  an  occupation  neurosis  of  these  parts.  As  a 
result  we  find  spasm,  cramp,  or  palsy  developing  to  such  a  degree  as  to 
incapacitate  the  patient.  The  most  common  neurosis,  because  the  pursuit 
is  most  common,  and  because  small  and  accurate  movements  are  required, 
is  that  due  to  writing,  the  so-called  scriveners'  palsy  or  writers'  cramp. 
Another  form  is  telegraphers'  cramp,  and  a  third  is  hammerers'  palsy. 
Less  common  forms  are  violinists'  cramp,  pianists'  cramp,  flute-players' 
cramp,  and  "sewing  spasm."  Milkers  and  cigarmakers  sometimes  suffer 
from  neuroses  of  this  character.  In  writers'  cramp  the  flexor  muscles 
suffer  chiefly,  while  in  telegraphers'  cramp  the  extensors  are  the  ones  most 
involved.  Various  disorders  of  sensation  in  the  hands  are  also  present  and 
consist  in  sensations  of  tingling,  tension,  or  numbness.  Localized  sweating 
or  excessive  dryness  of  the  skin  may  be  present.  Occasionally  the  condition 
depends  upon,  or  is  associated  with,  a  true  neuritis,  which  may  involve  the 
entire  brachial  plexus  and  cause  pain  in  the  upper  arm  and  even  in  the 
muscles  of  the  neck  and  head  on  the  aff'ected  side.  The  history  of  the  case 
in  many  instances  is  that  the  patient  first  experiences  for  some  days  a  feeling 
of  stiffness  and  lack  of  pliability  in  his  fingers,  which  is  generally  accom- 
panied by  a  certain  lack  of  co-ordination  in  the  movements  required.  This 
inability  to  move  the  fingers  rapidly  and  accurately  is  only  present  when 
the  sufferer  attempts  to  perform  the  movements  which  are  the  cause  of  the 
trouble,  and  almost  all  other  motions  can  be  gone  through  with  without 


OCCUPATION  NEUROSES  1073 

difficulty.  If  the  patient  now  insists  on  keeping  on  with  his  duties,  the 
stiffness  is  replaced  by  violent  cramps,  more  or  less  painful,  which  come  on 
suddenly  and  with  considerable  power.  Co-ordination  is  still  further  dis- 
ordered, and  all  attempts  at  a  repetition  of  the  offending  act  are  resented 
by  the  affected  centres  and  muscles  in  such  a  positive  manner  as  to  make  all 
movements  irregular  and  often  jerking  in  character.  Unless  absolute  rest 
and  avoidance  of  former  movements  is  permitted,  the  cramps,  etc.,  are 
followed  by  loss  of  power,  deepening  into  partial  paralysis.  Even  when 
paralysis  exists,  however,  it  is  surprising  to  see  how  many  unoffending 
movements  can  be  performed  without  discomfort  and  failure. 

Some  discussion  has  arisen  as  to  whether  the  several  symptoms  which 
the  disease  presents  are  each  in  their  turn  an  indication  of  a  more  advanced 
stage  in  the  disorder  or  are  merely  more  prominent  in  one  case  than  another 
by  chance  or  tendency  on  the  part  of  the  individual  to  any  one  of  them. 
Thus,  some  observers  have  held  that  the  first  sign  of  the  disorder  was  the 
feeling  of  distress  or  fatigue  in  the  overworked  extremity,  and  that  the  tremors 
followed  because  the  warning  given  by  the  fatigue  was  not  heeded.  Finally, 
the  disregard  of  this  second  sjnnptom  brought  about  the  spasm  or  cramp, 
or,  in  other  cases,  the  palsy.  Other  writers,  especially  those  of  the  present 
day,  have  attempted  to  prove  that  there  is  no  distinct  onward  march  of  the 
symptoms  from  fatigue  to  tremor  and  from  tremor  to  palsy  or  cramp,  but 
rather  that  the  disorder  is  to  be  di\aded  into  four  varieties,  each  one  of  which 
may  assert  itself  without  the  development  of  another. 

Thus,  Lewis  tells  us  that  in  some  cases  cramps  come  on,  in  others  palsy, 
and  in  others  tremors,  while  still  another  variety  is  separated  from  its  fellows 
by  the  predominance  of  certain  symptoms  associated  with  disturbances  of 
sensation.  He  states,  however,  that  the  disorder  of  sensation  is  always 
present  in  all  forms  of  the  trouble  in  some  degree,  and  that  it  is  only  in  cases 
where  the  trouble  consists  in  a  neuritis  that  the  symptom  rises  to  the  impor- 
tance of  marking  a  separate  variety. 

Many  very  prominent  writers  on  scriveners'  and  hammerers'  palsy  assert 
that  predisposition  is  one  of  the  prime  factors  in  the  causation  of  these 
maladies.  While  this  is  doubtless  true  to  a  certain  extent,  it  is  nevertheless 
a  fact  that  all  persons,  be  their  temperaments  nervous  or  otherwise,  are 
affected,  and  in  view  of  this  fact  the  writer  thinks  that  predisposition  should 
not  be  accorded  the  leading  position  in  the  causation  of  the  malady.  It  is, 
of  course,  probable  that  persons  whose  temperaments  are  nervous  and 
excitable  are  naturally  susceptible  to  nervous  disorders,  whereas  the  phleg- 
matic temperament  is  rather  opposed  to  the  conditions  which  are  necessary 
for  the  presence  of  this  disease. 

Rosenthal  calls  attention  to  the  fact  that  the  loss  of  power  is  limited 
entirely  to  those  centres  which  are  the  directors  of  the  particular  muscles 
involved,  and  states  in  substantiation  of  this  assertion  that  the  surrounding 
centres  for  other  groups  of  muscles  always  escape,  as  is  proved  by  the  fact 
already  mentioned,  that  other  acts  can  be  performed  without  difficulty. 
While  it  is  true  that  the  surrounding  centres  are  not  affected,  it  is  also  true 
that  the  centre  governing  like  movements  in  the  opposite  hand  is,  by  sym- 
pathy or  other  cause,  affected  with  its  fellow  to  a  certain  extent.  This  is 
68 


1074  DISEASES  OF   THE  NERVOUS  SYSTEM 

proved  by  the  fact  that  if  the  operator  learns  to  send  messages  with  this  well 
hand,  that  hand  very  soon  follows  the  fate  of  its  fellow. 

Experiments  performed  by  the  late  Dr.  N.  A.  Randolph  bear  so  strongly 
on  this  subject  that  they  may  be  quoted  at  this  point.  His  object  was  to 
discover  if  exhaustion  of  one  centre  in  the  brain  produced  any  effect  on 
the  corresponding  centre  on  the  opposite  side  of  the  brain ;  and  to  this  end 
he  proceeded  as  follows :  He  attached  a  small  lever  to  a  meter,  and  resting 
the  hand  of  the  subject  on  the  table,  as  when  writing,  he  directed  him  to 
place  the  tip  of  his  forefinger  on  the  end  of  the  lever  and  to  depress  it  as 
often  as  he  could.  Each  depression  was,  of  course,  registered  in  this  way. 
Dr.  Randolph  found  that,  normally,  the  right  forefinger  possessed  power 
for  100  movements,  the  left  forefinger  for  75  movements.  Having  decided 
this  primary  point  he  proceeded  to  search  after  the  main  object  of  his  exami- 
nation. He  found  that  if  the  left  forefinger  was  set  to  work  after  the  right 
forefinger  had  performed  its  100  depressions,  it  became  exhausted  at  50 
movements,  and  that  if  the  right  hand  was  set  to  work  after  the  left  fore- 
finger had  moved  75  times  it  could  only  move  75  times.  In  other  words, 
exhaustion  of  one  centre  produced  exhaustion  of  the  corresponding  centre 
on  the  opposite  side  of  the  brain. 

Careful  tests  prove  that  in  most  instances  exaggerated  reflexes  are 
present,  denoting  a  superexcitability  of  the  spinal  cord,  and  in  other  cases 
evidences  of  neuritis  of  the  nerve  trunks  have  undoubtedly  been  observed. 
In  some  cases  of  the  disease  a  species  of  pseudomuscular  hypertrophy  comes 
on,  due,  probably,  to  some  centric  nervous  lesion,  and,  perhaps,  in  part  to 
the  congested  condition  which  is  nearly  always  present  in  the  affected  mus- 
cles. Thus  we  find  the  bellies  of  the  muscles  hard,  firm,  and  projecting,  yet 
devoid  of  power. 

Treatment. — In  the  way  of  treatment  rest  is  the  best  measure  that  we 
possess  for  the  cure  of  the  affection;  but  although  absolute  rest  from  the 
exciting  cause  is  one  of  the  essential  factors  for  a  complete  recovery,  the 
affected  arm  should  be  used  in  every  other  motion  which  is  natural  and  easy, 
so  that  it  may  not  become  useless  from  disuse.  Next  to  rest  we  have  as  a 
therapeutic  agent  electricity,  which  is,  however,  only  indicated  in  those 
cases  where  very  slight  or  no  inflammatory  conditions  are  present,  either  in 
the  muscle,  nerve,  or  nerve  centre;  and  it  should  be  the  invariable  rule  to 
use  that  current  which  causes  the  most  contraction  with  the  least  pain. 
Galvanization  of  the  affected  muscles  should  be  performed  in  such  a  way 
that  the  disordered  nerve  centres  are  not  disturbed,  and  care  should  be  taken 
to  gradually  increase  the  exercise,  so  as  not  to  exhaust  or  overfatigue  the 
muscles  which  are  out  of  order.  Movements  which  are  slowly  performed 
with  the  affected  parts  are  also  useful,  following  the  method  of  muscle  train- 
ing proposed  by  Fraenkel  in  the  treatment  of  locomotor  ataxia. 

Finally,  the  administration  of  tonics,  such  as  arsenic,  iron,  and  strychnine, 
is  to  be  resorted  to,  and  these  measures  combined  with  massage  are  the 
best  methods  we  have  for  effecting  a  cure. 


ANGIONEUROTIC  (EDEMA  1075 


RAYNAUD'S    DISEASE. 

Definition. — Raynaud's  dsiease  is  a  condition  in  which  one  or  more  of  the 
fingers  or  toes,  and  rarely  the  nose  and  ears,  suffer  from  a  disorder  of  the 
local  bloodvessels,  with  the  result  that  these  parts  become  bloodless  and 
pallid  or  slate  colored  and  mottled  in  appearance.  The  affected  parts  are 
cold  and  sometimes  painful.  The  malady  usually  affects  persons  under 
thirty  years  of  age,  and  females  more  commonly  than  males.  The  cause 
is  unknown  save  that  it  seems  to  be  of  the  nature  of  a  paroxysmal  neurosis 
involving  the  bloodvessels  of  the  parts  affected.  Various  conditions,  all  of 
them  capable  of  causing  a  loss  of  normal  nerve  tone,  have  been  considered 
as  etiological  factors,  varying  from  diabetes  and  neurasthenia  to  fright  and 
exposure  to  cold  air  or  cold  water. 

Etiology. — ^The  onset  begins  with  a  sense  of  tingling,  or  of  heat  or  cold, 
in  the  parts  which  are  to  suffer  from  the  well-developed  state.  The  skin 
looks  shrunken  and  ashen  in  hue  and  numbness  is  present  to  a  more  or  less 
well-developed  degree,  but  complete  anaesthesia  does  not  occur.  The  con- 
dition may  last  for  a  few  hours  or  for  weeks.  ^Mien  it  disappears  it  nearly 
always  returns  in  a  short  time. 

When  the  disease  occurs  in  its  severe  form  local  gangrene  may  ensue. 
The  part  becomes  livid  and  dusky  and  small  blebs  develop  on  the  fingers. 
These  may  dry  up  and  recovery  take  place,  only  the  skin  being  destroyed, 
or  the  process  may  become  so  deep  that  the  entire  part  may  be  lost. 

This  condition  is  to  be  separated  from  senile  gangrene  by  the  youth  of 
the  patient,  from  frost-bite  by  the  absence  of  a  history  of  exposure  to  cold, 
and  from  chronic  ergotism  by  the  absence  of  any  history  of  eating  rye 
bread  contaminated  by  ergot. 

Treatment. — ^The  treatment  consists  in  the  use  of  tonics  and  every  possible 
measure  designed  to  re-establish  good  general  health.  Hydrotherapy  is 
often  of  value.  Locally  the  nutrition  of  the  affected  part  may  be  maintained 
to  some  extent  by  the  use  of  dry  or  moist  heat.  Great  care  should  be  taken 
to  protect  those  parts  which  are  usually  affected,  from  extremes  of  heat  and 
cold. 

ANGIONEUROTIC   (EDEMA. 

Definition  and  Symptoms. — Angioneurotic  oedema  is  a  condition  charac- 
terized by  the  sudden  appearance,  in  a  limited  area  in  one  or  more  parts  of 
the  body,  of  well-defined  swelling  due  to  some  perversion  of  the  normal 
functional  activity  of  the  vasomotor  nerve  supply,  so  that  the  bloodvessels 
of  the  part  become  dilated,  and,  in  all  probability,  an  extravasation  of  fluid 
takes  place.  The  condition  is  to  be  clearly  separated  from  that  character- 
istic of  inflammation.  The  temperature  of  the  part  is  often  lower,  but 
sometimes  it  is  higher  than  normal.  The  dimensions  of  the  affected  part 
vary  greatly,  but  it  is  rarely  more  than  a  few  inches  in  circumference.  The 
hue  of  the  area  affected  may  be  a  deep  red,  as  if  suffering  from  intense 
congestion,  or  so  pallid  as  to  be  cadaveric,     It  may  be  the  seat  of  a  sense  of 


1076  DISEASES  OF   THE  NERVOUS  SYSTEM 

tingling,  or  heat,  or  itching,  but  actual  pain  does  not  occur,  and  pitting  on 
pressure,  to  the  extent  that  it  appears  in  ordinary  oedema,  is  absent. 

Angioneurotic  oedema  occurs  most  commonly  on  the  face  or  hands.  It 
may  affect  the  body  and  quite  rarely  the  larynx  and  pharynx,  when  it  may 
produce  alarming  symptoms  by  interfering  with  respiration.  Instances  of 
death  due  to  this  cause  have  been  reported.  The  attacks  last  a  few  hours 
to  several  days,  and  are  prone  to  occur  at  irregular  intervals. 

Angioneurotic  oedema  occurs  more  frequently  during  the  third  decade 
of  life  than  at  any  other  period,  and  in  the  United  States  affects  females 
more  frequently  than  males,  although  the  reverse  of  this  holds  true  in  Europe. 
We  do  not  know  what  the  causative  factor  is,  but  it  is  known  that  exposure 
to  cold  and  causes  which  diminish  nervous  tone  bring  on  an  attack  in  those 
who  are  susceptible. 

In  some  cases  the  condition  is  induced  by  digestive  disorders,  or  by  the 
ingestion  of  some  food  which  is  toxic,  as  lobster,  fish,  or  other  animal  food 
that  is  not  fresh.  In  nearly  all  cases  the  patient  is  neurotic,  and  not  rarely 
has  a  neurotic  family  history,  or  even  a  direct  inheritance  of  the  disorder 
from  the  parents. 

Diagnosis. — Angioneurotic  oedema  must  be  separated  from  the  local 
vasomotor  disturbances  of  hysteria.  This  is  done  by  the  fact  that  in  hysteria 
there  are  associated  paralysis  of  motion  or  anaesthesia  and,  it  may  be,  hysteri- 
cal contractures.  Again,  the  oedema  of  hysteria  is  often  persistent,  whereas 
this  is  temporary.  From  severe  attacks  of  urticaria  it  is  differentiated  by  the 
fact  that  "hives"  are  usually  scattered  widely  over  the  body,  and  if  they 
appear  on  the  hands  are  characterized  by  multiple  lesions.  In  most  cases  of 
hives,  or  urticaria,  additional  lesions  can  be  produced  by  rubbing  a  part. 

Prognosis.  The  prospect  of  complete  cure  in  the  sense  of  an  escape  from 
all  future  attacks  is  not  encouraging.  The  general  health  is  usually  good 
between  the  attacks,  and  unless  the  part  affected  be  the  larynx  the  prospect 
of  any  serious  result  is  unlikely. 

Treatment. — ^The  treatment  can  be  directed  only  along  those  lines  which 
will  tend  to  improve  the  general  health,  of  which  the  most  useful  are  an 
out-door  life,  hydro  therapeutics,  and  the  internal  use  of  tonics,  such  as  iron 
and  arsenic  if  there  is  ansemia,  and  nux  vomica  and  quinine  if  the  nervous 
system  is  atonic.  Phosphorus  may  also  be  useful.  When  litheemic  or  gouty 
conditions  are  present,  the  iodides,  salicylates,  and  colchicum  may  be  of 
great  value.  It  is  needless  to  add  that  all  causes  known  by  the  experience 
of  the  patient  to  be  provocative  of  an  attack  should  be  sedulously  avoided, 
for  there  can  be  little  doubt  that  the  occurrence  of  one  attack  predisposes  to 
another. 

ERYTHROMELALGIA. 

Definition. — This  condition  was  first  described  by  Weir  Mitchell  in  1872. 
It  consists  in  a  hypersemia  of  the  foot  and  leg,  rarely  the  hand,  associated 
with  pain  which  may  vary  in  degree  from  a  sense  of  weight  and  heaviness 
to  exceedingly  severe  suffering.  The  malady  first  affects  the  neighborhood 
of  the  ball  of  the  foot,  and  thence  it  spreads  to  the  entire  plantar  surface. 


MIGRAINE  1077 

In  other  cases  the  heel  is  first  affected.  Although  exercise  greatly  increases 
the  suffering,  it  is,  as  a  rule,  worse  at  night.  The  pain  may  be  intermittent 
or  continuous.  The  skin  is  often  not  only  hypersemic,  but  is  often  marbled 
or  mottled  in  appearance.  Elevation  of  the  part,  by  decreasing  the  conges- 
tion, diminishes  the  pain. 

Etiology. — The  causes  of  the  malady  are  several.  In  rare  instances  it 
seems  to  depend  upon  lesions  in  the  spinal  cord,  in  others  it  apparently 
depends  upon  diabetes  mellitus,  and  in  still  others  arteriocapillary  fibrosis 
seems  to  be  the  underlying  factor. 

Diagnosis. — Before  determining  the  diagnosis  of  erythromelalgia  it  is 
essential  that  gout  and  diseases  of  the  soft  and  hard  tissues  of  the  foot  be 
excluded.  In  the  vast  majority  of  cases  the  symptoms  will  probably  be  due 
to  such  causes,  for  true  erythromelalgia  is  a  very  rare  malady  indeed,  and 
but  few  cases  have  been  recorded. 

Treatment. — ^Treatment  often  fails  to  give  much  relief.  The  part  should 
be  kept  in  an  elevated  posture  as  much  as  possible,  cool  lotions  may  be 
applied  to  it,  and  if  the  patient  be  lithsemic  the  alkalies  and  salicylates 
should  be  given. 

MIGRAINE. 

Definition. — Much  confusion  exists  as  to  the  exact  nature  of  the  condition 
which  is  called  migraine.  By  all  authors  it  is  used  to  describe  a  condition 
of  severe  pain,  more  or  less  limited  to  one  side  of  the  head,  often  accompanied 
by  some  disturbance  of  vision  in  one  or  both  eyes,  and  by  nausea  and  vomit- 
ing, which  often  do  not  develop  until  toward  the  end  of  the  attack.  Certain 
clinicians  have  expressed  the  belief  that  migraine  is  an  hereditary  affection, 
and  even  go  so  far  as  to  regard  it  as  a  manifestation  of  nervous  instability 
not  far  removed  from  epilepsy.  This,  however,  is  certainly  incorrect  in 
the  vast  majority  of  cases.  It  may  be  true  that  certain  neurotic  individuals 
who  are  subject  to  hysterical  or  epileptic  manifestations  often  suffer  from 
migraine.  But,  on  the  other  hand,  it  cannot  be  denied  that  in  the  majority 
of  instances  the  condition  is  a  toxic  neurosis  due  to  the  manufacture  and 
retention  in  the  body  of  abnormal  products  of  metabolism.  These  products 
are  chiefly  the  result  of  a  disturbed  action  of  the  liver,  either  in  the  sense 
that  the  liver  fails  to  destroy  poisons  which  are  absorbed  from  the  intestines, 
or  in  the  sense  that  it  develops  substances  which  it  does  not  produce  when 
in  health.  As  a  matter  of  fact  migraine,  as  a  toxic  condition,  is  rarely  the 
result  of  any  disorder  of  function  in  a  single  organ,  but  is  produced  by 
several  causes,  an  undue  development  of  poison,  a  deficient  action  of  the 
liver  in  destroying  these  poisons,  and  a  torpid  condition  of  the  kidneys, 
whereby  toxins  are  not  speedily  eliminated.  It  naturally  follows  that  in  high- 
strung,  nervous  individuals,  and  in  those  who  have  neurotic  tendencies, 
these  toxic  products  can  readily  disturb  the  functions  of  the  sensory  nerves 
of  the  head  and  so  produce  a  seizure. 

Among  the  active  causes  in  provoking  an  attack  of  migraine,  aside  from 
the  effects  of  autointoxication,  there  can  be  no  doubt  that  nervous  tire,  or 
exhaustion,  aids  materially  in  causing  an  attack,  particularly  if  in  addition 


1078  DISEASES  OF   THE  NERVOUS  SYSTEM 

to  such  stress  there  is  added  undue  sexual  activity,  or  other  forms  of  abuse. 
All  these  factors  diminish  the  nervous  energy  which  supports  vital  processes 
and  so  tend  to  cause  perversions  of  metabolism,  and  at  the  same  time  they 
diminish  the  resistance  of  the  nervous  and  vascular  system  to  the  action  of 
such  poisons. 

The  disease  occurs  most  frequently  in  w^omen  and  rarely  develops 
before  the  age  of  puberty.  It  is  particularly  prone  to  attack  those  who 
have  a  gouty  ancestry.  Certain  schools  of  ophthalmologists  have  strongly 
urged  the  view  that  all  cases  of  migraine  are  due  to  errors  of  refraction. 
There  can  be  no  doubt  that  in  many  instances  this  cause  of  nervous 
exhaustion  is  a  potent  factor.  The  important  point  for  the  physician  to 
remember  in  studying  this  malady  is  that  various  causes  may  be  responsible 
for  it;  and  if  the  patient  is  to  be  permanently  relieved,  one  or  more  of  these 
causes  must  be  discovered  and  removed. 

S3miptoms. — The  mode  of  onset  of  an  attack  varies  greatly.  Some  patients 
state  that  for  several  days  prior  to  a  paroxysm  they  feel  generally  out-of-sorts 
and  anything  but  well.  Often  the  chief  symptom  is  mental  depression. 
Other  patients  have  no  premonitory  symptoms  whatever.  Arising  in  the 
morning  in  perfect  health,  they  are  seized  at  some  time  during  the  day 
with  blurring  of  the  vision  in  one  or  both  eyes,  soon  followed  by  a  sharp 
attack  of  pain,  or  pain  may  be  the  first  and  only  symptom,  and  its  onset 
may  be  so  sudden  and  severe  as  to  completely  incapacitate  the  patient.  To 
this  form  of  migraine  the  terms  "fulgurating"  or  "fulminant"  have  been 
applied.  In  most  cases  the  pain  exists  chiefly  in  one  side  of  the  head,  and 
involves  the  supraorbital  region  and  the  eyeball.  When  it  is  fully  developed 
the  entire  head  may  suffer.  The  character  of  the  pain  is  throbbing  and  the 
sensation  in  the  head  is  tense.  Not  rarely  photophobia  is  present,  and  in 
some  cases  vision  may  be  so  much  interfered  with  that  actual  hemianopsia 
is  described  by  the  patient.  In  addition  to  the  pain  the  patient  not  infre- 
quently has  some  vertigo,  is  mentally  heavy  and  dull,  and  not  rarely  slightly 
aphasic. 

After  the  attack  has  lasted  from  one  to  several  hours  the  patient  quite 
frequently  becomes  nauseated  and  then  vomits.  As  a  rule,  the  stomach  does 
not  contain  undigested  food;  on  the  contrary,  digestion  seems  to  have  gone 
on  with  undue  rapidity.  The  material  vomited  is  usually  small  in  amount 
and  excessively  acrid  and  acid.  I  am  firmly  convinced  that  this  fluid  is  the 
result  of  an  attempt  on  the  part  of  the  stomach  to  eliminate  poisonous 
materials,  just  as  this  organ  eliminates  oxydimorphine  in  morphine  poison- 
ing. If  the  vomiting  persists  for  any  length  of  time  bilious  materials  may 
be  brought  up  by  reason  of  the  drawing  of  bile  through  the  pylorus  in  the 
act  of  retching.  It  is  a  question  whether  this  vomiting  is  the  result  of  the 
action  of  the  poison  which  produces  the  symptoms,  or  whether  it  is  in  large 
part  due  to  the  severity  of  the  pain  which,  when  it  affects  the  eyeball,  closely 
resembles  the  sickening  pain  produced  by  an  injury  to  the  testicle.  During 
an  attack  the  patient's  face  is  usually  pallid  and  betokens  severe  pain, 
having  an  anxious  and  hunted  expression  or  one  of  profound  depression. 
Sometimes  the  radial  pulse  is  small  and  hard,  and  not  rarely  the  temporal 
artery  on  the  affected  side  stands  out  like  a  whipcord.    The  attacks  rarely 


MIGRAINE  1079 

come  oftener  than  once  a  week,  and  sometimes  much  more  rarely  than  this, 
unless  the  patient  by  errors  in  diet  and  by  various  excesses  produces  the 
provoking  condition  frequently.  Sometimes  patients  state  that  the  attack 
comes  on  in  the  midst  of  perfect  health.  Thus,  I  have  heard  a  patient 
remark  that  she  felt  so  well  that  she  was  sure  she  was  going  to  be  sick  the 
next  day,  as  it  had  been  her  experience  that  a  sensation  of  well-being  was 
not  rarely  followed  by  a  nervous  explosion.  In  rare  cases  a  certain  degree 
of  'paralysis  of  the  extraocular  muscles  may  be  present  during  the  attack. 
In  still  more  rare  instances  the  face  is  flushed  instead  of  being  pallid.  Not 
rarely  during  the  attack  the  urine  is  scanty  and  high  colored,  but  as  the 
attack  subsides  the  urine  is  frequently  passed  in  large  quantities  and  is 
exceedingly  limpid.  Speedy  recovery  usually  follows  the  vomiting  of  the 
acrid  fluid  already  named. 

Treatment. — The  treatment  depends  upon  the  underlying  cause  of  the 
malady.  All  excesses  as  to  eating  and  sexual  activity  must  be  prevented. 
If  the  patient  is  run  down  and  neurasthenic,  a  vacation  or  a  rest  cure  is 
essential.  If  the  kidneys  fail  to  excrete  a  suflScient  quantity  of  urinary  solids 
per  day,  the  various  potassium  salts,  such  as  the  acetate,  citrate,  or  bitar- 
trate  of  potassium,  must  be  given  in  5  or  10  grain  doses  three  or  four  times 
a  day,  in  copious  draughts  of  water  to  increase  urinary  elimination.  If 
there  are  any  evidences  that  the  liver  is  persistently  or  occasionally  inactive, 
its  function  should  be  stimulated  by  the  use  of  calomel,  blue  mass,  or  podo- 
phyllin.  Many  of  these  cases  do  very  well  if  5  to  10  grains  of  blue  mass  are 
taken  every  week  or  ten  days,  and  then  followed  by  a  saline  purge.  In  those 
instances  in  which  the  patient  leads  a  sedentary  life,  active  out-door  exercise 
to  ensure  perfect  oxidation  processes  in  the  body  are  essential-  In  those 
patients  who  suffer  from  gastrointestinal  catarrh,  a  dose  of  Hunyadi  or 
Apenta  water,  taken  hot  and  in  sips,  before  breakfast,  will  often  be  efficient 
not  only  in  moving  the  bowels,  but  preventing  the  attacks.  Often  diluting 
one  of  these  waters  one-half  with  hot  water  makes  it  an  efficient  purgative. 
The  use  of  salol  in  the  dose  of  5  to  10  grains  a  day  as  an  intestinal  antiseptic 
is  often  advantageous. 

Of  all  forms  of  preventive  treatment,  that  which  is  devoted  to  the  in- 
creased activiy  of  the  intestines,  the  liver,  and  the  kidneys  is  of  most  impor- 
tance. If  the  patient  is  gouty,  or  suffers  from  that  condition  commonly  but 
erroneously  called  "uricacidsemia,"  not  only  should  the  treatment  just 
recommended  be  employed,  but  the  use  of  other  more  active  salicylates,  such 
as  the  salicylate  of  strontium  in  5  or  10  grain  doses  three  times  a  day,  are 
advisable.  If  errors  in  refraction  exist,  carefully  fitted  glasses  should  be 
provided,  and  if  the  nasal  mucous  membrane  is  hypertrophied  or  other 
abnormalities  exist  in  this  region,  they  should  be  treated.  For  the  relief 
of  the  attack  many  measures  have  been  suggested.  In  those  instances 
where  the  patient  has  prodromal  symptoms,  a  brisk  saline  cathartic,  such  as 
Seidlitz  powder,  citrate  of  magnesia,  or  Rochelle  salt,  should  be  given,  with 
the  idea  of  sweeping  out  from  the  bowels  poisonous  material.  This  may 
be  followed  in  half  an  hour  to  an  hour  by  2  grains  of  caffeine  with  10  grains 
of  bromide  of  sodium.  The  best  way  to  give  this  is  in  granular  effervescent 
salts.     In  some  instances  a  small  dose  of  phenacetin  or  acetanilid  should 


1080  DISEASES  OF   THE  NERVOUS  SYSTEM 

be  added.  If  high  arterial  tension  is  present,  nitroglycerin  is  valuable. 
For  the  relief  of  the  pain  when  it  is  very  severe  phenacetin,  antipyrin,  and 
acetanilid  are  useful,  but  it  must  always  be  remembered  that  the  stomach 
is,  as  a  rule,  excreting  rather  than  absorbing,  and  that  the  mere  administra- 
tion of  a  palliative  at  this  time  may  be  fruitless  for  this  reason.  Under  these 
circumstances  it  may  be  necessary  to  give  these  drugs  by  the  rectum,  or  to 
empty  the  stomach  by  vomiting  or  by  the  use  of  the  stomach  tube  before 
they  are  administered.  Sometimes  the  stomach  can  be  stimulated  to  absorp- 
tion by  ^  grain  of  strychnine.  In  certain  cases  the  use  of  a  full  dose,  10, 15, 
or  20  drops,  of  the  tincture  of  gelsemium  with  a  grain  of  an  active  extract  of 
cannabis  indica  gives  the  greatest  relief.  The  use  of  cologne-water  contain- 
ing 5  to  10  grains  of  menthol  to  the  ounce  applied  over  the  course  of  the 
painful  nerve  may  give  much  relief.  In  many  instances  it  is  impossible  for 
any  of  these  remedies  to  do  good  unless  the  patient  will  lie  down  in  a  quiet 
and  dark  room  for  several  hours. 


SUNSTROKE. 

Definition. — Sunstroke,  more  accurately  called  heatstroke,  insolation,  or 
thermic  fever,  and  by  the  French  coup  de  soleil,  is  a  condition  of  the  body 
produced  by  exposure  to  great  heat.  In  rare  instances  the  temperature  of 
the  patient  does  not  rise,  but  falls,  and  to  this  condition  is  given  the  name 
heat  exhaustion. 

Etiology. — ^The  chief  factor  in  producing  heatstroke  is  the  presence  of 
great  heat  associated,  as  a  rule,  with  marked  humidity  of  the  atmosphere. 
It  is  important  to  bear  in  mind  the  fact  that  exposure  to  the  rays  of  the  sun 
is  not  necessary  for  the  development  of  heatstroke.  Cases  are  constantly 
met  with  in  which  the  illness  of  the  patient  is  due  to  artificial  heat,  and  heat- 
stroke may  occur  in  the  night  as  well  as  in  the  day  if  the  atmosphere  is  hot 
and  moist.  Dry  heat  is  better  borne  by  all  persons  than  is  moist  heat, 
probably  because  evaporation  on  the  skin  proceeds  rapidly  in  dry  air,  and  so 
the  body  is  cooled  by  the  function  of  perspiration,  whereas  in  a  moist  atmos- 
phere the  imperfect  evaporation  results  in  an  accumulation  of  heat  in  the 
body.  For  this  reason  heatstroke  is  ^ery  rare  on  the  western  plains  of  the 
United  States,  where  the  temperature  in  summer  often  reaches  105°  in  the 
shade,  whereas  in  Philadelphia,  where  the  air  is  humid,  heatstroke  is  exceed- 
ingly common  when  the  thermometer  registers  a  temperature  of  90°.  In  the 
one  case  evaporation  is  so  rapid  that  the  heat  of  the  body  is  kept  at  a  normal 
level,  whereas  in  the  latter  case  the  perspiration  lies  on  the  skin  in  great  beads. 
A  second  factor  in  producing  heatstroke  is  the  use  of  alcoholic  drinks  in  any 
form.  There  can  be  no  doubt  that  all  such  beverages  greatly  predispose  to 
the  development  of  this  state.  So,  too,  renal  disease  and  a  feeble  heart  may 
act  as  predisposing  factors.  Loss  of  sleep  and  torpidity  of  the  bowels  are 
also  possessed  of  an  evil  influence. 

Certain  French  clinicians  have  asserted,  with  notable  facts  in  support  of 
their  views,  that  sunstroke  is  really  a  form  of  infection  which  develops  under 
the  atmospheric  states  already  named. 


SUNSTROKE  1081 

Pathology  and  Morbid  Anatomy. — While  a  very  considerable  number  of 
clinicians  in  America  and  in  the  East  Indies  described  sunstroke  symp- 
tomatically  in  the  early  part  of  the  last  century,  it  was  not  till  H.  C,  Wood 
collated  our  knowledge  and  enriched  it  by  further  experimentation  that  the 
profession  began  to  fully  grasp  the  facts  concerning  its  production  and  the 
lesions  which  ensued. 

The  pathology  of  the  disorder  resides  in  the  inability  of  the  heat-regulating 
mechanism  of  the  body  to  maintain  a  normal  body  temperature.  The 
primary  difficulty  lies  in  a  decreased  power  of  the  body  to  carry  out  an 
efficient  heat  dissipation,  and  this  is  followed  by  an  unrestrained  heat  pro- 
duction, due,  in  Wood's  opinion,  to  failure  of  the  inhibitory  heat  centres,  in 
the  pons,  to  check  oxidation  processes.  With  diminished  heat  dissipation 
and  increased  heat  production  it  is  not  difficult  to  perceive  why  the  tem- 
perature of  the  body  rises  until  a  state  of  hyperpyrexia  is  reached. 

The  morbid  anatomy  consists  in  changes  in  the  tissues  which  in  turn  per- 
mit decomposition  to  set  in  very  rapidly,  being  preceded  by  well-marked 
rigor  mortis.  The  veins  of  the  brain  and  lungs  are  found  distended  with 
fluid  blood,  and  everywhere  the  blood  fails  to  clot  as  it  does  in  the  vessels 
of  the  ordinary  cadaver.  If  an  autopsy  is  made  very  soon  after  death,  the 
left  ventricle  is  found  in  firm  systole,  but  the  right  ventricle  is  distended  with 
blood.    The  liver  and  kidneys  are  also  found  to  be  intensely  engorged. 

Symptoms. — ^The  symptoms  of  sunstroke  consist,  in  the  preliminary  stage, 
in  oppression  and  dizziness.  If  these  evidences  of  heat  are  ignored,  the  stage 
of  sudden  unconsciousness  develops,  and  is  often  ushered  in  by  a  convulsion 
which  may  be  exceedingly  violent.  In  other  cases  no  convulsion  develops, 
but  deep  stupor  with  stertorous  breathing  comes  on.  The  face  is  at  first  livid 
and  later  deeply  cyanotic,  the  great  vessels  of  the  neck  and  upper  extremities 
being  distended.  The  temperature  of  the  patient  speedily  rises  to  a  height 
never  seen  in  any  other  disease,  sometimes  reaching  112°  or  more,  the 
average  being  from  105°  to  110°.  The  pupils  may  be  contracted  or  widely 
dilated.  If  the  fever  cannot  be  reduced  and  the  cardiac  and  pulmonary 
congestion  are  not  relieved,  death  ensues  within  twelve  to  thirty-six  hours. 
When  improvement  takes  place,  a  relapse  some  hours  later  often  ensues.  A 
patient  who  has  sunstroke  may  subsequently  become  very  ill  and  die  from 
a  secondary  meningitis.  Persons  who  have  had  sunstroke  are  very  suscep- 
tible to  high  temperatures,  and  when  exposed  in  after  years  may  be  greatly 
distressed  by  an  atmospheric  temperature  as  low  as  80°,  if  the  air  is  moist. 

Diagnosis. — ^There  are  only  two  other  states  that  resemble  heatstroke, 
namely,  uraemia  and  apoplexy.  The  first  can  be  excluded  by  the  absence 
of  hyperpyrexia  and  albumin  in  the  urine.  The  second  is  excluded  by  the 
same  lack  of  temperature,  except  in  those  cases  in  which  the  pons  is  involved, 
when  the  fever  may  be  high,  but  pontile  hemorrhage  is  usually  speedily  fatal 
and  the  paralysis  severe.  Sunstroke  and  ursemia  may,  however,  exist 
simultaneously.  The  history  of  the  patient  will  exclude  epilepsy  which  is 
also  excluded  by  the  high  fever. 

Prognosis. — The  prognosis  depends  on  the  height  of  the  fever  and  the 
resistance  which  it  offers  to  treatment.  Do  what  we  will  a  large  number  of 
these  cases  die. 


1082  DISEASES  OF   THE  NERVOUS  SYSTEM 

Treatment. — The  treatment  of  sunstroke,  if  it  is  to  be  followed  by  satis- 
factory results,  must  be  bold  and  vigorous.  In  most  cases  three  things  are 
essential:  First,  that  the  temperature  must  be  reduced  until  it  is  at  a  safe 
level,  by  the  application  of  cold  water  or  ice.  This  is  best  carried  out  by 
stripping  the  patient,  laying  him  upon  a  canvas  cot,  and  then  directing  a 
stream  of  cold  water  upon  his  body  from  a  hose,  the  patient  being  actively 
and  vigorously  rubbed  at  the  same  time  by  one  or  more  attendants,  with  the 
object  of  producing  reaction,  of  overcoming  internal  congestion,  of  bringing 
the  blood  to  the  surface,  whereby  it  may  be  cooled,  and  of  increasing  the 
dissipation  of  heat,  for  frictions  increase  the  dissipation  of  heat  during  the 
application  of  cold  nearly  fifty  per  cent.  During  this  procedure  ice  should 
be  applied  to  the  head  constantly.  In  other  instances,  the  patient  may  be 
immersed  in  a  tub  of  cold  water,  and  if  necessary  pieces  of  ice  may  be  placed 
in  this  water.  If  the  tub  is  used,  active  frictions  are  as  essential  as  in  the 
case  just  stated.  Care  should  be  taken  that  the  temperature,  when  it  once 
begins  to  fall,  does  not  drop  too  rapidly,  so  that  the  patient  passes  into  hypo- 
thermia and  collapse.  If  the  patient  is  robust  and  there  is  evidence  of 
venous  engorgement,  free  venesection  should  be  practised.  Many  physicians 
of  large  experience  believe  that  venesection  is  of  almost  equal  importance 
with  the  use  of  cold.  Venesection  should  be  followed  by  hypodermo- 
clysis  or  by  the  intravenous  injection  of  normal  salt  solution.  By  these  two 
measures  engorgement  of  the  right  side  of  the  heart  is  diminished  and 
toxsemia  combated.  If  the  circulation  on  the  left  side  of  the  heart  seems 
failing,  hypodermic  injections  of  Hoffmann's  anodyne  and  strychnine  may 
be  administered.  The  use  of  alcohol  should  be  avoided.  If  the  bowels  are 
confined,  citrate  of  magnesia  should  be  given  in  full  purgative  dose  to  relieve 
them,  and  where  the  patient  is  unconscious  and  unable  to  swallow  so  large 
a  dose,  |  of  a  grain  of  elaterium  may  be  used  not  only  to  move  the  bowels, 
but  diminish  cerebral  congestion.  The  violent  headache  which  often  follows 
sunstroke  may,  in  some  instances,  yield  to  the  ordinary  coal-tar  products 
combined  with  the  use  of  bromide  of  sodium  and  cafl^eine.  Where  it  does 
not  do  so,  and  there  are  any  evidences  of  meningeal  or  cerebral  congestion, 
free  venesection  should  be  practised,  not  only  for  the  relief  of  pain,  but  in 
order  to  prevent  the  development  of  secondary  meningitis.  This  is  a  matter 
of  very  great  importance,  but  is  often  treated  as  of  little  moment. 

In  the  after-treatment  of  the  patient  it  is  essential  that  the  temperature 
should  be  carefully  watched,  as  it  nearly  always  has  a  tendency  to  rise  a 
second  time.  Such  a  tendency  should  be  combated  by  the  application  of 
cold  to  the  head,  and  by  cold  bathing  if  actual  hyperpyrexia  develops.  Per- 
fect rest  in  bed  for  a  number  of  days  after  the  sunstroke  should  be  insisted 
upon,  and  the  patient  should  be  warned  that  any  exposure  to  heat  for  several 
days  will  be  liable  to  produce  another  attack. 

HEAT  EXHAUSTION. 

Heat  exhaustion  is  a  condition  produced  by  the  same  causes  as  heatstroke, 
but  instead  of  hyperpyrexia  developing  the  temperature  becomes  subnormal, 
the  patient's  skin  may  be  bedewed  with  a  cold  sweat,  and  all  the  evidences 


PERIODICAL  PARALYSIS  1083 

of  severe  collapse  may  be  present.  This  condition  is  to  be  treated  by  immers- 
ing the  patient  in  hot  water,  and  by  the  application  about  his  body,  after  the 
removal  from  the  bath,  of  hot  bottles  or  hot  bricks  to  maintain  body  tem- 
perature. A  failing  circulation  should  be  supported  by  hypodermic  injec- 
tions of  Hoffmann's  anodyne  and  atropine.  Care  should  be  taken  that  cold- 
ness of  the  extremities  is  not  mistaken  for  true  heat  exhaustion,  for  it  some- 
times happens  that  the  extremities  are  cold  in  thermic  fever,  although  the 
temperature  of  the  body  may  be  far  above  normal.  This  point  must  be 
determined  by  taking  the  rectal  temperature.  If  the  rectal  temperature  is 
found  to  be  very  high,  the  treatment  for  heatstroke  should  be  instituted  and 
the  circulation  equalized  by  active  rubbing.  A  hot  bath  in  such  a  case  is 
not  advisable. 

FACIAL  HEMIATROPHY. 

This  is  a  condition  in  which  one  side  of  the  face  undergoes  a  slowly  pro- 
gressive wasting.  As  a  rule  it  begins  between  the  ages  of  ten  and  twenty 
years.  The  cause  is  unknown,  although  it  is  without  doubt  due  to  some 
localized  degenerative  change  in  the  nervous  system.  In  an  autopsy  upon 
a  case  of  this  character  Mindel  found  degeneration  of  the  trifacial  nerve  in 
its  efferent  fibres  and  atrophy  of  the  substantia  nigra. 

When  the  malady  first  develops,  the  skin  of  the  affected  part  begins  to  be 
thin  and  glossy  and  seems  to  be  stretched.  The  fine  hairs  fall  out  and  the 
sebaceous  glands  atrophy,  so  that  the  part  is  unduly  dry.  After  that  the 
subcutaneous  tissues  atrophy  so  that  the  natural  fulness  of  the  face  is  dimin- 
ished, and,  in  the  later  stages  of  the  affection,  even  the  underlying  bone  may 
be  atrophied  or  absorbed.  The  muscular  tissues  escape  the"  atrophy  to  a 
greater  extent,  and  do  not  undergo  degenerative  changes.  The  eye  may 
become  sunken  from  wasting  of  the  orbital  part,  and  the  pupil  may  be  in  a 
state  of  mydriasis.  Usually  the  condition  is  painless,  but  local  spasm  of  the 
muscles  of  the  part  may  occur.  No  treatment  is  of  any  avail  in  arresting 
the  progress  of  the  disease. 

PERIODICAL  PARALYSIS. 

This  term  is  applied  to  an  extraordinary  condition  of  paralysis  involving 
widely  distributed  groups  of  muscles  in  the  arms,  legs,  and  trunk,  which 
develops  rapidly  in  apparently  healthy  individuals  without  any  apparent 
exciting  cause.  Not  rarely  several  members  of  a  family  are  affected  by  the 
malady.  The  patient  may  go  to  bed  in  perfect  health  and  wake  to  find  him- 
self paralyzed,  or  the  paralysis  develops  after  a  preliminary  sense  of  weak- 
ness in  the  affected  parts.  As  a  rule,  the  legs  suffer  chiefly.'  Very  rarely  the 
muscles  of  the  neck  are  affected,  but  the  cranial  nerves  always  escape. 
The  reflexes  are  minus,  and  the  muscles  and  nerve  trunks  lose  their 
reaction  to  faradic  stimulation.  The  paralysis  lasts  from  a  few  hours  to  a 
day,  and  speedy  and  perfect  recovery  ensues,  but  relapses  frequently  take 
place 

The  condition  is  apparently  a  form  of  autointoxication,  and  is  said  to  be 
benefited  by  the  use  of  alkaline  diuretics. 


INDEX. 


ABDOMINAL  fades  in  ascites,  650 
Abducens  nerve,  paralysis  of,  1022 
Abscess  of  brain,  941 

in  bronchiectasis,  387 
in  erysipelas,  192 
hepatic,  653.    See  Hepatic  abscess 
of  liver  in  dysentery,  232 
of  lung,  423 

in  croupous  pneumonia,  148,  151, 
157 
of  mediastinum,  452,  455 
parotid,  551 
perinephritic,  737 

treatment  of,  737 
peritoneal,  643 
pulmonary,  in  septicaemia,  195 

in  typhoid  fever,  42 
in  smallpox,  82 
of  spleen,  764 
Acetone  in  urine,  test  for,  799 
Achylia-gastrica  nervosa,  604 
Acquired  idiocy,  928 
Acromegaly,   837 

dehaition  of,  837 
diagnosis  of,  839 

from  gigantism,  839 
from  leontiasis  ossea,  839 
from   myxoedema,  839 
from  osteitis  deformans,  839 
from    pulmonary    hypertrophic 
osteo-arthropathy,  839 
etiology  of,  837 
symptoms  of,  837 
Actinomycosis,   273 
cerebral,  274 
definition  of,  273 
diagnosis  of,  275 
etiology  of,  274 
morbid  anatomy  of,  274 
pathology  of,  274 
ray  fungus  in,  273 
streptothrix  actinomyces  in,  273 
symptoms  of,  274 
treatment  of,  275 
Acute  anterior  poliomyelitis,  970 
Addison's  disease,  760 

anaemia  in,  761 
asthenia  in,  761 
atrophic  changes  in,  760 
definition  of,  760 
diagnosis  of,  762 

from  diabetes  bronz6,  762 


Addison's  disease,  diagnosis  of,  from  hyper- 
trophic   cirrhosis    of   liver, 
762 
from  pregnancy,  762 
from  prolonged  use  of  arsenic, 
762 
etiology  of,  760 
history   of,   760 
languor  in,  761 
morbid  anatomy  of,  760 
pathology  of,  760 
pigmentation  of  skin  in,  761,  762 
prognosis  in,  763 
symptoms  of,  761 
treatment  of,  763 
tuberculosis  in,  760 
Adenitis,  cervical,  300 

tropical,  226 
Adenoma  of  kidney,  732 
of  pancreas,  695 
of  thyroid  gland,  751 
Adhesive  pericarditis,  chronic,  463 
Adiposis  dolorosa,  836 
Adrenal  apoplexy,  761 
iEstivo-autumnal  parasite  of  malarial  fever. 

866 
African  lethargy,  879,  See  Sleeping  sickness. 
Agraphia,  931 

Ague  cake  in  malarial  fever,  868,  875 
Ainhum,  841 

treatment  of,  841 
Albuminuria,   741 

in  acute  diffuse  nephritis,  701 
of  adolescence,  741 
cyclic,  741 

in  diabetes  mellitus,  796 
in  diphtheria,  176,  177 
.  orthostatic,  741 
in  pneumonic  plague,  223 
tests  for,  742 
in  typhoid  fever,  41 
in  ulcerative  endocarditis,  487 
in  yellow  fever,  216 
Albuminuric  neuro retinitis,  714 
papillitis,   714 

retinitis  in  chronic  parenchymatous 
nephritis,  706 
degenerative,  714 
hemorrhagic,  714 
typical,   714 
Albumosuria,  myelopathic,  746 
AlcohoHsm,  843 

(  1085  ) 


1086 


INDEX 


Alcoholism,  acute,  symptoms  of,  843 
treatment  of,  843 
chronic,  844 

morbid  anatomy  of,  845 
symptoms  of,  845 
treatment  of,  845 
dietetic,  846 
definition  of,  843 
etiology  of,  843 
Alexia,  931 

Algid  form  of  yellow  fever,  216 
Alimentary  canal,  tuberculosis  of,  334 
AUochiria  in  locomotor  ataxia,  962 
Alopecia,  syphilitic,  284 
Amaurosis,  ureemic,  722 
Ambh'opia,  in  whooping-cough,  122 
Amimia,  931 
Amoeba,  dysenterise,  229 
Amoebic  abscess  of  liver,  654 

dysentery,  227 
Amok,  1066 

Amphoric  breathing,  319 
Amyloid  degeneration  of  heart,  474 
disease  of  kidney,  718 
liver,  667 
Amyotrophic  lateral  sclerosis,  980 
Anaemia,  773 

in  Addison's  disease,  761 

brickmakers',  887 

in  chronic  lead  poisoning,  854 

definition  of,  773 

in  diphtheria,  180 

essential,  775 

in  gastric  ulcer,  582 

infantum,  785 

blood  changes  in,  785 
definition  of,  785 
treatment  of,  785 
miners',  887 
pernicious,  777 

blood  changes  in,  778 
definition  of,  777 
diagnosis  of,  779 
etiology  of,  777 
morbid  anatomy  of,  778 
prognosis  in,  779 
symptoms  of,  778 
treatment  of,  779 
Porto  Rican,  887 
primary,  775 
secondarj^  773 
causes  of,  773 
diagnosis  of,  774 
symptoms  of,  774 
treatment  of,  774 
in  septicaemia,  194 
splenic,  765 

blood  in,  766 

clinical  characteristics  of,  766 
definition  of,  765 
diagnosis  of,  766 
etiology  of,  765 
morbid  anatomy  of,  765 
pathology  of,  765 
prognosis  in,  766 


Anaemia,  splenic,  spleen  in,  765 
symptoms  of,  765 
treatment  of,  766 
in  sprue,  244 
in  syphilis,  284 
in  typhoid  fever,  34 
tunnel,  888 
in  uncinariasis,  890 
Anaesthesia  in  hysteria,  1049 
Anaesthetic  leprosy,  349 
Aneurysm,  534 

of  abdominal  aorta,  542 

cardiac,  479 

definition  of,  534 

"dissecting,"  534 

embolic,  534 

etiology  of,  534 

false,  534 

frequency  of,  535 

fusiform,  534 

haematemesis  in,  605 

of  hepatic  artery,  543 

morbid  anatomy  of,  534 

mycotic,   534 

pathology  of,  534 

of  renal  artery,  543 

sacculated,  534 

of  splenic  artery,  543 

of  superior  mesenteric  artery,  543 

of  thoracic  aorta,  536 

complications  of,  538 
diagnosis  of,  539 
prognosis  in,  540 
sequelae  of,  537,  538 
symptoms  of,  536 
treatment  of,  540 
operative,  541 
TufneU,  540 
varicose,  534 
Aneurysmal  varix,  534 
Angina  Ludovici,  552 
pectoris,  523 

definition  of,  523 
diagnosis  of,  525 
etiology  of,  523 
pathology  of,  523 
prognosis  in,  525 
symptoms  of,  524 
treatment  of,  525 
Angiomata,  cavernous,  of  liver,  668 

of  kidney,  732 
Angioneurotic  oedema,  1075 
definition  of,  1075 
diagnosis  of,  1076 
prognosis  of,  1076 
treatment  of,  1076 
Angiosclerosis,  532 

Animal  parasites,  diseases  due  to,  863 
Ankle  clonus  in  lateral  sclerosis,  979 
Ankylosis  in  gonorrhceal  arthritis,  187 
Ankylostomiasis,  887 
Ankylostomum  duodenale,  887 
Annular  stricture  of  oesophagus,  561 
Anorexia  nervosa,  604 
Anthracosis,  41 X 


INDEX 


1087 


Anthrax,  257 

bacillus  of,  257 
definition  of,  257 
diagnosis  of,  260 
etiology  of,  257 
frequency  of,  258 
lesion  of,  259 
morbid  anatomy  of,  258 
oedema,  malignant,  259 
pathology  of,  258 
prevention  of,  258 
prognosis  in,  260 
symptoms  of,  259 
treatment  of,  261 
Antirabic  serum,  265 

Antisepsis,  intestinal,  in  tj^phoid  fever,  56 
Anuria,  737 

treatment  of,  737 
Aorta,  abdominal,  aneurysm  of,  542 

thoracic,  aneurysm  of,  536 
Aortic  regurgitation,  508 

Corrigan  pulse  in,  510 
definition  of,  508 
diagnosis  of,  512 
Duroziez  sign  in,  512 
etiology  of,  508 
murmur  in,  511 
ox-heart  in,  509 
pathology  of,  508 
physical  signs  of,  509,  511 
pistol-shot  sound  in,  512 
prognosis  in,  512 
Quincke's  pulse  in,  510 
symptoms  of,  509 
trip-hammer  pulse  in,  511 
water-hammer  pulse  in,  511 
stenosis,  504 

definition  of,  504 
diagnosis  of,  507 
etiology  of,  505 
physical  signs  of,  506 
prognosis  in,  507 
symptoms  of,  506 
Aphasia,  930 

in  apoplexy,  920 
in  brain  tumor,  934 
conduction,  931 
definition  of,  930 
symptoms  of,  930 

transitory,  in  croupous  pneumonia,  160 
Aphemia,  931 
Aphonia,  hysterical,  1050 
in  smallpox,  83 
in  tuberculous  laryngitis,  375 
Aphthae  tropicse,  242 
Aphthous  stomatitis,  546 
Apoplectiform  attack,  913 
bulbar  paralysis,   913 
type  of  yellow  fever,  216 
Apoplexy,  913 
adrenal,  761 
aphasia  in,  920 
astereognosis  in,  920 
athetosis  in,  921 
bed-sores  in,  920 


Apoplexy,  contractures  in,  921 
definition  of,  913 
in  diabetes  mellitus,  797 
diagnosis  of,  922 

from  acute  alcoholism,  922 
from  coma  of  diabetes,  922 

of  ursemia,  922 
from  embolism  of  cerebral  vessels. 

922 
from  epilepsy,  922 
from  general  paralysis  of  insane, 

923 
from  opium  poisoning,  922 
from  sunstroke,  923 
from  syncope,  922 
from  thrombosis  of  cerebral  vessels, 
922 
etiology  of,  913 
frequency  of,  913 
hemiansesthesia  in,  920 
hemianopsia  in,   920 
hemiplegia  in,  919 
Hutchinson's  pupil  in,  921 
ingravescent,  922 
muscular  atrophy  in,  921 
ocular  symptoms  of,  919 
paralysis  in,  919,  920 
pathology  of,  914 
prognosis  in,  923 
pulse  in,  918 
reflexes  in,  919 
sequelae  of,  921 
stertorous  breathing  in,  918 
symptoms  of,  917 

premonitory,  917 
treatment  of,  921 
unconsciousness  in,  919 
ursemic,  923 
Appendicitis,  615 
abscess  in,  619 
catarrhal,  617 
definition  of,  615 
diagnosis  of,  621 

from  hepatic  colic,  621 
from  intestinal  obstruction,  621 
from,  ovarian  inflammation,  621 
from  renal  colic,  621 
from  tuberculosis,  621 
from  typhoid  fever,  621 
etiology  of,  615 
gangrenous,  617 
McBurney's  point,  620 
morbid  anatomy  of,  617 
muscular  rigidity  in,  620 
obliterative,  617 
pathology  of,  617 
perforative,  617 
prognosis  in,  622 
symptoms  of,  619 
treatment  of,  622 
in  typhoid  fever,  30,  39 
ulcerative,  617 
vomiting  in,  620 
Apraxia,  931 


1088 


INDEX 


Aran-Duchenne    type    of    chronic   anterior 

poliomyelitis,  975 
Argyll-Robertson  pupil   in  dementia   par- 
alytica, 952 
in  disseminated  sclerosis,  956 
in  locomotor  ataxia,  962 
Arhythmia,  522 
Arsenical  poisoning,  850 

chronic,  etiology  of,  850 
prognosis  in,  851 
pseudotabes  in,  851 
symptoms  of,  851 
treatment  of,  851 
Arteries,  diseases  of,  528 
Arteriocapillary  fibrosis,  529 
Arteriosclerosis,  529 
definition  of,  529 
etiology  of,  529 
morbid  anatomy  of,  530 
pathology  of,  530 
symptoms  of,  533 
treatment  of,  533 
Arteritis,  syphilitic,  281 
Artery  of  cerebral  hemorrhage,  915 
Arthritis  in  cerebrospinal  fever,  137 
in  croupous  pneumonia,  161 
deformans,  818 

definition  of,  818 
diagnosis  of,  822 
etiology  of,  819 
Hay  garth's  nodosities  in,  820 
Heberden's  nodes  in,  821 
morbid  anatomy  of,  820 
prognosis  in,  822 
symptoms  of,  820 
treatment  of,  822 
gonorrhoeal,  186 

ankj'losis  in,  187 
chronic,  186 
endocarditis  in,  187 
symptoms  of,  186 
treatment  of,  188 
infections,  in  cholera,  209 
in  mumps,  118 

in  rheumatic  fever,  acute,  199 
rheumatoid,  818 

in  bronchiectasis,  386 
septic,  in  scarlet  fever,  103 
in  smallpox,  83 
in  typhoid  fever,  44 
Articular    rheumatism,    acute,    196.       See 

Rheumatic  fever,  acute. 
Ascariasis,  884 

symptoms  of,  885 
treatment  of,  885 
Ascaris  lumbricoides,  884 
Ascending  myelitis,  983 

paralysis,  acute,  1000 
Ascites,  650 

definition  of,  650 
diagnosis  of,  652 

from  hepatic  enlargement,  652 
from  ovarian  cyst,  652 
from  splenic  enlargement,  652 
dyspnoea  in,  651 


Ascites,  etiology  of,  650 

paracentesis  abdominis  in,  653 
physical  signs  of,  650 
symptoms  of,  650 
treatment  of,  653 
Asiatic  cholera,  204 
Aspiration  pneumonia,  398 
Astasia-abasia,  1067 
definition  of,  1067 
symptoms  of,  1067 
Astereognosis  in  apoplexy,  920 
Asthenia  in  Addison's  disease,  761 
Asthma,  bronchial,  390 

Charcot-Lej^den  cry'stals  in,  392 
Curschmann's  spirals  in,  392 
definition  of,  390 
diagnosis  of,  393 

from  pulmonary  cfidema,  393 
etiology  of,  390 
Harrison's  groove  in,  392 
morbid  anatomy  of,  391 
pathology  of,  391 
pigeon-breast  in,  392 
prognosis  of,  394 
sputum  in,  392 
symptoms  of,  392 
treatment  of,  394 

bronchitis  tent  in,  396 
cardiac,  391 
renal,  391 
Asymmetrical  stricture  of  oesophagus,  561 
Ataxia,  family,  967 
Friedreich's,  967 
hereditary,  967 
locomotor,  958 

Marie's  cerebellar  hereditary,  970 
Atheroma,  531 
Athetosis  in  apoplexy,  921 
Athyrea,  756 
Atonic  dilatation  of  oesophagus,  562 

gastrectasis,  578 
Atriplicism,  860 

treatment  of,  860 
Atrophic  cirrhosis  of  liver,  659 
emphysema,  413 
enteritis  of  tropics,  242 
nasal  catarrh,  366 
paralysis,  acute,  970 
rhinitis,  365 

spinal  paralysis,  chronic,  974 
Atroph}^  of  heart,  474 
of  liver,  red,  666 

yellow,  acute,  670 
muscular,  progressive,  974 
of  peroneal  type,  1037 
in  apoplexy,  921 
optic,   1014 
Auctioneers'  sore  throat,  555 
Auditory  nerve,  disease  of,  1028 
deafness  in,     1028 
tinnitus  in,   1028 
vertigo  in,  1029 
Aura  in  epilepsy,  1054,  1056 
Autumnal  catarrh,  367 
fever,  17 


INDEX 


1089 


BABINSKI  reflex  in  amyotrophic  lateral 
sclerosis,  981 
in  lateral  sclerosis,  979 
Bacillary  dysentery,  227 
Bacillus  aerogenes  capsulatus  in  pneumo- 
pericardium, 467 
of  amoebic  dysentery,  227,  231 
of  anthrax,  257, 
of  Asiatic  cholera,  204,  207 
coli  communis  in  typhoid,  18 
of  diphtheria,  172 
dysenterise,  18 
of  Eberth,  17 
leprae,  345 

mallei  in  glanders,  272 
para-colon,  18 
pertussis  Eppendorf,  119 
pestis,  219,  220 

of  Pfeiffer  in  influenza,  125,  126 
of  tetanus,  267 

of  tuberculosis,  method  of  staining,  322 
typhosus,  17 
of  typhoid  fever,  17 
Banti's  disease,  767 
Barlow's  disease,  831 

Barrel-shaped  chest  in  chronic  hypertrophic 
tonsillitis,  559 
in  emphysema,  413 
Basedow's  disease,  751 
Basilar  meningitis,  301 
Bath,  Brand,  in  typhoid  fever,  53 
Baths,  Nauheim,  in  myocarditis,  478 
Bed-sores  in  typhoid  fever,  33 
Beef-worm,  901 
Benign  goitre,  749 
Beriberi,  249,  1007 

acute  pernicious,  255 
blood  in,  256 
cardiac  changes  in,  255 
definition  of,  249 
diagnosis  of,  256 
distribution  of,  250 
etiology  of,  250,  251 
forms  of,  254 
frequency  of,  252 
incubation  of,  252 
mild,  255 

morbid  anatomy  of,  253 
pathology  of,  253 
prognosis  in,  256 
prophylaxis  of,  253 
rudimentary,  255 
symptoms  of,  254 
treatment  of,  256 
urine  in,  256 
Bile-ducts,  catarrh  of,  acute,  671 
chronic,  673 
treatment  of,  673 
constriction  of,  674 
inflammations  of,  suppurative,  673 
diagnosis  of,  674 
symptoms  of,  674 
treatment  of,  674 
occlusion  of,  674 
congenital,  674 

69 


Bilharzia  disease,  904,  905 
diagnosis  of,  907 
distribution  of,  905 
etiology  of,  905 
haematuria  in,  906 
pathology  of,  906 
prognosis  in,  907 
schistosoma  haematobium  in,  905 
symptoms  of,  906 
treatment  of,  907 
Biliary  calculi,  677 
cohc,  679 

passages, 'malignant  growths  of,  683 
tract,  diseases  of,  671 
Bilious  fever,  874 

remittent  fever,  874 
Bilocular  heart,  527 

stomach,  598 
Birth  palsy,  1007 
"Black"  measles,  112 
smallpox,  81 

vomit  in  yellow  fever,  216 
-water  fever,  875 
Bladder,  tuberculosis  of,  340 
Blepharofacial  spasm,  1027 
Blepharospasm,  1027 
Blindness,  word-,  931 
Blood  in  beriberi,  256 

in  cerebrospinal  fever,  138 
changes  in  anaemia  infantum,  785 

in  pneumonic  plague,  223 
in  chlorosis,  775 
in  diabetes  mellitus,  794 
in  diphtheria,  176 
diseases  of,  773 
in  Hodgkin's  disease,  768 
in  malarial  fever,  changes  in,  867 
in  pernicious  anaemia,  778 
in  septicaemia,  194 
-spitting  in  mitral  regurgitation,  497 
in  splenic  anaemia,  766 
in  splenomedullary  leukaemia,  781 
in  stools,  tests  for,  584 
in  typhoid  fever,  25,  33 
in  urine,  738 
in  yellow  fever,  214 
Blue  line  on  gums  in  chronic  lead  poisoning, 

853 
Boas'  reagent,  593 

test  meal  in  gastric  cancer,  593 
Boils  in  typhoid  fever,  34 
Bone-marrow  in  malarial  fever,  868 
Bones,  syphilis  of,  286 
Bossy  frontals  in  rickets,  827 
Bothriocephalus  cordatus,  903 
cristatus,  903 
latus,  903 
Bouquet  fever,  131 
Bovine  tuberculosis,  291 
Bowel,  hemorrhage  from,  in  typhoid  fever, 
36 
treatment  of,  57 
obstruction  of,  623 

by  congenital  malformations,  624 
by  fecal  impaction,  624 


1090 


INDEX 


Bowel,  obstruction  of,  by  foreign   bodies, 
624,  628 
by  internal  strangulation,  624,  626 
by  intussusception,  624 
by  stricture,  624 
by  tumors,  624 
by  volvulus,  627 
perforation  of,   in  typhoid  fever,   30, 
37 
diagnosis  of,  38 
treatment  of,  58 
Bradycardia,  522 
Brain,  abscess  of,  941 

in  bronchiectasis,  387 
definition  of,  941 
diagnosis  of,  943 
etiology  of,  941 
morbid  anatomy  of,  942 
pathology  of,  942 
prognosis  in,  944 
symptoms  of,  942 
treatment  of,  944 
cancer  of,  932 
diseases  of,  913 
echinococcus  cyst  of,  932 
fibroma  of,  932 
glioma  of,  932 
gumma  of,  932 
hemorrhage  into,  913 
neuroma  of,  932 
osteoma  of,  932 
sarcoma  of,  932 
softening  of,  in  croupous  pneumonia, 

160 
syphilis  of,  285 
tabes  of,  952 
tubercle  of,  932 
tuberculosis  of,  343 
tumors  of,  932 

aphasia  in,  934 
diagnosis  of,  939 

from  localized  meningitis,  939 
etiology  of,  932 
frequency  of,  932 
headache  in,  933 
morbid  anatomy  of,  932 
optic  neuritis  in,  934 
paralysis  in,  934 

bilateral,  934,  935 
crossed,  934 
pathology  of,  932 
prognosis  in,  940 
symptoms  of,  933 
table  of  cerebral  locahzing  symp- 
toms in,  938 
treatment  of,  940 
surgical,  941 
vascular,  932 
vertigo  in,  933 
vomiting  in,  933 
Weber's  syndrome  in,  934 
Brand  bath  in  typhoid  fever,  53 
Breakbone  fever,  131 
Breathing,  stertorous,  in  apoplexy,  918 
Brickmakers'  anaemia,  887 


Bright's  disease,  acute,  700 

chronic,  703 
Bromatotoxismus,  855 
Bronchi,  diseases  of,  377 
Bronchial  asthma,  390 
Bronchiectasis,  383 

brain  abscess  in,  387 
complications  of,  386 
cough  in,  385 

in  croupous  pneumonia,  158 
definition  of,  383 
diagnosis  of,  386 

from  pulmonary  tuberculosis,  386 
etiology  of,  383 
forms  of,  383 
haemoptysis  in,  386 
morbid  anatomy  of,  383 
pathology  of,  383 
prognosis  in,  387 
pulmonary  gangrene  in,  387 

osteoarthropathy  in,  387 
rheumatoid  arthritis  in    386 
sputum  in,  385 
sj^mptoms  of,  385 
treatment  of,  387 
Bronchitis  actinomycotica,  chronic,  274 
capillary,  402 
catarrhal,  acute,  377 

definition  of,  377 
distribution  of,  377 
etiology  of,  378 
morbid  anatomy  of,  380 
pathology  of,  380 
prevention  of,  380 
sjanptoms  of,  380 
treatment  of,  381 
chronic,  382 

definition  of,  382 
treatment  of,  382 
in  croupous  pneumonia,  149 
fibrinous,  388 

definition  of,  388 
diagnosis  of,  390 

from  diphtheria,  390 
etiology  of,  388 
pathology  of,  388 
prognosis  of,  390 
symptoms  of,  389 
treatment  of,  390 
in  influenza,  126 
in  measles,  110,  111 
in  smallpox,  83 
tent  in  bronchial  asthma,  396 
in  whooping-cough,  123 
Bronchocele,  749 
Bronchopneumonia,  397 
complications  of,  404 
definition  of,  397 
diagnosis  of,  404 

from  acute  bronchitis,  404 
from  croupous  pneumonia,  404 
from  malarial  infection ,  405 
from  tulierculous  infection,  405 
in  diphtheria,  176,  178,  179 
distribution  of,  397 


INDEX 


1091 


Bronchopneumonia,  duration  of,  403 

etiology  of,  397 

frequency  of,  398 

in  measles,  110,  112 

morbid  anatomy  of,  399 

pathology  of,  399 

prevention  of,  398 

prognosis  of,  405 

in  scarlet  fever,  103 

in  smallpox,  83 

symptoms  of,  400 

treatment  of,  406 

types  of,  398 

in  whooping-cough,  122 
Brown  induration  of  heart,  474 
Bubo,  climatic,  226 

parotid,  551 

tropical,  226 
Buboes  in  bubonic  plague,  222 
Bubonic  plague,  219 
Buccal  psoriasis,  550 
Bucket  fever,  131 
Bulbar  paralysis,  977 

apoplectiform,  913 
Bulimia,  604 


CACHEXIA,  miners',  887 
in  pellagra,  858 
Caecum,  tuberculosis  of,  336 
Caisson  disease,  1001 

treatment  of,  1002 
palliative,  1002 
prophylactic,  1002 
Calcareous  degeneration  of  heart,  474 
Calculi,  biliary,  677 
Calculus,  coral,  of  kidney,  733 
"hemp-seed,"  of  kidney,  734 
mulberry,  of  kidney,  734 
pancreatic,  693 
renal,  733 
Cancer  of  brain,  932 
of  kidney,  732 
of  oesophagus,  563 
of  peritoneum,  649 
of  stomach,  588 
Cancrum  oris,  548 
Canker,  548 

CapUlary  bronchitis,  402 
Capsular  cirrhosis  of  liver,  665 
Carcinoma  of  biliary  ducts,  683 
of  gall-bladder,  683 
of  liver,  668 
in  lung,  428 
of  mediastinum,  452 
of  thyroid  gland,  751 
Carcinosarcoma  of  thyroid  gland,  751 
Cardiac  aneurysm,  479.     See  Heart,  aneu- 
rysm of. 
asthma,  391 
changes  in  beriberi,  255 

in  croupous  pneumonia,  149 
in  yellow  fever,  214 
complications  in  rheumatic  fever,  200, 
201 


Cardiac  defects,  congenital,  527 

dilatation,  468,  471,     See  Heart,  dila- 
tation of. 
hypertrophy,    468,    469.      See   Heart, 

hypertrophy  of. 
palpitation,  521 
valvular  anomalies,   528 
Cardiospasm,  601 

treatment  of,  602 
Caseative  nephritis,  725 
Cataract  in  diabetes  mellitus,  797 
Catarrh,  autumnal,  367 

of  bile-ducts,  acute,  671 

chronic,  673 
gastric,    acute,  564.     See   Gastric    ca- 
tarrh, 
nasal,  atrophic,  366 

definition  of,  366 
etiology  of,  366 
pathology  of,  366 
prognosis  of,  366 
symptoms  of,  366 
treatment  of,  366 
chronic,  365 

definition  of,  365 
etiology  of,  365 
pathology  of,  365 
symptoms  of,  365 
treatment  of,  366 
suffocative,  acute,  400,  402 
Catarrhal  appendicitis,  617 
bronchitis,  acute,  377 

chronic,  382 
cholecystitis,  675 
dysentery,  acute,  227 
enteritis,  609 
laryngitis,  acute,  369 

chronic,  371 
pneumonia,  397 
pyelonephritis,  726 
stomatitis,  546 
Cerebral  actinomycosis,  274 
embolism,  913 
hemorrhage,  913 

artery  of,  915 
meningitis,  946 
paralysis,  infantile,  925 
syphilis,  285,  286 
thrombosis,  913 
Cerebritis,  acute,  944 

definition  of,  944 
diagnosis  of,  945 
etiology  of,  944 
morbid  anatomy  of,  944 
pathology  of,  944 
prognosis  of,  945 
symptoms  of,  945 
treatment  of,  945 
Cerebrospinal  fever,  134 
arthritis  in,  137 
blood  in,  138 
complications  of,  139 
croupous  pneumonia  in,  139 
definition  of,  134 
delirium  in,  137 


1092 


INDEX 


Cerebrospinal  fever,  diagnosis  of,  139 

from  croupous  pneumonia,  140 
diplococcus         intracellularis 

meningitides  in,   134 
from  influenza,  140 
lumbar  puncture  as  aid  to,  140 
from  tuberculous  meningitis, 

140 
from  typhoid  fever,  139 
of  Weichselbaum  in,  134,  139 
eruption  in,  137 
etiology  of,  135 
fever  in,  138 
forms  of,  138 
chronic,  138 
intermittent,  138 
malignant,   138 
moderate,  137 
typhoid,  138 
frequency  of,  136 
headache  in,  137 
herpes  in,  137 
history  of,  135 
incubation  of,  137 
Kemig's  sign  in,  138 
morbid  anatomy  of,  136 
pathology  of,  136 
prevention  of,  136 
prognosis  of,  142 
respiration  in,  137 

Cheyne-Stokes,  137 
sequelae  of,  139 
symptoms  of,  137 
treatment  of,  142 
meningitis,   134 
Cervical  adenitis,  300 
Cervicobrachial  neuritis,  1006 
Cestodes,  900 
Ceylon  sour  mouth,  242 
Chalicosis,  411 
Chancre,  280,  283,  284 

leprous,  348 
Charcot  joint  in  locomotor  ataxia,  963 
Charcot-Leyden  crystals,  392 

in  distomatosis  of  lung,  908 
in  uncinariasis,  890 
Charcot-Marie-Tooth   form   of   progressive 

muscular  atrophy,  1037 
Cheyne-Stokes  respiration  in  cerebrospinal 

fever,  137 
Chicken-breast  in  rickets,  828 
Chickenpox,  90.     *See  Varicella. 
Chickpea  disease,  859 
Chigger,  911 

treatment  of,  911 
Chloroma,  784 
Chlorosis,  775 
blood  in,  775 
complications  of,  776 
definition  of,  775 
diagnosis  of  776 

from  pernicious  anaemia,  776 
Egyptian,  887 
etiology  of,  775 
florida,  776 


Chlorosis,  pathology  of,  775 
prognosis  in,  777 
symptoms  of,  776 
tarda,  775 
treatment  of,  777 
tropical,  888 
Cholangitis,  acute,  671 

diagnosis  of,  672 
acute,  etiology  of,  671 
prognosis  in,  672 
symptoms  of,  671 
treatment  of,  672 
chronic,  673 

treatment  of,  673 
suppurative,   673 

diagnosis  of,  674 

from  catarrhal  cholangitis,  674 
from  hepatic  abscess,  674 
symptoms  of,  674 
treatment  of,  674 
Cholecystitis,  acute,  675 
definition  of,  675 
diagnosis  of,  676 

from  acute  appendicitis,  676 

pancreatitis,  676 
from  gastric  ulcer,  676 
from  hepatic  colic,  676 
from    intestinal    obstruction, 
676 
etiology  of,  675 
morbid  anatomy  of,  675 
symptoms  of,  676 
treatment  of,  677 
catarrhal,  671 
in  typhoid  fever,  40 
Cholelithiasis,  677 
colic  in,  679 
complications  of,  680 
Courvoisier's  law  in  681 
definition  of,  677 
diagnosis  of,  680 

from  appendicitis,  680 

from  gastralgia,  680 

from  gastric  crises  of  ataxia,  680 

ulcer,  681 
from  pleurisy,  681 
from  renal  stone,  681 
enlargement  of  gaU-bladder  in,  680 
etiology  of,  677 
jaundice  in,  678 
pathology  of,  677 
perforation  in,  680 
sequelae  in,  680 
symptoms  of,  678 
treatment  of,  681 
in  typhoid  fever,  41 
urine  in,  679 
Cholera,  204 

arthritis,  infectious,  in,  209 
Asiatic,  204 
bacillus  of,  204,  207 
collapse  in,  208 
complications  of,  209 
definition  of,  204 
diagnosis  of,  209 


INDEX 


1093 


Cholera,  diarrhoea  in,  207 
distribution  of,  204 
etiology  of,  204 
facial  expression  in,  208 
gangrene  in,  208,  209 
history  of,  204 
incubation  in,  207 
infantum,  613 

definition  of,  613 

etiology  of,  613 

morbid  anatomy  of,  613 

pathology  of,  613 

prognosis  in,  614 

symptoms  of,  613 

treatment  of,  614 
liver  in,  206 

morbid  anatomy  of,  206 
nephritis  in,  209 
oedema  of  lungs  in,  209 
parotitis  in,  209 
pathology  of,  206 
prevention  of,  205 

inoculations  for,  205 
prognosis  in,  209 
purging  in,  208 
sequela;  of,  209 
sicca,  209 
stools  in,  208 
symptoms  of,  207 
treatment  of,  210 

irrigation  of  bowel  in,  211 
variations  in  symptoms  of,  208 
visceral  changes  in,  206 
vomiting  in,  208 
Cholerine,  208 
Chondroma  in  lung,  428 
Chorea,  acute,  1043 

in  acute  rheumatic  fever,  201 
electrical,  1047 
gravidarum,   1043 
hereditary,  1046 

prognosis  in,  1047 

symptoms  of,  1046 

treatment  of,  1047 
Huntington's,   1047 
insaniens,   1045 
minor,  1043 

complications  of,  1045 

definition  of,  1043 

diagnosis  of,  1045 

from  hysteria,  1045 
from  infantile  cerebral  palsy 
1045 

duration  of,  1045 

endocarditis  in,  1045 

etiology  of,  1043 

exciting  causes  of,  1043 

frequency  of,  1044 

hysteria  in,  1045 

mental  state  in,  1045 

morbid  anatomy  of,  1044 

movements  in,  1044 

pathology  of,  1044 

prognosis  in,  1045 

symptoms  of,  1044 


Chorea  minor,  treatment  of,  1046 
paralytic,  1045 
Sydenham's,   1043 
Chvostek's  sign  in  gastric  tetany,  576 

of  tetany,  1065 
Chyluria,  744 

"  Cinder-sifting"  kidney,  696 
Circulatory  disturbances  in  kidney,  698 

system,  diseases  of,  457 
Circumscribed  peritonitis,  643 
Cirrhosis  of  kidney,  710 

of  liver,  658 
Claw-hand  in  chronic  anterior  poliomyeUtis, 

975 
Clergymen's  sore  throat,  555 
Climatic  bubo,  226 

definition  of,  226 
symptoms  of,  226 
treatment  of,  227 
Coffee-ground  vomit    605 
Coin  sound  in  hydropneumothorax,  451 
Cold  bathing  in  typhoid  fever,  52 
Colic,  biliary,  679 

in  chronic  lead  poisoning,  854 
painters',  854 
renal,  735 
Colica  pictonum,  854 
Cohtis,  636 
acute,  636 

symptoms  of,  637 
treatment  of,  637 
croupous,  638 

treatment  of,  638 
follicular,  638 
mucous,  637 

definition  of,  637 
treatment  of,  637 

counterirritation  in,  638 
diet  m,  638 
rest  in,  637 
nodular,  638 
pseudomembranous,  639 
Collapse  in  cholera,  208 
"  Collar  of  brawn"  in  scarlet  fever,  99 
Colloid  goitre,  750 
Colon,  dilatation  of,  639 

by  foreign  bodies,  640 
by  gas,  639 

treatment  of,  640 
idiopathic,  640 
by  obstruction,  640 
Coma  in  chronic  parenchymatous  nephritis, 
706 
diabetic,  796,  797 
in  uraemia,  721 
vigil  in  typhoid  fever,  43 
Comma  bacillus  of  Asiatic  cholera,  204,  207 
Compensatory  emphysema,  413 
Compression  of  spinal  cord,  993 
Conduction  aphasia,  931 
Condylomata,  syphilitic,  284 
Confluent  smallpox,  81 
Congenital  cardiac  defects,  527 
hydronephrosis,  728 
malformations  of  bowel,  624 


1094 


INDEX 


Congenital  myxoedema,  758 

stenosis  of  pylorus,  595,  597 
wryneck, 1033 
Congestion  of  lungs,  425 
definition  of,  425 
diagnosis  of,  427 

from     catarrhal    pneumonia, 

427 
from     croupous     pneumonia, 

427 
from  pleural  effusion,  428 
dyspnoea  of,  427 
etiology  of,  425 
hypostatic,  426 
pathology  of,  425 
prognosis  of,  428 
symptoms  of,  427 
treatment  of,  428 
Conjunctiva,  diphtheria  of,  179 
Conjunctival    hemorrhages    in   whooping- 
cough,  122 
Conjunctivitis  in  measles,  113 
Constitutio  lymphatica,  770 
Contracted  kidney,  710 
Contractures  in  apoplexy,  921 
Convulsions  in  acute  anterior  poliomyelitis, 
972 
in  chronic  lead  poisoning,  853 
in  croupous  pneumonia,  155 
in  epilepsy,  1054 
in  hysteria,  1048 

in  infantile  cerebral  paralj'sis,  927 
in  mumps,  118 
in  typhoid  fever,  44 
in  uraemia,  721 
in  yellow  fever,  215 
Cor  bovinum  in  aortic  regurgitation,  509 
Corrigan  pulse  in  aortic  regurgitation,  510 
Coryza  in  measles,  110 
acute,  363 

definition  of,  363 
diagnosis  of,  364 
diplococcus  coryzse  in,  363 
etiology  of,  363 
morbid  anatomy  of,  363 
pathology  of,  363 
symptoms  of,  363 
transmission  of,  363 
treatment  of,  364 
Coup  de  soleil,  1080 
Courvoisier's  law,  681 
Cracked-pot  sound,  319 
Cramp,  flute-players',  1072 
pianists',  1072 
telegraphers',  1072 
violinists',  1072 
writers',  1072 
Cranial  nerves,  diseases  of,  1012 
Craniotabes,  827 
Crawcraw,  894 
Cretinism,  758 

definition  of,  758 
diagnosis  of,  759 
prognosis  in,  759 
symptoms  of,  758 


Cretinism,  treatment  of,  759 

thyroid  gland  in,  759 
Crisis  in  croupous  pneumonia,  155 
Croup,  false,  374 

spasmodic,  374 
Croupous  colitis,  638 

pharyngitis,  555 

pneumonia,      143.       See   Pneumonia, 
croupous. 
Curschmann's  spirals,  392 
Cyclasterion  scarlatinalis,  97 
Cyanosis  in  croupous  pneumonia,  151 

in  mitral  regurgitation,  497 

in  oedematous  laryngitis,  373 
Cyclic  albuminuria,  741 

vomiting,  607 
Cylindrical  stricture  of  oesophagus,  561 
Cynanche  gangrsenosa,  552 
Cyst,  hydatid,  of  spleen,  764 
Cystadenoma  of  pancreas,  694 
Cystic  adenoma  of  peritoneum,  649 

disease  of  kidney,  730 
of  liver,  668 

epithelioma  of  pancreas,  694 

goitre,  749 
Cysticercusmediocanellata,  901 
Cystitis  in  typhoid  fever,  42 
Cysts  of  mediastinum,  453 

of  pancreas,  694 
Cytoryctes  vaccinae  as  a  cause  of  smallpox, 

Cytoscopy  in  pleurisy  with  effusion,  440 


DACTYLITIS,  syphilitic,  286 
Dandy  fever,   131 
Deafness,  1028 
word-,  931 
Delirium  in  acute  rheumatic  fever,  201 
in  cerebrospinal  fever,  137 
cordis  in  diphtheria,  179 
in  croupous  pneumonia,  152,  154,  156 
ferox  in  typhus  fever,  64 
in  relapsing  fever,  70 
in  smallpox,  79 
in  typhoid  fever,  28,  43 
Dementia  paralytica,  950 

Argyll-Robertson  pupil  in,  952 
definition  of,  950 
diagnosis  of,  953 
etiology  of,  951 
morbid  anatomy  of,  951 
pathology  of,  951 
prognosis  in,  954 
symptoms  of,  952 
treatment  of,  954 
Dengue,  131 

chill  in,  132 
crisis  in,  132 
definition  of,  131 
desquamation  in,  133 
diagnosis  of,  133 

from  influenza,  133 
from  rotheln,  133 
from  scarlet  fever,  133 


INDEX 


1095 


Dengue,  diagnosis  of,  from  syphilitic   rose- 
ola, 133 
distribution  of,  131 
eruption  in,  133 
erythema  in,  132 
history  of,  131 
pathology  of,  131 
prognosis  in,  133 
relapse  in,  133 
symptoms  of,  132 
treatment  of,  133 
Dentition  in  rickets,  828 
Dermatobia  cyaniventris,  912 
Dermoid  cyst  in  lung,  428 

of  mediastinum,  453 
Descending  myelitis,  983 
Desquamation  in  dengue,  133 
in  scarlet  fever,  104,  108 
Desquamative  nephritis,  chronic,    704 
Dhobie  itch,  909 

definition  of,  909 
etiology  of,  909 
treatment  of,  910 
types  of,  909 
Diabetes  insipidus,  806 

definition  of,  806 
diagnosis  of,  807 
etiology  of,  806 
morbid  anatomy  of,  806 
prognosis  in,  807 
symptoms  of,  806 
treatment  of,  807 
urine  in,  807 
mellitus,  789 

albuminuria  in,  796 
blood  changes  in,  794 
carbuncles  in,  795 
coma  in,  796,  797 
complications  of,  795 
dyspeptic,  796 
nervous,  796 
ocular,  797 
pulmonary,  796 
definition  of,  789 
diagnosis  of,  797 

blood  tests  in,  798 
urinary  tests  in,  799 
distribution  of,  789 
dyspeptic  symptoms  in,  796 
emaciation  in,  795 
etiology  of,  790 
frequency  of,  789 
gangrene  in,  795 
glycosuria  in,  794,  795 
kidney  changes  in,  793 
Kussmaul's  coma  in,  797 
morbid  anatomy  of,  793 
nervous  system  in,  changes  in,  793 
pathology  of,  790 
prognosis  in,  800 
sequelae  of,  795 
symptoms  of,  794 
treatment  of,  801 

dietetic,  801,  802,  803 
medicinal,  804 


Diabetes  meUitus,  urine  in,  795 

"  phosphatic,"  745 
Diarrhoea,  608 
alba,  242 
in  cholera,  207 
hill,  240 

definition  of,  240 
etiology  of,  240 
pathology  of,  241 
symptoms  of,  241 
treatment  of,  241 
in  influenza,  127 
in  measles,  112 
serous,  608 

causes  of,  608 
treatment  of,  608 
Simla,  241 
in  sprue,  243 
in  typhoid  fever,  27,  30 
Diazo  reaction  of  urine  in  typhoid  fever,  50 
Dibothriocephalus  latus,  901,  903 
Dietl's  crises  in  movable  kidney,  697 
Digestive  tract,  diseases  of,  545 
Dilatation  of  colon,  639 
of  oesophagus,  561 
of  stomach,  572 
acute,  578 
Dilatation  of  the  stomach,  paralytic,  578 
Diphtheria,   171 

albuminuria  in,  176,  177 
anaemia  in,  180 
antitoxin,  183,  184 

administration  of,  184 
disagreeable  effects  of,  185 
results  of  administration,  185 
bacillus  of,  172 
blood  in,  176 

bronchopneumonia  in,  176,  178,  179 
complications  of,  179 
of  conjunctiva,  179 
definition  of,  171 
"delirium  cordis"  in,  179 
diagnosis  of,  180 

bacteriological,   180 
from  tonsillitis,  181 
distribution  of,  172 
emphysema  in,  176 
etiology  of,  172 

glandular  enlargement  in,  176,  177 
heart  failure  in,  179 

lesions  in,  175 
hemorrhage  in,  180 
kidney  lesions  in,  176 
laryngeal,  178 
local  lesion  of,  174 
lymphatic  enlargements  in,  176 
in  measles,  113 
morbid  anatomy  of,  174 
myositis,  acute,  in,  175 
nasal,  178 
nephritis  in,  176 

nervous  manifestations  of,  176,  177 
neuritis  in,  176,  1010 
paralysis,  facial,  in,  180 

local  or  widespread,  in,  179 


1096 


INDEX 


Diphtheria,  paralysis  of  phrenic  nerve  in,179 
pathology  of,  174 
poliomyelitis,  anterior,  acute  in,  176 
prognosis  of,  182 
prophylaxis  of,  182 
sequelae  of,  179 
sore  throat  in,  177 
spleen  in,  176 
symptoms  of,  176 
transmission,  mode  of,  172 
treatment  of,  183 
local,  185 
serum,  183,  184 
visceral  lesions  of,  175 
Diphtheritic  dysentery,  227 

gastritis,  568 
Diplegia,  spastic,  926 
Diplococcus  coryzEe,  363 

of  Weichselbaum  in  cerebrospinal  fever, 
134 
Diplopia  in  kubisagari,  362 

in  locomotor  ataxia,  963 
Diptera,  infection  by  larvse  of,  911 
Dipylidium  caninum,   901 
"Dissecting  aneurj'sm,"  534 
Disseminated  myelitis,  983 

sclerosis,  954 
Distomatosis,  904 
of  liver,  908 

symptoms  of,  909 
of  lung,  904,  907 

pathology  of,  908 
prognosis  of,  908 
symptoms  of,  90S 
treatment  of,  908 
Diverticula  of  oesophagus,  pressure,  561 

traction,  561 
Dracontiasis,  896 
Dracunculus  medinensis,  896 
Drop-foot  in  chronic  anterior  poliomyelitis, 

975 
Dropsy  in  mediastinal  tumor,  454 
Dry  mouth,  551 

pleurisy,  432 
Dubini's  disease,  1047 
Duchenne's   type  of    ascending    paralysis, 

975 
Ductless  glands,  diseases  of,  749 
Dum  dum  fever,  883 
Dumb  rabies,  264 

Duodenal  ulcer,  628.     See  Ulcer,  duodenal. 
Duroziez  sign  in  aortic  regurgitation,  512 
Dwarf  tapeworm,  901 
Dysbasia,  1068 
Dysentery,  227 
amoebic,  227 

diagnosis  of,  231 
hepatic  abscess  in,  232 

changes  in,  231 
intestinal  perforation  in,  234 
pathology  of,  231 
peritonitis  in,  234 
symptoms  of,  233 
bacillary,  227 

pathology  of,  230 


Dysenterj',  bacillar\",  Shiga's  bacillus  in,  230 

specific  treatment  of,  238 
catarrhal,  227 

pathology  of,  232 

s}Tnptoms  of,  234 
definition  of,  227 
diagnosis  of,  234 
diphtheritic,  227 

pathology  of,  232 

sj'mptoms  of,  234 
etiology  of,  227 
frequency  of,  230 
morbid  anatomy  of,  230 
pathology  of,  230 
prevention  of,  229 
prognosis  in,  235 
stools  in,  233 
sjonptoms  of,  232 
treatment  of,  236 

diet  in,  236 

local,  238 
Dysphagia   in    dilatation    of    oesophagus, 
562 
in  tuberculous  laryngitis,  375 
Dyspnoea  in  acute  pernicious  beriberi,  255 
in  ascites,  652 

in  croupous  pneumonia,  151 
in  emphysema  of  lung,  417 
in  exophthalmic  goitre,  754 
in  Hodgkin's  disease,  768 
in  mitral  regurgitation,  497 
in  pleurisy  with  effusion,  437 
in  pneumothorax,  450 
in  uraemia,  722 
Dystrophy,  muscular,  1035 

definition  of,  1035 

Erb's  juvenile,  1036 

etiology  of,  1035 

Landouzy-Dejerine  type  of,  1037 

morbid  anatomy  of,  1035 

pathology  of,   1035 

treatment  of,  1037 


EARACHE  in  smallpox,  83 
Echinococcic  strumitis,  749 
Echinococcus  cyst  of  brain,  932 
exogena,  903 
multilocularis,  903 
Eclampsia,  1062 
infantile,   1062 

diagnosis  of,  1063 
prognosis  in,  1063 
treatment  of,  1063 
puerperal,  1063 

treatment  of,  1063 
Ectopia  cordis,  528 
Eczema  of  tongue,  549 
Effusion,  pericardial,  461 

pleural,  436 
Egyptian  chlorosis,  887 
Ehrlich's  reaction  in  tj^hoid  fever,  50 
Electrical  chorea,  1047 
Elephantiasis,  895 
Elephantoid  fever  in  filariasis,  895 


INDEX 


1097 


Embolic  aneurysm,  534 
Embolism,  cerebral,  913 

in  croupous  pneumonia,  162 
in  typhoid  fever,  35 
Embrj'ocardia  in  typhoid  fever,  34 
Emphysema  in  diphtheria,  176 
of  lungs,  413 

acute,  413,  419 
atrophic,  413 

barrel-shaped  chest  in,  413 
chronic,  413 
compensatory,  413,  419 
definition  of,  413 
diagnosis  of,  417 
dyspnoea  in,  417 
etiology  of,  413 
frequency  of,  413 
hvpertrophic,  413 
interstitial,  413,  419 
morbid  anatomy  of,  413 
pathology  of,  413 
physical  signs  of,  415 
prognosis  in,  417 
senile,  413 
small-lunged,  420 

treatment  of,  420 
subjective  signs  of,  417 
surgical,  413 
symptoms  of,  415 
treatment  of,  418 
venesection  in,  419 
in  whooping-cough,  122 
Emprosthotonos  in  tetanus,  269 
Empyema,  430,  443 

complications  of,  446 
in  croupous  pneumonia,  157 
definition  of,  443 
diagnosis  of,  446 

from  serous  effusion,  446 
etiology  of,  443 
micro-organisms  in,  444 
necessitatis,  446 
perforation  in,  446 
physical  signs  of,  446 
prognosis  in,  447 
sepsis  in,  446 
in  septicaemia,  195 
symptoms  of,  445 
in  typhoid  fever,  43 
treatment  of,  447 

aspiration  in,  447 
Encephalitis,  acute,  944 
Encephalomyelitis,  983 
Encephalopathia  saturnina,  853 
Endarteritis,  obliterative,  532 

in  typhoid  fever,  26 
Endemic  hsematuria,  904 
haemoptysis,  904 
multiple  neuritis,  249 
Endocarditis,  482 
acute,  482 

complications  of,  485 
diagnosis  of,  485 
etiology  of,  482 
malignant,  482 


Endocarditis,  acute,  morbid   anatomy   of, 
484 
pathology  of,  484 
prognosis  in,  485 
symptoms  of,  484 
in  tonsillitis,  557 
treatment  of,  485 
benign,  482 
chronic,  488 

valvular  disease  as  result  of,  489 
in  croupous  pneumonia,  149,  159 
definition  of,  481 
gonorrhoea!,  187 
mural,  482 
papillary,  482 

in  rheumatic  fever,  acute,  200 
simple,  482 

tuberculous  vegetative,  343 
ulcerative,  485 

albuminuria  in,  487 
cerebral  type  of,  487 
compUcations  of,  487 
definition  of,  485 
diagnosis  of,  488 
in  erysipelas,  192 
etiology  of,  486 
haematuria  in,  487 
malarial  type  of,  487 
morbid  anatomy  of,  486 
pathology  of,  486 
prognosis  in,  488 
septic  form  of,  487 
splenic  enlargement  in,  487 
symptoms  of,  486 
treatment  of,  488 
senma  in,  488 
typhoid  type  of,  487 
valvular,  482 
verrucous,  482 
Endothelioma  of  kidnej',  732 
in  lung,  428 
of  thyroid  gland,  751 
Enteric  fever,  17.     See  Typhoid  fever. 

intussusception  of  bowel,  624 
Enteritis,  atrophic,  of  tropics,  242    ' 
catarrhal,  609 

symptoms  of,  609 
treatment  of,  609 
Enteroptosis,  632 

definition  of,  632 
diet  in,  635 
etiology  of,  632 
symptoms  of,  634 
treatment  of,  634 
surgical,  635 
Ephemeral  fever,  351 
Epidemic  gangrenous  proctitis,  239 
definition  of,  239 
etiology  of,  239 
pathology  of,  240 
symptoms  of,  240 
treatment  of,  240 
parotitis,  117 
roseola,  115 
Epididymitis  in  typhoid  fever,  42 


1098 


INDEX 


Epilepsy,  1052 

apoplexy  in,  1058 

aura  in,  1054,  1056 

complications  of,  1057 

convulsions  in,  1054 

cry  in,  1054 

definition  of,  1052 

diagnosis  of,  1058 

from  alcoholic  epilepsy,  1058 
from  hysteria,  1058,  1059 
from  petit  mal,  1059 
from  syncope,  1059 
from  tetanus,  1059 
from  uraemia,  1059 

etiology  of,  1052 

Jacksonian,  1061 

localized,  1061 

minor,  1061 

motor  paralysis  in,  1057 

pathology  of,  1054 

prognosis  in,  1060 

risus  sardonicus  in,  1055 

spinal,  1039.  See  Paramyoclonus  multi- 
plex. 

symptoms  of,  1054 

traumatisms  in,  1057 

treatment  of,  1061 
Epiphysitis,  syphilitic,  286 
Epistaxis,  369 

etiology  of,  369 

in  leprosy,  348 

treatment  of,  369 
Epithelioma,  cystic,  of  pancreas,  694 
Erb's  juvenile  muscular  dystrophy,  1036 

sign  in  gastric  tetany,  576 
of  tetany,  1065 
Ergotism,  856 
Erosive  gastritis,  569 
Eructation,  nervous,  603 
Eruption  in  cerebrospinal  fever,  137 

in  dengue,  133 

in  frambesia,  359 

in  leprosy,  348 

in  measles.  111 

in  pellagra,  858 

in  rubella,  116 

in  scarlet  fever,  100 

in  smallpox,  75,  77 

in  tick  fever,  355 

in  varicella,  91 

in  verruga,  361 
Erysipelas,  189 

abscess  in,  192 

complications  of,  191 

definition  of,  189 

endocarditis  in,  192 

etiology  of,  189 

facial,  191 

frequency  of,  189 

incubation  of,  190 

migrans,  191 

morbid  anatomy  of,  190 

pathology  of,  190 

pericarditis  in,  192_ 

pleuritis,  purulent  in,  192 

prognosis  in,  192 


Erysipelas,  sequelae  of,  191 

in  smallpox,  83 

symptoms  of,  190 

treatment  of,  192 
local,  192 

in  typhoid  fever,  34 

in  varicella,  92 
Erythema  in  acute  rheumatic  fever,  201 

in  dengue,  133 
Erythromelalgia,  1076 

definition  of,  1076 

diagnosis  of,  1077 

etiology  of,  1077 

treatment  of,  1077 
Esbach's  method  for  quantitative  estima- 
tion of  albumin  in  urine,  742 
Essential  emphysema,  413 
Ewart's  sign  of  pericardial  effusion,  461 
Exhaustion,  heat,  1082 
Exophthalmic  goitre,  751 
Exophthalmos     in     exophthalmic      goitre, 

753 
Exudative  nephritis,  701 
Eyeballs,    protrusion   of,    in   exophthalmic 
goitre,  753 


FACIAL  erysipelas,  191 
expression  in  cholera,  208 

in  typhoid,  27 
hemiatrophy,  1083 
nerve,  paralysis  of,  1025 

diagnosis  of,  1026 
etiology  of,  1025 
prognosis  in,  1027 
symptoms  of,  1026 
treatment  of,  1027 
spasm,  1027 

prognosis  in,  1028 
treatment  of,  1028 
Fallopian  tubes,  tuberculosis  of,  342 
False  aneurysm,  534 

croup,  374 
Family  ataxia,  967 
Famine  fever,  68 
Farcv,  272 
buds,  _  273 
chronic,  273 
Fatty  degeneration  of  heart,  473 

liver,  668 
Febricula,  351 

definition  of,  351 
diagnosis  of,  351 
etiology  of,  351 
symptoms  of,  351 
treatment  of,  351 
Febris  recurrens,  68 

Fecal  impaction  as  cause  of  intestinal  ob- 
struction, 624 
Fehling's  solution,  799 
Fetid  stomatitis,  546 
Fibrinous  bronchitis,  388 
pericarditis,  459 
pleurisy,  430 
pneumonia,  143 
Fibroma  of  brain,     932 


INDEX 


1099 


Fibroma  in  lung,  428 

of  mediastinum,  453 
Fibromata  of  kidney,  732 
Filaria  nocturna,  892 

sanguinis  hominis,  892 
Filariasis,  892 

definition  of,  892 
elephantiasis  in,  895 
filaria  Demarquaii  in,  892 
diurna  in,  892 
loa  in,  892 
Magalhffisi  in,  892 
microscopic  demonstration  of,  891 
nocturna  in,  892,  893 
Ozzardi  in,  892 
perstans  in,  892 
haematochyluria  in,  895 
lymph  scrotum  in,  896 
morbid  anatomy  of,  894 
pathology  of,  894 
symptoms  of,  895 
treatment  of,  896 
varicose  groin  glands  in,  896 
Fingers,  club-shaped,  in  mitral  regurgita- 
tion, 497 
Flatulence  in  sprue,  243 
Flea,  sand,  911 
Floating  kidney,  696 
Fluke,  lung,  904 
Flukes,  904 

Flute-players'  cramp,  1072 
FoUicular  colitis,  638 
pharyngitis,  556 
stomatitis,  546 
Food  poisoning,  855 
Foot-and-mouth  disease,  356 

definition  of,  356 
Foramen  ovale,  persistence  of,  527 
Forchheimer's  spots  in  rubella,  116 
Foreign  bodies  in  bowel,  624,  628 
Frambesia,  358 

definition  of,  358 
diagnosis  of,  360 

from  syphilis,  360 
from  verruga,  360 
eruption  in,  359 
etiology  of,  358 
incubation  of,  359 
prognosis  of,  360 
symptoms  of,  359 
treatment  of,  360 
tropica,  358 
Friedreich's  ataxia,  967 

definition  of,  967 
diagnosis  of,  969 

from  hereditary   cerebellar 
ataxia,  969 
etiology  of,  967 
gait  in,  968 
inco-ordination  in,  968 
morbid  anatomy  of,  967 
pathology  of,  967 
prognosis  in,  970 
speech  in,  969 
symptoms  of,  968 


Friedreich's  ataxia,  treatment  of,  970 

disease,  967,  1039.   See  Paramyoclonus 
multiplex. 
Fulminant  migraine,  1078 
Fulminating  purpura,  786 
Fungus  foot  of  India,  275 
Funnel  chest  in  chronic  hypertrophic  tonsil- 
litis, 559 
Fusiform  aneurysm,  534 


GAIT  in  Friedreich's  ataxia,  968 
in  locomotor  ataxia,  961 
Galactotoxismus,  857 
GaU-bladder,  carcinoma  of,  683 
diagnosis  of,  685 
etiology  of,  683 
carcinoma  of,  jaundice  in,  684 
inflammation  of,  acute,  675 
morbid  anatomy  of,  683 
pathology  of,  683 
prognosis  in,  685 
symptoms  of,  683 
treatment  of,  685 
malignant  growths  of,  683 
perforation  of,  680 
Gallstone  crepitus,  680 
Gallstones,  677 
Gangrene  in  cholera,  208,  209 
diabetic,  795 
of  lung,  420 

cough  in,  422 

in  croupous  pneumonia,  148,  157 
diagnosis  of,  422 
etiology  of,  420 
frequency  of,  420 
morbid  anatomy  of,  421 
odor  of  breath  in,  421 
pathology  of,  421 
septic  diarrhoea  in,  422 
sputum  in,  422 
symptoms  of,  421 
treatment  of,  422 
surgical,  423 
pulmonary,  in  bronchiectasis,  387 
in  Raynaud's  disease,  1075 
of  skin  in  smallpox,  83 
in  typhoid  fever,  33 
Gangrenous  appendicitis,  617 
pancreatitis,  689 
proctitis,  epidemic,  239 
pyelonephritis,  726 
stomatitis,  548 
Gastralgia,  603 
Gastrectasis,  572 
acute,  578 

diagnosis  of,  578 

from  acute  indigestion,  578 
from  volvulus,  578 
etiology  of,  578 
lavage  in,  579 
morbid  anatomy  of,  578 
prognosis  in,  579 
symptoms  of,  578 
treatment  of,  579 


1100 


INDEX 


Gastrectasis,  atonic,  578 

toxic,  578 
Gastric  cancer,  588 

diagnosis  of,  592 

from  gastric  ulcer,  593 
from  pernicious  anaemia,  592 
microscopic,  594 
test  meal  in,  593 
duration  of,  594 
etiology  of,  589 
haematemesis  in,  592,  605 
mode  of  spreading,  589 
morbid  anatomy  of,  589 
Oppler-Boas  baciUus  in,  594 
prognosis  in,  594 
symptoms  of,  591 
treatment  of,  595 
vomiting  in,  592 
catarrh,  acute,  564 

definition  of,  564 
diagnosis  of,  565 
etiology  of,  564 
symptoms  of,  564 
treatment  of,  565 
chronic,  568 

changes  in  yellow  fever,  215 
crises  in  locomotor  ataxia,  962 
dilatation,  572 
acute,  578 
definition  of,  572 
diagnosis  of,  576 
etiology  of,  572 
morbid  anatomy  of,  573 
pathology  of,  573 
physical  signs  of,  574 
symptoms  of,  573 
treatment  of,  576 
vomiting  in,  573 
fever,  17 
ectasy,  572 
hyperperistalsis,  602 

treatment  of,  602 
juice,  hypersecretion  of,  604 

hyposecretion  of,  604 
neuralgia,  603 
neuroses,  601 
tetany,  575 

Chvostek's  sign  in,  576 
Erb's  sign  in,  576 
Trousseau's  sign  in,  575 
Tiirck's  gyromele  in,  575 
ulcer,  579 

anaemia  in,  582 
classes  of,  580 
chronic,  582 
definition  of,  579 
diagnosis  of,  584 

from  duodenal  ulcer,  584 

tests  for  blood  in  stools, 
584 
from  gallstone  colic,  584 
from  gastric  cancer,  584 
from    gastric    crises   of   loco- 
motor ataxia,  584 
from  gastric  neuralgia,  584 


Gastric  ulcer,  etiology  of,  579 
frequency  of,  579 
gastroenterostomy  in,  587 
haematemesis  in,  582,  604 
hemorrhage  in,  treatment  of,  587 
hour-glass  contraction  in,  581 
morbid  anatomy  of,  580 
pathology  of,  580 
perforation  in,  583 
prognosis  in,  585 
symptoms  of,  581 
treatment  of,  586 
dietetic,  586 
surgical,  587,  588 
in  typhoid  fever,  36 
Gastritis,  catarrhal,  acute,  564 
chronic,  568 
definition  of,  568 
diagnosis  of,  570 

from  gastric  cancer,  570 
diet  in,  572 
etiology  of,  568 
lavage  in,  571 
morbid  anatomy  of,  569 
pathology  of,  569 
prognosis  in,  570 
symptoms  of,  569 
tongue  in,  570 
treatment  of,  570 
diphtheritic,  568 
erosive,  569  , 
mycotic,  568 
phlegmonous,  566 
definition  of,  566 
diagnosis  of,  567 
etiology  of,  567 
symptoms  of,  567 
treatment  of,  568 
polyposa,  569 
toxic,  acute,  565 

diagnosis  of,  566 
etiology  of,  565 
morbid  anatomy  of,  566 
symptoms  of,  566 
treatment  of,  566 
Gastrodiaphany,  575 
Gastrodynia,  603 
Gastrointestinal  paralysis,  578 
Gastroptosis,  632 
Gastrorrhagia,  604 

Genito-urinary   complications    of    typhoid 
fever,  41 
system,  tuberculosis  of,  338 
Geographical  tongue,  549 
Gerhard's  test  for  acetone  in  urine,  800 
German  measles,  115.     See  Rubella. 
Gibralter  fever,  245 
Gingko  poisoning,  861 
Gland,  thymus,  diseases  of,  772 
Glanders,'  271 

bacillus  mallei  in,  272 
chronic,  273 
definition  of,  271 
diagnosis  of,  273 

from  carbuncles,  273 


INDEX 


1101 


Glanders,  diagnosis  of,  from   multiple    ab- 
scesses, 273 
etiology  of,  272 
morbid  anatomy  of,  272 
pathology  of,  272 
symptoms  of,  273 
treatment  of,  273 
Glands,  ductless,  diseases  of,  749 

suprarenal,  diseases  of,  760 
Glandular  enlargement  in  bubonic  plague, 
222 
in  diphtheria,  176,  177 
in  rubella,  116 
in  scarlet  fever,  99,  103 
in  whooping-cough,  122 
fever,  353 

definition  of,  353 
diagnosis  of,  353 
etiology  of,  353 
glandular  enlargements  in,  353 
nephritis,  acute,  in,  353 
prognosis  in,  354 
symptoms  of,  353 
treatment  of,  354 
tuberculosis,  299 
Glaucoma,   hemorrhagic,   in  chronic  inter- 
stitial nephritis,  715 
Glenard's  disease,  632 
Glioma  of  brain,  932,  933 
Globus  in  hysteria,  1050 
Glomerular  nephritis,  700 
Glomerulo  nephritis,  chronic,  704 
Glosso-labio-laryngeal  paralysis,  977 
Glossopharyngeal  nerve,  paralysis  of,  1030 
Glottis,  spasm  of,  in  tetanus,  269 
Glycosuria,  794,  795 
Goitre,  749 

benign,  749 
colloid,  750 
cystic,  749 
definition  of,  749 
etiology  of,  750 
exophthalmic,  751 
definition  of,  751 
dyspnoea  in,  754 
etiology  of,  752 
exophthalmus  in,  753 
frequency  of,  752 
Mobius'  sign  in,  753 
morbid  anatomy  of,  752 
nervous  symptoms  of,  754 
pathology  of,  752 
prognosis  in,  755 
Stelwag's  sign  in,  753 
symptoms  of,  753 
tachycardia  in,  753 
treatment  of,  755 
tremor  in,  754 
von  Graefe's  sign  in,  753 
hyperplastic,  749 
lingual,  750 
malignant,  749 
mixed,  749 
neoplastic,  749 
parenchymatous,  749 


Goitre,  simple,  749 

symptoms  of,  750 

treatment  of,  750 

vascular,  749 
Gold-dust  complaint,  412 
Gonorrhoeal  arthritis,  ankylosis  in,  187 
chronic,  186 
symptoms  of,  186 
temporary,   186 
treatment  of,  188 

endocarditis,  187 

infection,   186 

diagnosis  of,  187 
prognosis  of,  188 

pysemia,   186 

rheumatism,  187 
Gout,  808 

acute,  813 

symptoms  of,  813 

cardiovascular  changes  in,  812 

chronic,  814 

symptoms  of,  814 

definition  of,  80S 

diagnosis  of,  815 

from  arthritis  deformans,  816 

etiology  of,  808 

frequency  of,  809 

irregular,  symptoms  of,  814 

joint  changes  in,  811 

morbid  anatomy  of,  811 

pathology  of,  809 

prognosis  in,  816 

retrocedent,  815 

symptoms  of,  813 

treatment  of,  816 
dietetic,  817 
Gouty  lesions  in  chronic  lead  poisoning,  853 
Grain  shovellers'  disease,  411 
Grand  mal,  1052 
Granular  kidney,  710 

meningitis,  301 
Graves'  disease,  751 
Green  sickness,  776 
Grindstone  consumption,  412 
Ground  itch,  889 
Guinea-worm,  896 

definition  of,  896 

disease,  896 

distribution  of,  896 

symptoms  of,  897 

treatment  of,  898 
Gull's  disease,  756 
Gumma  of  brain,  932,  933 
Gummata,  syphilitic,  281,  284 


H^MAMCEBA  malarise,  863 
in  man,  865 
in  mosquito,  867 
Hsematemesis,  604 
in  aneurysm,  605 

diagnosis  of,  from  haemoptysis,    607 
in  gastric  cancer,  592,  605 

ulcer,  582,  604 
in  haemophilia,  605 


1102 


INDEX 


Hsematemesis  in  hepatic  cirrhosis,  605 
in  purpura,  605 
in  smallpox,  605 
in  yeUow  fever,  605 
Hsematinuria,  739 

treatment  of,  740 
Hgematitis,  suppurative,  780 
Hsematochyluria  in  filariasis,  895 
Hsematuria,  738 

in  bilharzia  disease,  906 
causes  of,  738 
endemic,  904 
in  movable  kidney,  697 
treatment  of,  738 
in  ulcerative  endocarditis,  487 
Hsemoglobinuria,  739 

in  croupous  pneumonia,  155 
in  malarial  fever,  877 
Hsemopericardimn,  467 
Haemophilia,  787 

definition  of,  787 
epistaxis  in,  788 
etiology  of,  787 
hsematemesis  in,  605 
morbid  anatomy  of,  788 
pathology  of,  788 
prognosis  in,  788 
symptoms  of,  788 
treatment  of,  788 
Hsemoptysis,  607 

in  bronchiectasis,  386 
endemic,  904,  907 
parasitic,  904,  907 
in  pulmonary  tuberculosis,  316 
Hammerer's  palsy,  1072 
Hanot's  cirrhosis  of  liver,  664 
Harrison's  groove  in  rickets,  828 
Haut  mal,  1052 
Hay  fever,  367 

definition  of,  367 
distribution  of,  367 
etiology  of,  367 
morbid  anatomy  of,  367 
pathology  of,  367 
prognosis  of,  368 
symptoms  of,  367 
treatment  of,  368 
Hay  garth's    nodosities   in    arthritis   defor- 
mans, 820 
Head  tetanus,  271 
Heart,  aneurysm  of,  479 
causes  of,  480 
forms  of,  479 
symptoms  of,  481 
atrophy  of,  474 
bilocular,  527 
brown  induration  of,  474 
congenital  defects  of,  527 
degeneration  of,  amyloid,  474 
calcareous,  474 
fatty,  474 
hyaUne,  474 
parenchymatous,  473 
dilatation  of,  468,  471 
causes  of,  471 


Heart,  dilitation  of,  definition  of,  468 
physical  signs  of,  472 
prognosis  in,  472 
sjTnptoms  of,  471 
treatment  of,  472 
diseases  of,  468 
failure  in  diphtheria,  179 
in  typhoid  fever,  35 
hypertrophy  of,  468,  469 
definition  of,  468 
diagnosis  of,  470 

from  cardiac  dilatation,  470 
from  pericardial  effusion,  470 
from  tobacco  heart,  470 
physical  signs  of,  469 
prognosis  in,  470 
symptoms  of,  469 
treatment  of,  471 
-muscle,  changes  in,  in  typhoid  fever,26 
neuroses  of,  521 

definition  of,  521 
treatment  of,  522 
palpitation  of,  521 
fragmentation  of,  474 
pulmonary  valves  of,  disease  of,  515 
segmentation  of, -474 
-sounds  in  typhoid  fever,  34 
trilocular,  527 
tuberculosis  of,  343 
valves  of,  mechanism  of,  490 
valvular  anomalies  of,  528 
disease  of,  chronic,  489 
causes  of,  489 
treatment  of,  516 
valves  affected  in,  489 
wounds  of,  481 
Heat  exhaustion,  1082 
Heatstroke,  1080 

Heat  test  for  albumin  in  urine,  742 
Heberden's   nodes   in   arthritis   deformans, 

821 
Hematoma  of  dura  mater,  947 
Hemiansesthesia  in  apoplexy,  920 

in  hysteria,  1049 
Hemianopsia,  1015 
in  apoplexy,  920 
binasal,     1015 
bitemporal,  1015 
homonymous,   1015 
Hemiatrophy,  facial,  1083 
Hemiplegia  in  apoplexy,  919 
in  croupous  pneumonia,  160 
in  malarial  fever,  876 
pneumonique,  159 
spastic,  925 
in  typhoid  fever,  44 
in  ursemia,  722 
Hemorrhage,  cerebral,  913 
in  diphtheria,  180 
in  duodenal  ulcer,  630 
from  lungs,  607 
into  pancreas,  695 
in  pneumonic  plague,  223 
in  pulmonary  tuberculosis,  316 
retinal,  in  malarial  fever,  876 


INDEX 


1103 


Hemorrhage  into  spinal  cord,  990 

definition  of,  990 

diagnosis  of,  991 

etiology  of,  990 

prognosis  of,  991 

symptoms  of,  990 

treatment  of,  991 

membranes,  991 
from  stomach,  604 

symptoms  of,  605 
subconjunctival    in     whooping-cough, 

122 
in  typhoid  fever,  30,  36,  37 

diagnosis  of,  36 

symptoms  of,  36 

treatment  of,  57 
Hemorrhagic  affections  of  newborn,  786 
albuminuric  retinitis,  714 
cysts  of  pancreas,  694 
glaucoma  in  chronic  interstitial  neph- 
ritis, 715 
internal  pachymeningitis,  947 
measles,  112 
nephritis,  701 
pancreatitis,  acute,  695 
peritonitis,  643 
smallpox,  81 
Henoch's  purpura,  786 
Hepatic  abscess,  653 

amoebae  dysenterise  in,  656 

diagnosis  of,  657 

from  empyema,  658 

from  infection  of  gall-ducts, 

657 
from  malarial  infection,  657 

in  dysentery,  232 

etiology  of,  653 

fever  in,  656 

morbid  anatomy  of,  654 

multiple,  655 

pathology  of,  654 

prognosis  in,  658 

pysemic,  654 

single  large,  654 

symptoms  of,  656 

traumatic,  653 

treatment  of,  658 

tropical,  654 
artery,   aneurysm  of,   543 
bloodvessels,  affections  of,  666 
changes  in  croupous  pneumonia,  149 

in  yellow  fever,  215 
cirrhosis,  658.     See  Liver,  cirrhosis  of. 

haematemesis  in,  605 
congestion,  666 

fever  of  Charcot,  intermittent,  679 
tuberculosis,  338 
Hepatitis,  acute,  653 

definition  of,  653 

etiology  of,  653 
Hepatization  of  lung.  426 

in  croupous  pneumonia,  147 
Hereditary  ataxia,  967 

Marie's  cerebellar,  970 
ataxic  paraplegia,  967 


Hereditary  chorea,   1046 

syphilis,  286 
Herpes  in  cerebrospinal  fever,  137 
in  croupous  pneumonia,  151 
in  typhoid  fever,  31 
HiU  diarrhoea,  240 

definition  of,  240 
etiology  of,  240 
pathology  of,  241 
symptoms  of,  241 
treatment  of,  241 
Hip,  spontaneous  dislocation  of ,  in  typhoid 

fever,  44 
Hippocratic  facies  in  acute  peritonitis,  644 
in  cholera,  208 
in  yellow  fever,  216 
Hob-nail  liver,  659 
Hodgkin's  disease,  767 

blood  changes  in,  768 
bronzing  of  skin  in,  768 
definition  of,  767 
diagnosis  of,  769 

from  true  leukaemia,  769 
from     tuberculous     lymph 
glands,  769 
dyspnoea  in,  768 
etiology  of,  767 
morbid  anatomy  of,  767 
oedema  in,  768 
pathology  of,  767 
prognosis  in,  770 
symptoms  of,  767 
treatment  of,  770 
Hoffman's  sign  of  tetany,  1065 
Hookworm  disease,  888 
Horseshoe  kidney,  696 
Hour-glass   stomach,    598.      See   Stomach, 

hour-glass. 
Hunger  typhus,  61 
Huntington's  disease,   1046 
Hutchinson's  pupil  in  apoplexy,  921 

teeth  in  syphilis,  286 
Hyaline  degeneration  of  heart,  474 
Hybrid  scarlet  fever,  115 
Hydatid  cyst  of  mediastinum,  453 
of  peritoneum,  649 
of  spleen,  764 
Hydrocephalus,  927 
Hydronephrosis,  728 
acquired,  728 
congenital,  728 
definition  of,  728 
diagnosis  of,  729 
etiology  of,  728 
pathology  of,  728 
prognosis  of,  729 
in  tuberculosis  of  kidney,  342 
symptoms  of,  729 
treatment  of,  729 
Hydropericardium,  466 
prognosis  of,  466 
symptoms  of,  466 
treatment  of,  467 
Hydrophobia,  261 
definition  of,  261 


1104 


INDEX 


Hydrophobia,  diagnosis  of,  265 

from  pseudohj'drophobia,  265 
from  tetanus,  265 

distribution  of,  262 

etiology  of,  262 

frequency  of,  262 

morbid  anatomv  of,  262 

pathology  of,  262 

prevention  of,  262 

prognosis  of,  265 

S}Tnptoms  of,  in  animals,  263 
in  man,  264 

treatment  of,  265 
b}'  serum,  265 
Hydropneumothorax,  449 

coin  sound  in,  451 

in  croupous  pneumonia,  157 

metallic  tinkling  in,  451 

physical  signs  of,  451 

Skodaic  resonance  in,  451 
Hydrotherapy  in  typhoid  fever,  52 
Hj^dro thorax,  448 
Hyperemia  of  kidney,  acute,  699 
chronic,  699 

of  liver,  666 
Hj'perhsemocytosis  in  scarlet  fever,  99 
Hymenolipsis  nana,  901 
Hypercesthesia  of  stomach,  603 
Hypernephromata  of  kidney,  732 
Hyperperistalsis,  gastric,  602 
Hj'perplastic  goitre,  749 

tuberculosis,  chronic,  296 
Hypertrophic  cirrhosis  of  liver,  663 

emphysema,  413 

pulmonary  osteoarthropathy,   840 

rhinitis,  365 

stenosis  of  pylorus,  595 

tonsillitis,  chronic,  558 
Hypertrophy,  pseudomuscular,  1035 
Hypodermoclysis  in  cholera  infantum,  614 
Hvpoglossal  nerve,  disease  of,  1034 
Hysteria,   1047 

ansesthesia  in,  1049 

aphonia  in,  1050 

con\ailsion  in,  1048 

in  chorea  minor,  1045 

definition  of,  1047 

diagnosis  of,  1051 

from  organic  nervous  disease,  1051 

disturbances  of  special  sense  in,  1049 

etiologj^  of,  1047 

globus  in,  1050 

hemiansesthesia  in,  1049 

major,  1048 

merycismus  in,  1050 

ovarian  tenderness  in,  1050 

paralvsis  of  motion  in,  1050 

pathology  of,  1048 

prognosis  in,  1051 

pseudo-angina  in,  1050 

symptoms  of,   1048 
sensor}',  1049 

tachycardia  in,  1050 

treatment  of,  1051 
Hysteroepilepsy,  1051 


ICE,  infection  by,  in  tj^hoid  fever,  18 
"  Iced  hver,"  464 
Ichthyosis  liuguahs,  550 
Ichthyotoxismus,  856 
Icterus  neonatonmi,  686 
Idiocy,  acquired,  928 
Idiopathic  dilatation  of  colon,  640 

muscular  spasm,  1064 
Heocsecal  intussusception  of  bowel,  625 
Ileocolic  intussusception  of  bowel,  625 
Ileocohtis  of  childhood,  609 
definition  of,  609 
diagnosis  of,  612 

from  typhoid  fever,  612 
etiology  of,  609 
morbid  anatomy  of,  610 
patholog}'  of,  610 
prognosis  in,  612 
symptoms  of,  611 
treatment  of,  612 
Incarcerated  kidney,  696 
Inco-ordination  in  Friedreich's  ataxia,  968 

in  locomotor  ataxia,  961 
"India-rubber  bottle  stomach,"  589 
Indicanuria,   745 
test  for,  746 
Indurative  media stinoperi carditis,  463 
Infantile  cerebral  paralysis,  925 

eclampsia,  1062.   See  Eclampsia,  infan- 
tile, 
palsy,  acute,  970 
spinal  paralysis,  970 
scurvy,  831 
Infarct  of  spleen,  764 

in  septicsemia,  195 
Infarction  of  lung  in  typhoid  fever,  42 
Infection,  diseases  due  to  specific,  17 

latent  malarial,  878 
Inflammation    of    bile-ducts,    suppurative, 
673 
of  liver,  653 
of  salivary  glands,  551 
Influenza,   125 

bacillus  of  Pfeiffer  in,  125, 126 
bronchitis  in,  126 
chill  in,  126 
complications  of,  128 

cardiac,  128 
definition  of,  125 
diagnosis  of,  128 
diarrhoea  in,  127 
endemic-epidemic,  125 
etiology  of,  125 
fever  in,  126 
history  of,  125 
incubation  in,  126 
jaundice  in,  127 
kidneys  in,  128 
meningitis,  127 
mental  disturbances  in,  127 
nervous  manifestations  of,  127 
pleurisjr  in,  127 
pneumonia  in,  127 
prophylaxis  of,  130 
pulmonarj'  congestion  in,  127 


INDEX 


1105 


Influenza,  sequelae  of,  128 
symptoms  of,  126 
toxic  neuritis  in,  127 
treatment  of,  129 
vera,  125 
vomiting  in,  127 
Infusoria,  parasitic,  909 
Ingravescent  apoplexy,  922 
Inoculation  preventive  in  plague,  224 
Insolation,   1080 

Insomnia  in  croupous  pneumonia,  155 
in  typhoid  fever,  26 
treatment  of,  58 
in  uraemia,  722 
Insular  sclerosis,  954 
Intermittent  fever,  diagnosis  of,  872 
from  septicaemia,  872 
from  tuberculosis,  872 
from  ulcerative  endocarditis, 
872 
prognosis  of,  872 
treatment  of,  872 
hepatic  fever  of  Charcot,  679 
malarial  fever,  863 
Interstitial  emphysema,  413 
neuritis,  1003 
nephritis,  chronic,  710 
Intestinal  amcebiasis,  227 

antisepsis  in  typhoid  fever,  56 
changes  in  yellow  fever,  216 
hemorrhage  in  typhoid  fever,  36 

treatment  of,  57 
perforation  in  typhoid  fever,  37 

treatment  of,  58 
myiasis,  912 
obstruction,  623 
acute,  623 
causes  of,  623 
chronic,  623 

by  congenital  malformations,  624 
diagnosis  of,  624 
prognosis  of,  624 
symptoms  of,  624 
treatment  of,  624 
definition  of,  623 
by  foreign  bodies,  624,  628 
by  internal  strangulation,  624,  626 

symptoms  of,  627 
by  intestinal  paralysis,  624,  627 
by  intussusception,  624 
etiology  of,  625 
frequency  of,  625 
pathology  of,  625 
prognosis  in,  626 
symptoms  of,  625 
treatment  of,  626 
by  volvulus,  627 

prognosis  in,  627 
symptoms  of,  627 
treatment  of,  627 
ulcers  in  paratyphoid  fever,  59 
Intestines,  diseases  of,  608 
tuberculosis  of,  335 

chronic  hyperplastic,  336 
Intoxications,  843 

7Q 


Intubation  in  acute  catarrhal  laryngitis,  371 

in  oedematous  laryngitis,  374 
Intussusception,  624 

acute,  625 

enteric,  625 

etiology  of,  625 

frequency  of,  625 

ileocaecal,  625 

ileocolic,  625 

pathology  of,  625 

prognosis  in,  626 

retrograde,  625 

subacute,  625 

symptoms  of,  625 

treatment  of,  626 

ultra-acute,  625 
Iritis,  syphilitic,  284 
Itch,  dhobie,  909 


JACKSONIAN  epilepsy,  1061 
Japanese  river  fever,  357 

definition  of,  357 
etiology  of,  358 
fever  in,  358 
symptoms  of,  358 
treatment  of,  358 
Jaundice  in  acute  pancreatitis,  689 
in  cancer  of  gall-bladder,  684 
in  cholelithiasis,  678 
in  croupous  pneumonia,  155 
in  influenza,   127 
in  newborn,  686,  786 
in  relapsing  fever,  69 
in  typhoid  fever,  40 
in  yellow  fever,  216 
Joint  complications  in  typhoid  fever,  44 
Joints  in  gout,  changes  in,  811 

inflammation  of,   in  acute  rheumatic 

fever,  199 
in  verruga,  361 


KAKKE,  1007 
Kala-azar,  883 

definition  of,  883 
etiology  of,  883 
morbid  anatomy  of,  884 
pathology  of,  884 
symptoms  of,  884 
treatment  of,  884 
Keratitis  in  measles,  113 

syphilitic,  286 
Kernig's  sign  in  cerebrospinal  fever,  138 
Kidney,  adenoma  of,  732 
alveolar,  732 
papillary,  732 
amyloid  disease  of,  718 
definition  of,  718 
etiology  of,  718 
pathology  of,  719 
prognosis  in,  719 
symptoms  of,  719 
treatment  of,  719 
urine  in,  719 


1106 


INDEX 


Kidney,  angiomata  of,  732 
cancer  of,  732 
chronic  contracted,  710 
"  cinder-sifting,"  696 
circulatory  disturbances  in,  698 
cirrhosis  of,  710 
contracted,  710 
in  croupous  pneumonia,  149 
cystic  disease  of,  730 
cysts  of,  congenital,  730 
echinococcus,  731 
multiple,  730 
single,  730 
symptoms  of,  731 
in  diabetes  mellitus,  changes  in,  793 
diseases  of,  696 
endothelioma  of,  732 
fibromata  of,  732 
floating,  696 
granular,  710 
horseshoe,  696 
hyperaemia  of,  acute,  699 
treatment  of,  699 
chronic,   699 

albuminuria  in,  699 
diagnosis  of,  699 
symptoms  of,  699 
treatment  of,  699 
hypemephromata  of,  732 
incarcerated,  696 
in  influenza,  128 
large  white,  705 
lipomata  of,  732 

in  malarial  fever,  changes  in,  868 
malformations  of,  696 
movable,  696 

diagnosis  of,  697 
Dietl's  crises  in,  697 
etiology  of,  697 
hsematuria  in,  697 
symptoms  of,  697 
treatment  of,  698 
papilloma  of,  732 
sarcoma  of,  732 
in  scarlet  fever,  99  102 
sclerotic,  710 
small  white,  705 
stone  in,  733 

suppuration  of,  in  septicaemia,  195 
tuberculosis  of,  341 
tumors  of,  732 

malignant,  hsematuria  in,  733 
symptoms  of,  733 
in  typhoid  fever,  changes  in,  26 
in  typhus  fever,  63 
Klebs-Loeffler  bacillus  of  diphtheria,  172 
Knee-jerks  in  locomotor  ataxia,  961 
Knife-grinders'  rot,  412 
Kopf -tetanus,  271 
Koplik's  spots  in  measles,  111 
Korssakoff's  disease,  1009 
Kreotoxismus,  856 
Kubisagari,  362 

diplopia  in,  362 
paresis  in,  362 


Kubisagari,  ptosis  in,  362 

treatment  of,  362 
Kussmaul's    coma    in    diabetes    mellitus, 
797 


LACQUER  poisoning,  860 
treatment  of,  861 
La  grippe,   125.     See  Influenza. 
Landouzy-Dejerine        type     of      muscular 

dystrophy,  1037 
Landry's  paralysis,  1000 
Large-lunged  emphj^sema,  413 
Larval  plague,  symptoms  of,  223 
Laryngeal  diphtheria,  178 
tuberculosis,  314 
ulceration  in  typhoid  fever,  42 
Laryngitis,  catarrhal,  acute,  369 
definition  of,  369 
diagnosis  of,  370 
etiology  of,  369 
intubation  in,  371 
pathology  of,  370 
prognosis  of,  371 
symptoms  of,  370 
tracheotomy  in,  371 
treatment  of,  371 
chronic,  371 

diagnosis  of,  372 
pathology  of,  372 
symptoms  of,  371 
treatment  of,  372 
cedematous,  372 

cyanosis  in,  373 
definition  of,  372 
diagnosis  of,  373 

from  foreign  body,  373 
from  laryngeal  crises  in  loco- 
motor ataxia,  373 
etiology  of,  372 
intubation  in,  374 
pathology  of,  373 
prognosis  in,  373 
symptoms  of,  373 
tracheotomy  in,  374 
treatment  of,  373 
in  smallpox,  83 
spasmodic,  374 

definition  of,  374 
etiology  of,  374 
treatment  of,  374 
syphilitic,  376 

diagnosis  of,  377 

from   tuberculous  ulceration, 
377 
etiology  of,  376 
prognosis  of,  377 
symptoms  of,  377 
treatment  of,  377 
tuberculous,  375 

aphonia  in,  375 
cough  in,  375 
definition  of,  375 
diagnosis  of,  376 

from  carcinoma  of  larynx,  376 


INDEX 


1107 


Laryngitis,  tuberculosis,  diagnosis  of,  from 
syphilitic  laryngitis,  376 
dysphagia  in,  375 
etiology  of,  375 
lesion  in,  376 
pathology  of,  375 
prognosis  of,  376 
symptoms  of,  375 
treatment  of,  376 
Larynx,  diseases  of,  369 
Latah,  1066 
Lateral  sclerosis,  978 

amyotrophic,  980 
Lathyrism,  859 

definition  of,  859 
etiology  of,  859 
history  of,  859 
symptoms  of,  859 
treatment  of,  860 
Lavage  in  chronic  gastritis,  572 
Lead  poisoning,  851 
acute,  851 
chronic,  851 

anaemia  in,  854 
blue  line  on  gums  in,  853 
colic  in,  854 
convulsions  in,  853 
diagnosis  of,  854 

from  acute  poliomyelitis, 

854 
from    chronic    poliomev- 

litis,  854 
from  epilepsy,  854 
from  pressure  palsy,  854 
etiology  of,  852 
gouty  lesions  in,  853 
morbid  anatomy  of,  852 
neuritis  in,  853 
optic  neuritis  in,  853 
pathology  of,  852 
prevention  of,  852 
prognosis  in,  854 
squint  in,  853 
symptoms  of,  853 
treatment  of,  854 
wrist-drop  in,  853 
Leathery  stomach,  589 
Leontiasis,  349 
ossea,  840 
Leprosy,  344 

anaesthetic,  349 
bacillus  of,  345 
clinical  forms  of,  347 
definition  of,  344 
diagnosis  of,  349 
distribution  of,  344 
epistaxis  in,  348 
eruptions  in,  348,  349 
etiology  of,  345 
incubation  period  in,  348 
leontiasis  in,  349 
leprous  chancre  in,  348 
manner  of  infection  in,  345 
mixed,  349 
morbid  anatomy  of,  347 


Leprosy,  nodules  in,  348 
prognosis  in,  350 
prophylaxis  of,  351 
symptoms  of,  347 
treatment  of,  350 
tuberculous,  348 
Leptomeningitis,  948 
diagnosis  of,  949 
morbid  anatomy  of,  949 
pathology  of,  949 
symptoms  of,  949 
treatment  of,  950 
Lethargy,  African,  879 
Leucocythajmia,  780 
Leucocytosis  in  typhoid  fever, 

33 
Leukaemia,  780 

definition  of,  780 
diagnosis  of,  783 
etiology  of,  781 
lymphatic,  780,  782 

symptoms  of,  783 
morbid  anatomy  of,  781 
myelogenous,  780 
pathology  of,  781 
prognosis  in,  783 
splenomeduUary,  780,  781 
blood  changes  in,  781 
spleen  in,  782 
symptoms  of,  783 
treatment  of,  784 
Leukoplakia  buccalis,  550 
Lingual  goitre,  750 
Lipomata  of  kidney,  732 
Lithiasis,  411 
Lithuria,  746 
Little's  disease,  929 
Liver,  abscess  of,  653 

diagnosis  of,  657 
in  dysentery,  232 
etiology  of,  653 
multiple,  655 
pathology  of,  654 
prognosis  of,  658 
pyaemic,  654 
single  large,  654 
symptoms  of,  656 
traumatic,  653 
treatment  of,  658 
tropical,  654 
amyloid,  667 

symptoms  of,  667 
treatment  of.  667 
angiomata,  cavernous,  of,  668 
carcinoma  of,  668 

secondary,  668 
changes  in,  in  typhoid  fever,  25 
in  cholera,  206 
cirrhosis  of,  658 
atrophic,  659 

etiology  of,  660 
hepatic  coma  in,  662 
morbid  anatomy  of,  660 
pathology  of,  660 
physical  signs  of,  662 


1108 


INDEX 


Liver,  cirrhosis  of,   atrophic,  prognosis    in, 
662 
symptoms  of,  661 
treatment  of,  662 
capsular,  665 
definition  of,  658 
hypertrophic,  659,  663 
definition  of,  663 
diagnosis  of,  664 
etiology  of,  663 
Hanot's  type  of,  664 
morbid  anatomy  of,  663 
pathology  of,  663 
prognosis  in,  664 
symptoms  of,  664 
treatment  of,  664 
syphilitic,  664 

treatment  of,  665 
congestion  of,  666 

nutmeg  appearance  in,  666 
symptoms  of,  667 
treatment  of,  667 
cystic  disease  of,  668 
diseases  of,  653 
distomatosis  of,  908 
hyperfemia  of,  666 
fatty,  668 
flukes,  908 

varieties  of,  905 
"iced,"  464 
inflammation  of,  653 
in  malarial  fever,  changes  in,  868 
red  atrophy  of,  666 
sarcoma  of,  668 
syphilis  of,  281 
tuberculosis  of,  338 
timiors  of,  668 

diagnosis  of,  669 

from  echinococcus  cyst,  669 
from  gumma,  669 
from   hypertrophic    cirrhosis, 
669 
prognosis  in,  669 
symptoms  of,  669 
treatment  of,  669 
in  typhoid  fever,  changes  in,  40 
yellow  atrophy  of,  acute,  670 
definition  of,  670 
diagnosis  of,  670 
etiology  of,  670 
morbid  anatomy  of,  670 
pathology  of,  670 
prognosis  in,  671 
symptoms  of,  670 
treatment  of,  671 
Lobar  pneumonia,  143 
Lobular  pneumonia,  397 
Localized  epilepsy,  1061 

peritonitis,  643 
"Lock-jaw"  in  tetanus,  269 
Locomotor  ataxia,  958 

allochiria  in,  962 
Argyll-Robertson  pupil  in,  962 
Charcot  joint  in,  963 
crises  in,  962 


Locomotor,  ataxia,  definition  of,  958 
diagnosis  of,  964 

from  caries  of  vertebrae,  964 
from  cerebellar  tumor,  964 
from  general  paralysis  of  in- 
sane, 964 
from  paraplegia,  964 
from  peripheral  neuritis,  964 
diplopia  in,  963 
etiology  of,  958 
gait  in,  961 

girdle  sensations  in,  962 
inco-ordination  in,  961 
knee-jerk  in,  961 
lightning  pains  in,  962 
morbid  anatomy  of,  958 
ocular  symptoms  of,  962 
optic  atrophy  in,  963 
pathology  of,  958 
perforating  ulcer  of  foot  in,  964 
prognosis  in,  964 
Romberg's  symptom  in,  961 
symptoms  of,  960 
treatment  of,  965 
baths  in,  966 
electrical,  966 
Westphal's  symptom  in,  961 
Loculated  peritonitis,  643 
Lucilia  macellaria,  911 
Ludvig's  angina,  552 

symptoms  of,  552 
treatment  of,  552 
Lues,  276 

venerea,  276 
Liunbar  puncture  as   aid  to   diagnosis   of 

cerebrospinal  fever,  140 
"Lumpy  jaw,"  274 
Lung,  abscess  of,  423 

in  croupous  pneumonia,  148,  157 
congestion  of,  425 
diseases  of,  397 
distomatosis  of,  904,  907 
emphysema  of,  413 
fever,  143 
flukes,  907 
gangrene  of,  420 

in  croupous  pneumonia,  148,  162 
hemorrhage  from,  607 
hypostatic   congestion  of,   in  typhoid 
fever,  42 
in  typhus  fever,  63 
infarction  of,  in  typhoid  fever,  42 
oedema  of,  in  cholera,  209 
syphilis  of,  281 
tumors  in,  428 
Lupinosis,  859 

Lymph  nodes,  syphilitic,  283 
scrotum  in  filariasis,  896 
Lymphadenoma  of  mediastinum,  452 
Lymphatic  areas  of  stomach,  590 
constitution,  770 
glands,  tuberculosis  of,  299 
involvement  in  diphtheria,  176 
leukaemia,  780,  782 
system,  diseases  of ,  749 


INDEX 


1109 


Lymphoma  of  mediastinum,  452 
Lyssa,  261 


McBURNEY'S  point,  620 
Macular  syphilide,  284 
Madura  foot,  275 
Maidismus,  857 
Malarial  fever,  863 

sestivo-autumnal,  parasite  of,  866 
ague  cake  in,  868,  875 
blood  changes  in,  867 

examination  in,  869 
bone-marrow  in,  868 
chill  in,  869 
chronic,  863 

changes  in,  868 
complications  of,  875 

nervous,  876 
definition  of,  863 
distribution  of,  863 
etiology  of,  864 

mosquito  as,  864 
hemiplegia,  876 
hepatic  changes  in,  868 
intermittent,  863 
morbid  anatomy  of,  867 
nephritic  changes  in,  868 
pathology  of,  867 
pernicious,  863,  875 

symptoms  of,  875 
Plasmodium,  863 
prevention  of,  867 
quartan,  parasite  of,  866 
remittent,  863 
retinal  hemorrhages  in,  876 
sequelae  of,  875 
splenic  changes  in,  868 

enlargement  in,    876 
symptoms  of,  870 
tertian,  parasite  of,  865 
infection,  latent,  878 
Malformations,  congenital,  of  bowel,  624 

of  kidney,  696 
Malignant  anthrax  oedema,  259 
goitre,  749 

growths    of  gall-bladder    and    biliary 
ducts,  683 
of  spleen,  764 
of  vertebrse,  994 
Mali-maU,  1066 
Malta  fever,  245 

complications  of,  249 
definition  of,  245 
diagnosis  of,  247 
distribution  of,  245 
duration  of,  248 
etiology  of,  246 
fever  in,  247 
incubation  of,  247 
micrococcus  melitensis  in,  245 
pathology  of,  246 
prognosis  of,  248 
spleen  in,  246 
symptoms  of,  247 


Malta  fever,  treatment  of,  248 

Mania  in  ursemia,  722 

Marie's  cerebellar  hereditary  ataxia,  970 

disease,  837 
Measles,  108 

bacteriology  of,  109 

"black,"  112 

bronchitis  in,  110,  111 

bronchopneumonia  in,  110,  112 

chiU  in,  110 

complications  of,  112 
nervous,  113 

conjunctivitis  in,  113 

coryza  in,  110 

diagnosis  of,  113 

diarrhoea  in,  112 

diphtheria  in,  113 

distribution  of,  108 

eruption  of,  111 

etiology  of,  108 

fever  in,  111 

frequency  of,  110 

German,  115.     See  Rubella. 

hemorrhagic,   112 

incubation  of,  109 

keratitis  in,  113 

"Koplik's  spots"  in.  111 

meningitis  in,  113 

morbid  anatomy  of,  110 

noma  in,  112 

pathology  of,  110 

prevention  of,  109 

prognosis  in,  113 

respiratory  form  of,  111 

sequelae  of,  112 

stomatitis  in,  112 

symptoms  of,  110 

transmission  of,  mode  of,  109 

treatment  of,  114 

variations  of.  111 

vomiting  in,  112 

whooping-cough  in,  113 
Mediastinal        glands,      tuberculosis      of, 

300 
Mediastinopericarditis,  indurative,  463 
Mediastinum,  abscess  of,  452,  455 

carcinoma  of,  452 

dermoid  cyst  of,  453 

diseases  of,  452 

fibroma  of,  453 

hydatid  cyst  of,  453 

lymphadenoma  of,  452 

lymphoma  of,  452 

sarcoma  of,  452 

teratoma  of,  453 

tumors  of,  452 

abdominal  effusion  in,  454 
dropsy  in,  454 
dyspnoea  in,  454 
pain  in,  455 
symptoms  of,  453 
Medina  worm,  896 
Mediterranean  fever,  245 
Melanuria,  746 
Membranous  oesophagitis,  560 


1110 


INDEX 


Meniere's  disease,  1029 

treatment  of,  1030 
Meningeal  tuberculosis,  acute,  301 
Meningitis  in  acute  rheumatic  fever,  201 
basilar,  301 
cerebral,  946 

definition  of,  946 
etiology  of,  946 
cerebrospinal,   134 
in  croupous  pneumonia,  149,  159 
granular,  301 
in  influenza,   127 
in  measles,  113 
in  mumps,  118 
spinal,  997 

chronic,  999 

diagnosis  of,  999 
etiology  of,  999 
symptoms  of,  999         ^ 
treatment  of,  999 
definition  of,  997 
diagnosis  of,  998 
etiology  of,  997 
morbid  anatomy  of,  997 
pathology  of,  997 
prognosis  in,  998 
symptoms  of,  997 
treatment  of,  998 
in  typhoid  fever,  43,  44 
Meningoencephalitis,  950 
Mental  disturbances  in  influenza,  127 

state  in  chorea  minor,  1045 
Merycismus,  603 

in  hysteria,  1050 
Mesenteric  artery,   superior,   aneurysm  of, 
543 
glands,  tuberculosis  of,  300 
Metallic    tinkling    in    hydropneumothorax, 

451 
Metastatic  pneumonia,  408 
Micrococcus  lanceolatus  in  pneumonia,  143, 
147 
melitensis  in  Malta  fever,  245 
rheumaticus  in  acute  rheumatic  fever, 
198 
Microsporon  minutissimus  in  dhobie  itch, 

909 
Migraine,  1077 

definition  of,  1077 
fulgurating,  1078 
fulminant,  1078 
symptoms  of,  1078 
treatment  of,  1079 
Miliary  fever,  356 

definition  of,  356 
etiology  of,  357 
prognosis  in,  357 
symptoms  of,  357 
treatment  of,  357 
tubercle,  295 
tuberculosis,  acute,  297 
Milk,  infection  by,  in  typhoid  fever,  18 
sickness,  352 

definition  of,  352 
symptoms  of,  352 


Milk  sickness,  treatment  of,  352 
Miners'  ansemia,  887 
cachexia,  887 
disease,  887 
phthisis,  412 
Minor  epilepsy,  1061 
Mitral  regurgitation,  494 

blood-spitting  in,  497 
club-shaped  fingers  in,  497 
cyanosis  in,  497 
diagnosis  of,  498 
dyspnoea  in,  496 
oedema  in,  497 
pathology  of,  494 
physical  signs  of,  497 
prognosis  in,  498 
symptoms  of,  495 
objective,  497 
subjective,  496 
stenosis,  499 

definition  of,  499 
diagnosis  of,  503 

from  adhesive  pericarditis,  504 
from  Flint's  murmur,  503 
from  tricuspid  stenosis,  503 
etiology  of,  499 
pathology  of,  499 
physical  signs  of,  500 
prognosis  in,  504 
Mobius'  sign  in  exophthalmic  goitre,  753 
Monilia  Candida  in  thrush,  547 
Monoplegia  in  croupous  pneumonia,  160 

in  ursemia,  722 
MorbiUi,  108.     >See  Measles. 
Morbus  maculosus  neonatorum,  787 
Morphinism,  848 
chronic,  848 

symptoms  of,  848 
treatment  of,  849 
Morvan's  disease,  989 
Motor  neuritis,  1008 
Mountain  fever,  354 

Mouth  breathing  in   chronic  hypertrophic 
tonsillitis,  559 
diseases  of,  545 
dry,  551 

lesions  in  sprue,  243 
putrid  sore,  546 
Movable  kidney,  696 

spleen,  764 
Movements  in  chorea  minor,  1044 

in  paralysis  agitans,  1041 
Mucomembranous  enteritis,  637 
Mucous  colitis,  637 
patches,  550 

in  syphilis,  284,  286 
Muguet,  547 
Multiple  neuritis,  1007 
endemic,  249 
myoclonus,  1039 
sclerosis,  954 
serositis,  464 
Mumps,  117 

arthritis  in,  118 
complications  of,  117 


INDEX 


nil 


Mumps,  convulsions  in,  118 
definition  of,  117 
etiology  of,  117 
fever  in,  117 
incubation  of,  117 
meningitis  in,  118 
orchitis  m,  117 
pancreatitis  in,  118 
pathology  of,  117 
sequelae  of,  117 
symptoms  of,  117 
treatment  of,   118 
Mural  endocarditis,  482 
Musca  vomitoria,  912 

Muscle  changes  in  croupous  pneumonia,  149 
Muscles,  diseases  of,  1035 
Muscular  atrophy,  peroneal  type  of,  1037 
definition  of,  1037 
etiology  of,   1037 
morbid  anatomy  of,  1038 
pathology  of,   1038 
prognosis  in,  1038 
symptoms  of,  1038 
treatment  of,   1038 
in  apoplexy,  921 
progressive,  974,  1037 

Charcot-Marie-Tooth  form  of, 

1037 
neural,  of  Hoffman,  1037 
contractions  in  paramyoclonus  multi- 
plex, 1039 
dystrophies,   1035 

definition  of,  1035 
Erb's  juvenile,   1036 
etiology  of,  1035 
Landouzy-Dejerine  type  of,   1037 
morbid  anatomy  of,   1035 
pathology  of,  1035 
treatment  of,  1037 
rheumatism,  824 
rigidity  in  paralysis  agitans,  1042 

in  tetanus,  268 
spasm,  idiopathic,  1064 
tremors  in  typhoid  fever,  27 
Mycetoma,  275 

treatment  of,  276 
Mycotic  aneurysm,  534 

gastritis,  568 
Myelitis,  983 
acute,  983 

etiology  of,  983 
morbid  anatomy  of,  983 
paraplegia  in,  984 
pathology  of,  983 
prognosis  in,  985 
symptoms  of,  984 
treatment  of,  985 
ascending,  983 
central,  983 
chronic,  985,  988 

definition  of,  985 
diagnosis  of,  986 
etiology  of,  985 
morbid  anatomy  of,  986 
pathology  of,  986 


Myelitis,  chronic,  prognosis  in,  986 
symptoms  of,  986 
treatment  of,  986 
definition  of,  983 
descending,  983 
disseminated,  983 
subacute,  983 
transverse,  983 
Myelogenous  leukasmia,  780 
Myelomalacia,  987 
Myelopathic  albumosuria,  746 
Myiasis,  911 

intestinal,  912 
Myocarditis,  476 
acute,  476 
chronic,  476 
definition  of,  476 
Nauheim  baths  in,  478 
physical  signs  of,  477 
prognosis  in,  477 
in  rheumatic  fever,  acute,  201 
in  smallpox,  83 
symptoms  of,  477 
treatment  of,  477 
in  typhoid  fever,  35 
in  typhus  fever,  63 
Myocardium,  degeneration  of,  473 
amyloid,  474 
calcareous,  474 
fatty,  473 
hyaline,  474 
parenchymatous,  473 
prognosis  of,  475 
symptoms  of,  474 
disease  of,  473 
tuberculosis  of,  343 
Myoclonus,  1039.    See  Paramyoclonus  mul- 
tiplex, 
epilepticus,  1039 
multiple,  1039 
Myomalacia  cordis  in  syphilis,  281 
Myositis,  acute,  in  diphtheria,  175 

in  typhoid  fever,  45 
Myotonia  congenita,  1038 
definition  of,  1038 
symptoms  of,  1038 
Myriachit,  1066 
Mytilotoxismus,  856 

treatment  of,  856 
Myxoedema,  756 
congenital,  758 
definition  of,  756 
etiology  of,  756 
frequency  of,  757 
morbid  anatomy  of,  756 
pathology  of,  756 
prognosis  in,  757 
symptoms  of,  757 
treatment  of,  757 

thyroid  gland  in,  757 


N 


ASAL  catarrh,  atrophic,  366 
chronic,  365 
diphtheria,   178 


1112 


INDEX 


Nasha  fever,  245 

symptoms  of,  245 
Nauheim  baths  in  myocarditis,  478 
Neapolitan  fever,  245 
Nematodes,  884 
Neoplastic  goitre,  749 
Nephritic  changes  in  yellow  fever,  215 
Nephritis,  acute,  in  glandular  fever,  353 
caseative,  725 
in  cholera,  209 
desquamative,  chronic,  704 
diffuse,  acute,  700 

defhiition  of,  700 
diagnosis  of,  702 
etiology  of,  700 
morbid  anatomy  of,  700 
oedema  in,  701 
pathology  of,  700 
prognosis  of,  702 
symptoms  of,  701 
treatment  of,  702 
urine  in,  701 
chronic,  704 
in  diphtheria,  176 
exudatiA^e,  701 
glomerular,  700 
hemorrhagic,  701 
interstitial,  chronic,  703,  710 

hemorrhagic  glaucoma  in,  715 
Hirschberg's  vessels  in,  715 
pathology  of,  710 
prognosis  in,  716 
retinal  detachment  in,  715 

lesions  in,  714 
symptoms  of,  710 
cerebral,  713 
circulatory,  713 
respiratory,  713 
treatment  of,  717 
climatic,  718 
dietetic,  717 
medicinal,  717 
urine  in,  712 
parenchymatous,  chronic,  703,  704 
coma  in,  706 
definition  of,  703 
diagnosis  of,  707 
dropsy  in,  705 
etiology  of,  703 
frequency  of,  704 
morbid  anatomy  of,  705 
pathology  of,  705 
prognosis  in,  707 
retinitis  in,  706 
symptoms  of,  705 
treatment  of,  707 
dietetic,  707 
urine  in,  706 
in  scarlet  fever,  99,  102 
syphilitic,  281 
tubular,  chronic,  704 
in  typhoid  fever,  41 
in  varicella,  92 
Nephrolithiasis,  733 
colic  in,  735 


Nephrolithiasis,  definition  of,  733 
diagnosis  of,  735 

from  acute  appendicitis,  735 

from  gallstone  colic,  735 

from  hydronephrosis,  735 

from  neuralgia,  735 

from  twist  of  ureter,  735 
etiology  of,  733 
frequency  of,  734 
pathology  of,  733 
prognosis  in,  735 
symptoms  of,  735 
treatment  of,  736 
urine  in,  735 
Nerve,  abducens,  paralysis  of,  1022 
auditory,  diseases  of,  1028 
facial,  diseases  of,  1024 
glossopharyngeal,  paralysis  of,  1030 
hypoglossal,  diseases  of ,   1034 
oculomotor,  diseases  of,  1018 
olfactory,  diseases  of,  1012 
optic,  diseases  of,  1012 

paralysis  of,   1018 
pathetic,  paralysis  of,  1020 
trifacial,  paralysis  of,  1020 
vagus,  diseases  of  1030 
Nerves,  cranial,  diseases  of,  1012 
diseases  of,  1003 
inflammation  of,  1003 
Nervous  complications  of  acute  rheumatic 
fever,  201 

of  typhoid  fever,  43 
diseases,  functional,  1038 
disorders  of  gastric  secretion,  604 
eructation,   603 
exhaustion,  1068 
manifestations  in  influenza,  127 
system  in  diabetes  mellitus,  changes  in, 
793 

diseases  of,  913 
Neuralgia,  gastric,  603 
Neurasthenia,  1068 
definition  of,  1068 
diagnosis  of,  1069 
etiology  of,  1068 
prognosis  of,  1069 
symptoms  of,  1068 
treatment  of,  1069 
Neuritis,  1003 

cervicobrachial,  1006 

prognosis  in,  1006 

treatment  of,   1006 
in  croupous  pneumonia,  161 
definition  of,  1003 
diagnosis  of,  1004 
in  diphtheria,  176 
endemic  multiple,  249 
etiology  of,  1003 
interstitial,   1003 
morbid  anatomy  of,  1003 
motor,  1008 
multiple,  1007 

definition  of,  1007 

diagnosis  of,  1010 

etiology  of,  1007 


INDEX 


1113 


Neuritis,  multiple,  prognosis  in,  1010 
symptoms  of,  1007 
treatment  of,  1011 
obstetrical,  1007 
optic,  1012 

in  brain  tumor,  934 
in  chronic  lead  poisoning,  853 
symptoms  of,  1013 
treatment  of,  1014 
parenchymatous,  1003 
pathology  of,  1003 

periaxial,  of  Gombault  in  lead  poison- 
ing, 853 
peripheral,  1007 

in  chronic  arsenical  poisoning,  1009 
lead  poisoning,  853,  1009 
prognosis  in,  1004 
retrobulbar,   1013 
symptoms  of,  1004 
toxic,  in  influenza,  127 
treatment  of,  1004 
in  typhoid  fever,  44 
Neuroma  of  brain,  932 
Neuroretinitis,  albuminuric,  714 

in  syphilis,  285 
Neuroses,  gastric,  601 
of  heart,  521 
occupation,  1072 
traumatic,  1070 

definition  of,  1070 
etiology  of,  1071 
paralyses  in,  1071 
symptoms  of,  1071 
treatment  of,  1072 
Neurotic  atrophy,  1037 
Newborn,  hemorrhagic  affections  of,  786 

jaundice  in,  686,  786 
Nitric  acid  test  for  albumin  in  urine,  742 
Nodding  spasm,  1034 
Nodular  colitis,  638 
Nodules,  leprous,  348 
Noma,  548 

in  measles,  112 
Nose,  diseases  of,  363 
Nummular  sputum  in  tuberculosis,  316 
Nutrition,  diseases  of,  789 
Nystagmus  in  disseminated  sclerosis,  956 


OBESITY,  833 
definition  of,  833 
etiology  of,  833 
symptoms  of,  833 
treatment  of,  834 
dietetic,  835 
Obliterative  appendicitis,  617 
Obstetrical  neuritis,  1007 
Obstruction,  intestinal,  623 
Occupation  neuroses,  1072 
Ocular  complications  of  diabetes  mellitus, 
797 
muscles,    disturbances  of  motility   of, 

1022 
symptoms  in  apoplexy,  919 

in  disseminated  sclerosis,  956 


Ocular  symptoms  in  locomotor  ataxia,  962 
Oculomotor  nerve,  diseases  of,  1018 
paralysis  of,   1018 

diagnosis  of,  1019 
prognosis  in,  1019 
symptoms  of,  1019 
(Edema  in  acute  diffuse  nephritis,  701 
angioneurotic,  1075 
in  Hodgkin's  disease,  768 
of  larynx,  372 
of  limgs  in  cholera,  209 
malignant  anthrax,  259 
in  mitral  regurgitation,  497 
CEdematous  laryngitis,  372 
(Esophagismus,  562 
Qilsophagitis,  560 
chronic,  560 
membranous,  560 
in  typhoid  fever,  35 
(Esophagus,  cancer  of,  563 
prognosis  in,  563 
symptoms  of,  563 
treatment  of,  564 
dilatation  of,  561 
atonic,  562 
diagnosis  of,  562 
diffuse,  561 
dysphagia  in,  562 
etiology  of,  561 
localized,  561 
symptoms  of,  562 
treatment  of,  562 
diseases  of,  560 
spasms  of,  562 

treatment  of,  563 
stricture  of,  organic,  561 
annular,  561 
asymmetrical,  561 
cylindrical,  561 
multiple,  561 
single,  561 
symmetrical,  561 
symptoms  of,  561 
treatment  of,  561 
tuberculosis  of,  334 
ulceration  of,  in  typhoid  fever,  35 
Oidium  albicans  in  thrush,  547 
Olfactory  nerve,  diseases  of,  1012 
Ophthalmoplegia,  1023 
etiology  of,  1024 
externa,  1()23 
interna,   1023 
pathology  of,  1024 
symptoms  of,  1024 
treatment  of,  1024 
Opisthotonos  in  tetanus,  269 
Oppler-Boas  bacillus  in  gastric  cancer,  594 
Optic  atrophy,  1014 

in  diabetes  mellitus,  797 
diagnosis  of,  1015 
etiology  of,  1014 
in  locomotor  ataxia,  963 
pathology  of,  1014 
prognosis  in,  1015 
symptoms  of,  1014 


1114 


INDEX 


Optic  atrophy,  treatment  of,  1015 
nerve,  inflammation  of,  1012 
neuritis  in  brain  tumor,  934 

in  chronic  lead  poisoning,  853 
Orchitis  in  mumps,  117 
in  typhoid  fever,  42 
Oroya  fever,  361 
Orthostatic  albuminuria,  741 
Osteitis  deformans,  839 
Osteoarthritis,  818 

Osteoarthropathy,  pulmonary,    in  bronchi- 
ectasis, 387 
hypertrophic,  840 
in  pulmonary  tuberculosis,  318 
Osteoma  of  brain,  932 

in  lung,  428 
Osteomyelitis  in  typhoid  fever,  44 
Otitis  media,  acute,  in  typhoid  fever,  44 
in  croupous  pneumonia,  162 
in  scarlet  fever,  99,  103 
Ovaries,  tuberculosis  of,  342 
Ox-heart  in  aortic  regurgitation,  509 
Oxaluria,  745 
Oxyuris  vermicularis,  885 
Oysters,  infection  by,  in  typhoid  fever,  18 
Ozajna,  365,  366 


PACHYMENINGITIS,  947 
cervical,  hypertrophic,  996 
diagnosis  of,  947 
interna,  947 

morbid  anatomy  of,  948 
pathology  of,  948 
symptoms  of,  948 
morbid  anatomy  of,  947 
pathology  of ,  947 
prognosis  in,  947 
symptoms  of,  947 
treatment  of,  947 
Paget's  disease,  839 
Painters'  colic,  854 
Palpitation  of  heart,  521 
Palsy,  acute  infantile,  970 
birth,  1007 
hammerers',  1072 
scriveners',  1072 

shaking,  1040.     See  Paralysis  agitans, 
Pancreas,  adenoma  of,  695 
carcinoma  of,  695 
cystadenoma  of,  694 
cystic  epithelioma  of,  694 
cysts  of,  694 

hemorrhagic,  694 
hydatid,  694 
proliferation,  694 
pseudo-,  694 
retention,  694 
diseases  of,  687 
gumma  of,  695 
hemorrhages  into,  695 
sarcoma  of,  695 
tumors  of,  695 
Pancreatic  calculus,  693 

symptoms  of,  693 


Pancreatic  calculus,  treatment  of,  694 
cysts,  694 

diagnosis  of,  695 
prognosis  in,  695 
symptoms  of,  694 
treatment  of,  695 
tumors,  695 
Pancreatitis,  687 
acute,  687 

constipation  in,  689 
diagnosis  of,  689 

from  fulminating  appendicitis 

690 
from    intestinal    obstruction, 

689 
from  perforation  of  duodenum 
689 
of    gastric  ulcer,  689 
from  rupture  of  gall-bladder, 

690 
from    suppurative    cholecyst- 
itis, 690 
etiology  of,  687 
fat-necrosis  in,  688 
jaundice  in,  689 
morbid  anatomy  of,  688 
pathology  of,  688 
prognosis  in,  690 
symptoms  of,  688 
treatment  of,  690 
chronic,  687,  691 

diagnosis  of,  692 

from  cancer  of  head  of  pan- 
creas, 692 
from    gallstones    in    common 

duct,  692 
from  subphrenic  abscess,  692 
interacinar,  691 
interlobular,  691 
interstitial,  691 
intralobular,  691 
prognosis  in,  692 
symptoms  of,  692 
treatment  of,  693 
definition  of,  687 
gangrenous,   689 
hemorrhagic,  acute,  695 
in  mumps,  118 
subacute,  687 

symptoms  of,  690 
treatment  of,  691 
suppurative,  688 
Pani-Ghao,  889 
Papillary  endocarditis,  482 
Papillitis,  1013   ■ 

albuminuric,  714 
Papilloma  of  kidney,  732 
Paracentesis  abdominis  in  ascites,  653 

thoracic  in  pleurisy  with  effusion,  440, 
441 
Paracholecystitis,  675 
Paralysis  of  abducens  nerve,  1022 
agitans,   1040 

definition  of,  1040 
diagnosis  of,  1042 


INDEX 


1115 


Paralysis  agitans,  diagnosis  of,  from  multi- 
ple sclerosis,   1042 
from  senile  tremor,  1042 
etiology  of,  1040 
movements  in,  1041 
muscular  rigidity  in,  1042 
pathology  of,  1041 
prognosis  in,  1042 
symptoms  of,  1041 
treatment  of,  1042 
tremor  in,  1041 
ascending,  acute,  1000 

definition  of,  1000 
diagnosis  of,  1001 
•       etiology  of,  1000 

morbid  anatomy  of,  1000 
pathology  of,   1000 
prognosis  in,  1001 
symptoms  of,  1000 
treatment  of,  1001 
atrophic,  acute,  970 
of  bowel,  627 
in  brain  tumor,  934 
bulbar,  977 

apoplectiform,  913 
diagnosis  of,  977 
etiology  of,  977 
morbid  anatomy  of,  977 
pathology  of,  977 
prognosis  in,  977 
symptoms  of,  977 
treatment  of,  977 
cerebral,  infantile,  925 

convulsions  in,  927 
definition  of,  925 
deformities  in,  927,  928 
diagnosis  of,  928 

from    amaurotic    family 

idiocy,  929 
from    hereditary    spastic 
spinal  paralysis,  929 
etiology  of,  926 
lesions  in,  926 
morbid  anatomy  of,  926 
paralysis  in,  928 
pathology  of,  926 
prognosis  in,  929 
symptoms  of,  927 
in  diphtheria,  176,  178,  179 
of  facial  nerve,  1024 
gastrointestinal,  578 
general,  of  insane,  950 
glosso-labio-laryngeal,  977 
glossopharyngeal  nerve,   1030 
of  internal  and  external  muscles  of  eye- 
ball,  1023 
Landry's,   1000 
monoplegic,    in    croupous   pneumonia, 

160 
of  oculomotor  nerve,   1018 
of  pathetic  nerve,  1020 
periodical,  1083 

of  spinal  accessory  nerve,  1034 
atrophic,  chronic,  974 
infantile,  970 


Paralysis,  spinal  spastic,  syphilitic,  980 
of  trifacial  nerve,  1020 
in  whooping-cough,  122 
Paralytic  chorea,  1045 

dilatation  of  stomach,  578 
Paramyoclonus  multiplex,  1039 
definition  of,  1039 
diagnosis  of,  1040 

from  chorea.  1040 
from  electrical  chorea,  1040 
from  hysterical  spasm,  1040 
from  "maladie  des  tics  con- 
vulsifs,"  1040 
etiology  of,  1039 
muscular  contractions  in,  1039 
prognosis  in,  1040 
treatment  of,  1040 
Paraphasia,  931 

Paraplegia  in  acute  myelitis,  984 
ataxic,  hereditary,  967 
senile,  987 

symptoms  of,  987 
treatment  of,  987 
spastic,  978 
Parasites,  animal,  diseases  due  to,  863 
Parasitic  haemoptysis,  904 
infusoria,  909 
stomatitis,  547 
strumitis,  749 
Parasyphilitic  affections,  283 
Paratyphoid  fever,  59 

bacteriology  of,  59 
complications  of,  60 
diagnosis  of,  60 
intestinal  ulcers  in,  59 
pathology  of,  59 
prognosis  of,  61 
splenic  enlargement  in,  59 
symptoms  of,  60 
treatment  of,  61 
Parenchymatous     degeneration   of     heart, 
473 
goitre,  749 
neuritis,  1003 
Paresis,  950 

in  kubisagari,  362 
Parkinson's  disease,    1040      See    Paralysis 

agitans. 
Parotid  abscess,  551 

bubo,  551 
Parotitis,  epidemic,  117.     See  Mumps, 
in  cholera,  209 
chronic  indurative,  552 
in  croupous  pneumonia,  162 
in  scarlet  fever,  103 
suppurative  interstitial,  551 
in  typhoid  fever,  35 
Parry's  disease,  751 
Pathetic  nerve,  paralysis  of,  1020 

S3''mptoms  of,   1020 
Pectoriloquy,  319 
"  Peg"  teeth  in  syphilis,  286 
Peliomata  in  typhoid  fever,  32 
Peliosis  rheumatica,  786 
Pellagra,  857 


1116 


INDEX 


Pellagra,  cachexia  in,  858 
deiiaition  of,  857 
diarrhoea  in,  858 
eruption  in,  858 
etiology  of,  857 
pathology  of,  858 
symptoms  of,  858 
nervous,  858 
treatment  of,  859 
Pemphigus  contagiosus,  910 

neonatorum  in  sj-philis,  286 
Peptic  ulcer,  579 

Perforation  of  bowel  in  t5T)hoid  fever,  37,  38 
in  duodenal  ulcer,  629 

symptoms  of,  630 
in  empvema,  446 
of  gall-bladder,  680 
in  gastric  ulcer,  583 
Perforative  appendicitis,  617 
Pericardial  effusion  in  croupous  pneumonia , 
153 
diagnosis  of,  461 

from  aortic  aneur\^sm,  462 
from  cardiac  dilatation,  462 

hypertrophy,  462 
from  pleural  effusion,  462 
physical  signs  of,  461 
tuberculosis,  304 
"  Pericarditic  pseudo cirrhosis  of  liver,"  464 
Pericarditis,  acute,  457 

definition  of,  457 
diagnosis  of,  461 

from  phthisis,  461 
etiology  of,  457 
forms  of,  459 
frequency  of,  458 
pathology  of,  459 
physical  signs  of,  460 
prognosis  in,  462 
saddle-leather  sound  in,  460 
symptoms  of,  459 
treatment  of,  462 
chronic,  463 

adhesive,  463 

definition   of,   463 
diagnosis  of,  465 
pathology  of,  463 
physical  signs  of,  465 
prognosis  in,  466 
pulsus  paradoxus  in,  466 
symptoms  of,  465 
treatment  of,  466 
in  croupous  pneumonia,  149,  158 
in  erj'sipelas,  192 
externa  et  interna,  465 
in  rheumatic  fever,  acute,  201 
serofibrinous,  acute,  457 

symptoms  of,  461 
in  typhoid  fever,  34 
Pericardium,  diseases  of,  457 

tuberculosis  of,  304. 
Pericholecystitis,  675 
Perihepatitis,   665 
Perinephritic  abscess,  737 
Perineuritis,  1003 


Periodic  rhinitis,  367 
Periodical  paralysis,  1083 
Peripheral  neuritis,  1007 
Peristaltic  unrest,  602 
Peritoneal  abscess,  643 

tuberculosis,  304 
Peritoneum,  cancer  of,  649 
cystic  adenoma  of,  649 
diseases  of,  641 
hydatid  cyst  of,  649 
sarcoma  of,  649 
tuberculosis  of,  304 
Peritonitis,  acute,  641 

complications  of,  644 
definition  of,  641 
diagnosis  of,  645 

from  acute  hemorrhagic  pan- 
creatitis,  645 
from  gallstone  colic,  645 
from  hysteria,  645 
from    intestinal    obstruction, 

645 
from  perforation  of  stomach, 

645 
from  typhoid  fever,  645 
etiology  of,   641 
Hippocratic  fades  in,  644 
micro-organisms  in,  641 
morbid  anatomy  of,  642 
pathology  of,   642 
prognosis  in,  645 
sequelse  of,  644 
sjTnptoms  of,  643 
treatment  of,   646 

counterirritation  in,  647 
tympany  in,  644 
adhesive,  sclerotic,  chronic,  648 
in  amcebic  dysenter}',  232 
chronic,   647 
circumscribed,   643 
hemorrhagic,   643 
localized,   643 
loculated,  643 
putrid,  643 
in  scarlet  fever,  103 
septic,  642 
tuberculous,  304 
in  typhoid  fever,  36,  57 
diagnosis  of,  37 
Pernicious  anaemia,  777 

malarial  fever,  863,  875 
Pertussis,  119      See  Whooping-cough. 
Pestis  minor,  223 
Petechias  in  relapsing  fever,  68 
in  smallpox,   79 
in  typhoid  fever,  34 
in  typhus  fever,  64 
Petechial  fever,   134 
Petit  mal,   1061 

Peyer's  patches  in  typhoid  fever,  23 
Pharyngitis,  acute,  552 

definition  of,  552 
etiology  of,  552 
patholog}^  of,  553 
prognosis  in,  553 


INDEX 


1117 


Phatyngitis,  acute,  sjTnptoms  of,  553 
treatment  of,  553 
local,  554 
chrome,  555 

etiology  of,  555 
pathology  of,  555 
symptoms  of,  555 
treatment  of,  555 
croupous,  555 

etiology  of,  555 
treatment  of,  555 
follicular,  556 

etiology  of,  556 
treatment  of,  556 
phlegmonous,  554 
in  typhoid  fever,  34 
ulcerative,  554 

etiology  of,  554 
symptoms  of,  554 
treatment  of,  554 
Pharynx,  diseases  of,  552 

tuberculosis  of,  334 
Phlebosclerosis,  532 
Phlebitis  in  typhoid  fever,  35 
Phlegmonous  gastritis,  566 

pharyngitis,  554 
"Phosphatic  diabetes,"  745 
Phosphaturia,  745 
Phthisis,  syphilitic,  282 

ventriculi,  569 
Pianists'  cramp,  1072 
Pigeon-breast,  392 

in  chronic  hypertrophic  tonsUlitis,  559 
Pin-worm,  885 
Pistol-shot   sound   in   aortic  regurgitation, 

512 
Plagiomonas  urinaria,  909 
Plague,  219 

bacillus  of,  220 
bubonic,  219,  222 
buboes  in,  222 
fever  in,  222 

glandular  enlargements  in,  222 
symptoms  of,  222 
vomiting  in,  222 
definition  of,  219 
diagnosis  of,  225 
distribution  of,  219 
etiology  of,  220 
frequency  of,  222 
larval,  symptoms  of,  223 
mode  of  transmission  of,  221 
pathological  anatomy  of,  224 
pneumonic,  albuminuria  in,  223 
blood  changes  in,  223 
hemorrhage  in,  223 
relapses  in,  223 
sputum  in,  223 
symptoms  of,  223 
prognosis  in,  225 
prophylaxis  of,  223 
protective  inoculation  in,  224 
septicsemic,  symptoms  of,  223 
symptoms  of,  222 
treatment  of,  225 


Plasmodium  malarise,  863 
of  malarial  fever,  863 
Pleura,  diseases  of,  430 
Pleural  effusion,  436 
bloody,  449 
purulent,  443 
Pleurisy,  430 

chronic,  448 

definition  of,  448 
primitive  drj^  448 
in  croupous  pneumonia,  149,  156 
definition  of,  430 
dry,  430,  432 

cough  in,  434 
diagnosis  of,  434 

from  intercostal  neuralgia,434 
from  muscular   soreness,  434 
from    muscular    rheumatism, 
434 
fever  in,  434 
friction  sound  in,  433 

pleuropericardial,  433 
physical  signs  of,  433 
prognosis  in,  435 
symptoms  of,  433 
treatment  of,  435 
etiology  of,  430 
fibrinous,  430 
forms  of,  430 
frequency  of,  432 
in  influenza,  127 
purulent,  430 

in  er3-sipelas,  192 
serofibrinous,  430 
in  smallpox,  83 
tuberculous,  303,  430 
in  t3^phoid  fever,  43 
with  efi'usion,  436 

cytoscopy  in,  440 
diagnosis  of,  438 

from    hydatid     cyst     of 

liver,  439 
from  hj^ostatic   conges- 
tion, 439 
from      new-growths      in 

lung,  439 
from  pleurisy  -with  thick- 
ening, 439 
from  pneumonia,  439 
from  pneumothorax,  439 
from  pulmonars'  oedema, 

439 
from  subphrenic  abscess, 

439 
from  tubercular  consoli- 
dation, 439 
duration  of,  438 
dyspnoea  in,  437 
paracentesis  thoracis  in,  440, 

441 
physical  signs  of,  437 
posture  in,  437 
prognosis  in,  440 
sjrmptoms  of,  436 
treatment  of,  440 


1118 


INDEX 


Pleurisy  with  effusion,  treatment  of.  blisters 
in,  442 
diaphoretics  in,  442 
diuretics  in,  442 
purges  in,  442 
tapping  in,  441 
Pleuritis,  430.     See  Pleurisy. 
Plumbism,  851.     See  Lead  poisoning. 
Pneumogastric  nerve,  disease  of,  1030 
symptoms  of,  1032 
treatment  of,  1032 
Pneumonia,  aspiration,  398 
catarrhal,  397 
croupous,  143 

abscess  in,  148,  162 
aphasia,  transitory,  in,  160 
arthritis  in,  161 
brain  softening  in,  160 
bronchiectasis  in,  158 
bronchitis  in,  149 
cardiac  changes  in,  149 
in  cerebrospinal fe^er,  139 
chill  in,  150 
complications  of,  156 
congestion  of  lung  in,  147 
convulsions  in,  155 
cough  in,  151 
crisis  in,  155 

protracted,  156 
cyanosis  in,  151 
definition  of,  143 
delirium  in,  152,  154 
diagnosis  of,  163 

from  acute  pulmonary  tuber- 
culosis,  163 
from  appendicitis,  163 
from  catarrhal  pneumonia,  163 
from  hypostatic  congestion  cf 

lung,   163 
from   pleurisy   with   effusion, 

163  • 

from    pulmonary    infarction, 
163 
distribution  of,  145 
duration  of,  162 
dyspnoea  in,   151 
embolism  in,  161 
empyema  in,  157 
endocarditis  in,  149,  159 
engorgement  of  lung  in,  147 
etiology  of,  144 
frequency  of,   146 
gangrene  in,  148,  162 
gray  hepatization  in,  147 
hsemoglobinuria  in,  155 
headache  in,  151 
hemiplegia  in,  159 
hemiplegie  pneumonique,  160 
hepatic  changes  in,  149 
hepatization  in,  gray,  147 

red,   147 
herpes  in,  151 

hydropneumothorax  in,   157 
incubation  of,  150 
in  infants,  146 


Pneumonia,  croupous,  insomnia  in,  155 

jaundice  in,  155 

meningitis  in,  149,  159 

micrococcus   lanceolatus   in,    143, 
145 

monoplegia  in,  160 

morbid  anatomy  of,  147 

muscle  changes  in,   149 

nephritic  changes  in,  149 

nervous  symptoms  of,  154 

neuritis  in,  161 

otitis  media  in,  162 

pain  in,   150 

paralysis,  monoplegic,  160 

parotitis  in,  162 

pathology  of,  147 

pericardial  effusion  in,  153 

pericarditis  in,  149,  158 

physical  signs  of,  in  first  stage,  151 
in  well-developed   stage,    152 

pleurisy  in,  149,  156 

pneumococcus  of  Fraenkel,  143 

prevention  of,  146 

prognosis  in,  163 

pseudocrisis  in,  156 

pulse  in,  150,  151,   152 

rales  redux  in,  156 

red  hepatization  in,  147 

relapse  in,  162 

renal  changes  in,  149 

respirations  in,  150,  151 

sputum  in,  151 

sweating  in,  155 

symptoms  of,  150 

in  developed  stage,  151 
in  stage  of  onset,  150 
of  resolution,  155 

tongue  in,   154 

treatment  of,  166 

tympanites  in,  154 

unusual  changes  in  lung  in,  148 

urine  in,  153 

varieties  of,  162 

venous  thrombosis  in,  162 
fibrinous,   143 
in  influenza,   127 
lobar,  143 
lobular,  397 
metastatic,  408 

abscess  in,  410 

definition  of,  408 

embolism  in,  409 

etiology  of,  409 

pathology  of,  409 

prognosis  in,  411 

sputum  in,  409 

symptoms  of,  410 

treatment  of,  411 
pysemic,  410 
in  typhoid  fever,  29,  41 
Pneumonic  plague,  symptoms  of,  223 
Pneumonitis,   143 
Pneumonoconiosis,  411 
definition  of,  411 
etiology  of,  411 


INDEX 


1119 


Pneumonoconiosis,  pathology  of,  412 
prognosis  in,  412 
symptoms  of,  412 
treatment  of,  412 
Pneumopericardium,  467 

bacillus  aerogenes  capsulatus  in,  467 
prognosis  of,  468 
symptoms  of,  467 
treatment  of,  468 
Pneumothorax,  449 
definition  of,  449 
diagnosis  of,  451 

from  diaphragmatic  hernia,  451 
from  emphysema,  451 
from  pyopneumothorax  subphren 
icus,  451 
dyspnoea  in,  450 
etiology  of,  450 
physical  signs  of,  450 
prognosis  in,  451 
in  pulmonary  tuberculosis,  318 
symptoms  of,  450 
syncope  in,  451 
treatment  of,  452 
in  whooping  cough,  122 
Podagra,  808 
Poisoning,  alcoholic,  843 
acute,  843 
chronic,  844 
arsenical,  850 
by  cheese,  857 
by  coast  orach,  860 
by  ergot,  856 
by  fermented  maize,  857 
by  fish,  856 
food,  855 

by  gingko  tree,  861 
by  impure  milk,  857 
lacquer,  860 
lead,  acute,  851 
chronic,  851 
by  meat,  856 
morphine,  chronic,  848 
by  mussels,  856 
Poker  back,  821 
Polioencephalitis     superior    of     Wernicke, 

945 
Poliomyelitis,  983 

anterior,  acute,  970 

convulsions  in,  972 
definition  of,  970 
diagnosis  of,  973 
in  diphtheria,  1 76 
etiology  of,  970 
morbid  anatomy  of,  971 
paralysis  in,  972 
pathology  of,  971 
prognosis  in,  973 
symptoms  of,  972 
treatment  of,  973 
chronic,  974 

Aran-Duchenne  type  of,   975 
claw-hand  in,  975 
definition  of,  974 
diagnosis  of,  976 


Pohomyelitis,   anterior,  chronic,  diagnosis 
of,   from    amyotrophic 
lateral  sclerosis,  976 
from  muscular  dystrophy 

976 
from  neuritis,  976 
from  syringomyelia,   976 
drop-foot  in,  975 
etiology  of,  975 
morbid  anatomy  of,  975 
pathology  of,  975 
prognosis  in,  976 
symptoms  of,  975 
treatment  of,  976 
Polyneuritis,  1007 
Polyuria  in  typhoid  fever,  42 
Porencephaly,  926 
Pork-worm,  901 
Portal  vein,  thrombosis  of,  666 
Porto  Rican  anaemia,  887 
Posture  in  pleurisy  with  effusion,  437 
Potassium  ferrocyanide  test  for  albumin  in 

urine,  742 
Potters'  rot,  411 
Pox,  276 

Pregnancy,  typhoid  fever  complicating,  45 
Prevention  of  tetanus,  268 
Primitive  dry  pleurisy,  448 
Proctitis,  epidemic  gangrenous,  239 
Progressive  muscular  atrophy,  974 
Proliferation  cysts  of  pancreas,  694 
Prophylaxis  against  diphtheria,  182 

plague,  223 
Pseudoangina  in  hysteria,  1050 
Pseudocrisis  in  croupous  pneumonia,  156 
Pseudocysts  of  pancreas,  694 
Pseudohydrophobia,  265 
Pseudoleuksemia,  767 
Pseudolyssaphobia,  265 
Pseudomembranous  colitis,  639 

pyelonephritis,  726 
Pseudomuscular  hypertrophy,  1035 

prognosis  in,  1036 
Pseudotabes,  arsenical,  851 
Psilosis,  242 
Psoriasis,  buccal,  550 
Psorospermiasis,  879 
Ptosis  in  kubisagari,  362 
Ptyalism,  550 
Puerperal  eclampsia,  1063 
"  Puking  fever,"  352 
Pulex  penetrans,  911 
Pulmonary  abscess,  423 

diagnosis  of,  424 
etiology  of,  423 
multiple,  423 
prognosis  in,  425 
in  septicaemia,  195 
symptoms  of,  424 
treatment  of,  425 
in  typhoid  fever,  41 
complications  of  rheumatic  fever,  acute 

200 
congestion,  425 

in  influenza,  127 


1120 


INDEX 


Pulmonarj'  emphysema,  413 
gangrene,  420 

in  bronchiectasis,  387 
cedema  in  cholera,  209 
osteoarthropathy  in  bronchiectasis,  378 
hypertrophic,  840 
in  pulmonary  tuberculosis,  318 
regurgitation,  516 
stenosis,  516 
tuberculosis,  309 
valves  of  heart,  diseases  of,  515 
Pulsus  paradoxus  in  chronic  adhesive  peri- 
carditis, 466 
Purpura,  785 

causes  of,  785 
fulminating,  786 
htematemesis  in,  605 
hemorrhagica,  786 
Henoch's,  786 
micro-organisms  in,  785 
in  rheumatic  fever,  acute,  201 
rheumatica,  786 
treatment  of,  787 
Purulent  pericarditis,  459 
pleural  effusion,  443 
pleurisy,  430 
Pus  in  urine,  744 
Putrid  fever,  61 

peritonitis,  643 
sore  mouth,  546 
Pyaemia,  193.     See  Septicaemia. 

gonorrhoeal,   186 
Pygemic  abscess  of  liver,  653 

pneumonia,  410 
Pyelitis,  725 
Pyelonephritis,  725 
catarrhal,  726 
definition  of,  725 
diagnosis  of,  727 

from  aneurysm,  728 
from  malarial  fever,  727 
from  perinephritic  abscess,  727 
from  suppurative  cystitis,  727 
from  typhoid  fever,  727 
etiology  of,  725 
gangrenous,  726 
micro-organisms  in,  725 
morbid  anatomy  of,  726 
pathology  of,  726 
prognosis  in,  728 
pseudomembranous,  726 
suppurative,  726 
symptoms  of,  727 
treatment  of,  728 
Pylephlebitis,  suppurative,  666 
Pylorospasm,  602 

Pylorus,  stenosis  of,  congenital,  595,  597 
hypertrophic,  595 

definition  of,  595 
diagnosis  of,  596 

from  cicatricial    contrac- 
tion, 597 
from  gastric  cancer,  596 
etiology  of,  596 
piorbid  anatomy  of,  596 


Pylorus,  stenosis  of,  hvpertrophic.prognosis 

of,  598 
symptoms  of,  596 
treatment  of,  598 
Pyopericardium,  459 
Pyonephritis,  725 
Pyonephrosis,  725 

in  tuberculosis  of  kidney,  342 
Pyopneumothorax,  449 
Pyuria,  744 

treatment  of,  744 
in  typhoid  fever,  42 


QUARTAN  parasite   of    malarial  fever, 
866 
Quincke's  pulse  in  aortic  regurgitation,  510 

RABIES,  261 
dumb,  264 
Rachitic  rosary,  827 
Rachitis,  825 
Ragweed  fever,  367 

Rales  redux  in  croupous  pneumonia,  156 
Rashes  in  smallpox,  79 
Ray  fungus  in  actinomycosis,  273 
Raynaud's  disease,  1075 

definition  of,  1075 

etiology  of,  1075 

gangrene  in,  1075 

treatment  of,  1075 
Rectal  crises  in  locomotor  ataxia,  962 
Rectum,  tuberculosis  of,  336 
Red-light  treatment  of  smallpox,  87 
Reflexes  in  apoplexy,  919 
Regurgitation,  aortic  508 
mitral,  494 
pulmonary,  516 
tricuspid,  513 
Relapse  in  croupous  pneumonia,  162 
Relapsing  fever,  68 

chill  in,  69 

crisis  in,  70 

definition  of,  68 

delirium  in,  70 

distribution  of,  68 

etiology  of,  68 

fever  in,  70 

history  of,  68 

incubation  in,  68 

jaundice  in,  69 

morbid  anatomy  of,  68 

pathology  of,  68 

petechise  in,  68 

prognosis  of,  70 

relapse  in,  68 

spirillum  in,  68 

spleen  in,  68 

symptoms  of,  69 

treatment  of,  70 

vomiting  in,  69 
Remittent  fever,  bilious,  874 
complications  of,  875 
diagnosis  of,  877 


INDEX 


1121 


Remittent  fever,  hsemoglobinuria  in,  875 
sequelse  of,  875 
symptoms  of,  874 
treatment  of,  877 
Renal  artery,  aneurysm  of,  543 
asthma,  391 
calculus,   733 

changes  in  croupous  pneumonia,  149 
colic,  735 

disease,  acute,  in  typhoid  fever,  30 
tuberculosis,  341 
Respiratory  system,  diseases  of,  363 
Retention  cyst  of  pancreas,  694 
Retinal  hemorrhages  in  malarial  fever,  87  G 
lesions  in' chronic  interstitial  nephritis, 
714 
Retinitis,  albuminuric,  in  chronic  parenchy- 
matous nephritis,  706 
degenerative,  714 
hemorrhagic,  714 
in  puerperal  eclampsia,  1063 
typical,  714 
diabetic,  797 
Retrobulbar  neuritis,  1013 
Retro  cedent  gout,  815 
Retrograde  intussusception  of  bowel,  625 
Rheumatic  fever,  acute,  196 
arthritis  in,  199 
bacteriology  of,  198 
chorea  in,  201 
complications  of,  200 
definition  of,  196 
delirium  in,  201 
-    diagnosis  of,  201 

from  arthritis,  acute,  202 

septic,  202 
from  gonorrhoeal  rheum- 
atism, 202 
from    monoarticular    in- 

fianunation,  202 
from  osteomyelitis,  acute, 
202 
distribution  of,  196 
duration  of,  200 
endocarditis  in,  200 
etiology  of,  197 
joints  in,  199 
meningitis  in,  201 
micrococcus  rheumaticus,  198 
morbid  anatomy  of,  198 
myocarditis  in,  201 
pericarditis  in,  200,  201 
prognosis  of,  202 
pulmonary    complications  in, 

201 
purpura  rheumatica  in,  201 
rheumatic  nodules  in,  201 
sweating  in,  199 
symptoms  of,  199 
tongue  in,  199 
treatment  of,  202 
urine  in,  199 
urticaria  in,  201 
Rheumatism,    acute     articular,    196.     See 
Rheumatic  fever,  acute,  yf/ 
71 


Rheumatism,  chronic,  823 
definition  of,  823 
etiology  of,  823 
morbid  anatomy  of,  823 
symptoms  of,  823 
treatment  of,  823 

gonorrhoeal,   187 

muscular,  824 

treatment  of,  824 
Rheumatoid  arthritis,  818 

in  bronchiectasis,  386 
Rhinitis,  atrophic,  365 

hypertrophic,  365 

periodic,  367 

syphilitic,  286 
Rice-water  stools  in  Asiatic  cholera,  208 
Rickets,  825 

bossy  frontals  in,  827 

chicken-breast  in,  828 

definition  of,  825 

dentition  in,  828 

diagnosis  of,  828 

etiology  of,  825 

Harrison's  groove  in,  828 

morbid  anatomy  of,  826 

prognosis  in,  829 

symptoms  of,  827 

treatment  of,  829 
Ringworms,  909 
Risus  sardonicus  in  epilepsy,  1054 

in  tetanus,  269 
Rock  fever,  245 

Romberg's  symptom  in  locomotor  ataxia,961 
Rose  cold,  367 

rash  in  rubella,  116 

spots  in  typhoid  fever,  28 
Roseola,  epidemic,  115 

in  syphilis,  283 
Rotch's  sign  of  pericardial  effusion,  461 
Rotheln,  115.     See  RubeUa. 
Round-worm,  884 
RubeUa,  115 

definition  of,  115 

diagnosis  of,  116 

from  measles,  116 
from  scarlet  fever,  116 

eruption  in,  116 

etiology  of,  116 

Forchheimer's  spots  in,  116 

glandular  enlargements  in,  116 

incubation  of,  116 

prognosis  in,  116 

"rose  rash"  of,  116 

symptoms  of,  116 

treatment  of,  116 
Rubeola  notha,  115 
Running  amok,  1066 
Rupture  of  spleen,  764 
Russian  tapeworm,  901 


ST.  ANTHONY'S  FIRE,"  189 
St.  Gothard's  tunnel  disease,  887 
St.  Vitus'  dance,  1043 
Saccharomyces  albicans  in  thrush,  547 


1122 


INDEX 


Sacculated  aneurysm,  534 

Saddle-leather  sound  in  acute  pericarditis, 

460 
Salivary  glands,  diseases  of,  550 

functional  disorders  of,  550 
inflammation  of,  551 
Salivation,  550 
Sand  flea,  911 
Sanduhrmagen,  598 

Sansom's  sign  of  pericardial  effusion,  461 
Sarcoma  of  brain,  932,  933 
of  kidney,  732 
of  liver,  668 
in  lung,  428 
of  mediastinum,  452 
of  pancreas,  695 
of  peritoneum,  649 
of  thyroid  gland,  751 
Saturnine  epilepsy,  853 
Scarlatina,  93 
Scarlet  fever,  93 

bacteriology  of,  95 
bronchopneumonia  in,  103 
"collar  of  brawn"  in,  99 
complications  of,  102 
definition  of,  93 
desquamation  in,  104,  108 
^diagnosis  of,  103 

from  erythema  scarlatiniform, 

104 
from  German  measles,  104 
from  nephritic  eruption,  104 
from  rash  of  sepsis,  105 
from  rose  rash  of  indigestion, 

104 
from  syphilitic  rash,  104 
distribution  of,  93 
eruption  in,  100 

peculiarities  of,  100 
etiology  of,  93 
fulminant  form  of,  102 
glandular  enlargements  in,  99,  103 
hybrid,  115 

liyperhsemocytosisin,  99 
incubation  period  of,  99 
kidneys  in,  99,  102 
malignant,  101 
morbid  anatomy  of,  98 
mortality  of,  105 
nephritis  in,  99,  102 
otitis  in,  99,  103 
parotitis  in,  103 
pathology  of,  98 
peritonitis  in,  103 
prognosis  of,  105 
prophylaxis  of,  97 
septic  arthritis  in,  103 

infections  in,  99 
sequelse  of,  102 
sore  throat  in,  99,  100,  101 
■"strawberry  tongue"  in,   104 
■suppression  of  urine  in,  101 
surgical,   102 
treatment  of,  105 
hygienic,  105 


Scarlet  fever,  valvular  disease  of  heart  in,103 

vomiting  in,  99 
"Schluck-pneumonie,"  398 
Schonlein's  disease,  786 
Scleroderma,  840 

treatment  of,  840 
Sclerosis,  disseminated,  954 

Argyll-Robertson  pupil  in,  956 
definition  of,  954 
diagnosis  of,  957 

from    general    paralysis    of 

insane,  957 
from  hysteria,  957 
from  locomotor  ataxia,  957 
from  paralysis  agitans,  957 
from  spastic  paraplegia,  957 
etiology  of,  954 
morbid  anatomy  of,  955 
nystagmus  in,  956 
pathology  of,  955 
prognosis  in,  957 
symptoms  of,  955 
treatment  of,  957 
insular,  954 
lateral,  978 

amyotrophic,  980 

Babinski  reflex  in,  981 
definition  of,  980 
diagnosis  of,  982 

from  bulbar  paralysis,  982 
from  syringomyelia,  982 
etiology  of,  980 
pathology  of,  980 
prognosis  in,  982 
symptoms  of,  981 
treatment  of,  982 
ankle  clonus  in,  979 
Babinski  reflex  in,  979 
definition  of,  978 
diagnosis  of,  979 
etiology  of,  978 
morbid  anatomy  of,  978 
pathology  of,  978 
prognosis  in,  979 
Striimpell's  family  type  of,  978 
symptoms  of,  978 
treatment  of,  979 
multiple,  954 
Sclerotic  kidney,  710 
Scorbutus,  830 
Screw-worm,  911 

treatment  of  infection  by,  912 
Scriveners'  palsy,  1072 
Scrofula,  299 
Scurvy,  830 

definition  of,  830 
etiology  of,  830 
infantile,  831 
morbid  anatomy  of,  830 
pathology  of,  830 
symptoms  of,  831 
treatment  of,  832 
Seat-worm,  885 
Secondary  anaemia,  773 
Secretion,  gastric,  nervous  disorders  of,  604 


INDEX 


1123 


Secretion,    gastric,    nervous     disorders    of, 

treatment  of,   604 
Segmentation  of  heart  muscle,  474 
Senile  emphysema,  413 

paraplegia,  987 
Sepsis  in  empyema,  446 
Septic  arthritis  in  scarlet  fever,  103 
in  smallpox,  83 

peritonitis,   642 

pneumonia,  409 
Septicaemia,   193 

anaemia  in,  194 

blood  in,  194 

chill  in,  194 

chronic,  195 

definition  of,  193 

diagnosis  of,  195 

empyema  in,  195 

etiology  of,   193 

infarction  of  spleen  in,  195 

morbid  anatomy  of,   193 

pathology  of,  193 

pulmonary  abscess  in,  195 

subacute,  195 

suppuration  of  kidney  in,  195 

sweating  in,  194 

symptoms  of,  194 

treatment  of,  196 
Septicsemic  plague,  symptoms  of,  223 
Serofibrinous  pericarditis,  acute,  459,  461 

pleurisy,  430 
Serositis,  multiple,  465 
Serous  diarrhoea,  608 

membranes,  tuberculosis  of,  301 
Serum,  antirabic,  265 

antitubercle,  331 

treatment   of   ulcerative   endocarditis, 
488 
Seven  days'  fever,  68 
Sewing  spasm,  1072 

Shaking  palsy,  1040.    See  Paralysis  agitans 
Shiga's  bacillus  in  dysentery,  230 
Ship  fever,  61 
Siderosis,  411 
Simla  diarrhoea,  241 
Sitotoxismus,  856 
Skin  changes  in  typhoid  fever,  32 

eruptions,  syphilitic,  283,  286 

gangrene  of,  in  smallpox,  83 

in  Hodgkin's  disease,  768 

pigmentation  of,  in  Addison's  disease, 
761 
Skodaic  resonance  in  hydropneumothorax, 

451 
Sleeping  sickness,  879,  881 
diagnosis  of,  883 
etiology  of,  882 
pathology  of,  882 
prognosis  in,  883 
symptoms  of,  882 
treatment  of,  883 
"Slows"  in  cattle,  352 
Smallpox,  70 

aberrant  manifestations  of,  81 

abscesses  in,  82 


Smallpox,  aphonia  in,  8 
backache  in,  77 
bed-sores  in,  83 
black,  81 
bronchitis  in,  83 
bronchopneumonia  in,  83 
complications  of,  82 
confluent,  81 
cytoryctes  vaccinae  in,  71 
deafness  in,  83 
definition  of,  70 
delirium  in,  79 
diagnosis  of,  84 

from  chickenpox,  84 

from  measles,  84 

from  scarlet  fever,  84 

from  syphilides,  84 
distribution  of,  71 
earache  in,  83 
endocarditis  in,  83 
eruption  in,  75,  77 

development  of,  77 

forms  of,  78 

on  mucous  membrane,  79 

stages  of,  78 

variations  in,  79,  80 
erysipelas  in,  83 
etiology  of,  71 
forms  of,  81 
frequency  of,  73 
gangrene  of  skin  in,  83 
haematemesis  in,  605 
headache  in,  77 
hemorrhagic,  81 
history  of,  70 
incubation  of,  72 
laryngitis  in,  83 

mode  of  spreading  contagion,  71 
morbid  anatomy  of,  75 
myocarditis  in,  83 
pathology  of,  75 
pericarditis  in,  83 
pleurisy  in,  83 
in  pregnancy,  83 
prevention  of,  73 
prognosis  of,  85 
rashes  in,   79 
septic  arthritis  in,  83 
sequelae  of,  82 
symptoms  of,  77 
treatment  of,  86 

red-light,  87 
urine  in,  77 

vaccination  as  a  preventive,  73,  88 
varioloid,  82 
Smokers'  tongue,  550 
"Snuffles,"  286 
Soor,  547 

Sore  throat,  clergj^men's,  555 
in  diphtheria,  177 
in  scarlet  fever,  99,  100,  101 
ulcerated,  554 
Spasm,  facial,  1027 

muscular,  idiopathic,  1064 
nodding,  1034 


1124 


IXDEX 


Spasm  of  oesophagus,  562 

sewing,  1072 
Spasmodic  croup,  374 
laryngitis,  374 
wryneck,  1033 
Spasmus  nutans,   1034 
Spastic  diplegia,  926 
hemiplegia,  925 
paraplegia,   978 
Speech  in  Friedreich's  ataxia,  969 
Spinal  accessor}^  nerve,  disease  of,  1032 
symptoms  of,  1033 
paralysis  of,   1034 
cord,  compression  of,  993 
by  aneurysm,  995 
definition  of,  993 
by  disease  of  vertebrse,  993 
diagnosis  of,  994 
prognosis  in,  994 
symptoms  of,  994 
treatment  of,   994 
etiologj-  of,  993 

by    hypertrophic    cen.-ical 
pachymeningitis,  996 
symptoms  of,  996 
treatment  of,   996 
by  malignant  gro-vs^ths,  994 
hemorrhage  into,  990 
definition  of,  990 
diagnosis  of,  991 
prognosis  in,  991 
symptoms  of,  990 
treatment  of,  991 
inflammation  of,   983 
syphilis  of,  285,  286 
tuberculosis  of,  343 
epilepsy,  1039.       See    Paramyoclonus 

multiplex, 
membranes,  hemorrhage  into,  991 
definition  of,  991 
etiology  of,  991 
extrameningeal,  991 
intrameningeal,  991 
prognosis  in,  993 
symptoms  of,  992 
treatment  of,  993 
meningitis,   997 

chronic,  999 
paralysis,  atrophic,   chronic,  974 
infantile,  970 
spastic,  syphilitic,  980 
syphilis,  285,  "286 
Spirillum  cholerse  Asiatica,  204 

of  relapsing  feyer,  68 
Splanchnoptosis,  632 
Spleen,  abscess  of,  764 
diseases  of,  764 
in  diphtheria,  176 
enlargement  of,  in  paratyphoid  feyer, 

59^ 
in  hepatic  cirrhosis,  764 
hydatid  cj'st  of,  764 
infarct  of,  764 

in  septicfemia,  195 
in  malarial  feyer,  764 


Spleen  in  malarial  feyer,  changes  in,  868 
malignant  growths  of,  764 
in  ilalta  feyer,  246 
moyable,   764 
in  relapsing  feyer,  68 
rupture  of,  764 
in  splenic  ansemia.  765 
in  splenomedullary  leukaemia,  764,  782 
in  typhoid  feyer,  25,  27,  3o,  764 
in  typhus  feyer,  63 
wandering,   764 

treatment  of,  765 
Splenic  anaemia,  765 

artery,  aneur\'sm  of,  543 
Splenization  of  lung,  426 
Splenomedullary-  leukaemia,  780,  781 
Splenomegaly,  tropical,  883 
Spondylitis  deformans,  821  ■ 

rhizomelique,  821 
Spotted  feyer,  61,  134,  354 
Sprue,  242 

anaemia  in,  244 
definition  of,  242 
diagnosis  of,  244 
diarrhoea  in,  243 
etiolog}-  of,  242 
flatulence  in,  243 
mouth  lesions  of,  243 
•pathology  of,   242 
predisposing  causes  of,  242 
prognosis  in,  244 
symptoms  of,  243 
tongue  in,  243 
treatment  of,  244 
Sputum  in  bronchial  asthma,  392 
in  bronchiectasis,  385 
in  croupous  pneumonia,  151 
in  distomatosis  of  lung,  908 
in  metastatic  pneumonia,  409 
in  pneumonic  plague,  223 
in  pulmonary  gangrene,  422 
tuberculosis,   315,  316 

microscopic    examination   of, 
322 
Squint  in  chronic  lead  poisoning,  853 
St.  Anthony's  fire,  189 
St.  Gothard's  tunnel  disease,  887 
St,  Vitus'  dance,  1043.     See  Chorea  minor. 
Status  epilepticus,  1056 
Ijmiphaticus,  770 

definition  of,  770 
etiology  of,  770 
morbid  anatomy  of,  770 
pathology  of,   770 
sjTnptoms  of,  771 
tetany  of,  771 
treatment  of,   771 
Stelwag's  sign  in  exophthalmic  goitre,  753 
Stenosis,  aortic,  504 
mitral,  499 
pulmonary,  516 
of  pylorus,  congenital,  595,  597 

hypertrophic,  595 
tricuspid,  515 
Still's  chsease,  821 


INDEX 


1125 


Stokes-Adams  syndrome,  475 
Stomach,  bilocular,  598 
cancer  of,   588 

dilatation  of,  572.     See  Gastric  dilata- 
tion, 
paralytic,  578 
diseases  of,  564 
hemorrhage  from,   604 
hour-glass,  598 

definition  of,  598 
etiology  of,  599 
morbid  anatomy  of,  599 
pathology  of,  599 
physical  signs  of,  599 
symptoms  of,  599 
treatment  of,  601 
Woelfier's  "first  sign"  in,  599 
"second  sign"  in,  600 
hypersesthesia  of,  603 
symptoms  of,  603 
lymphatic  areas  of,  590 
neuroses  of,  601 
ulcer  of,  579.    See  Gastric  ulcer. 
Stomatitis,  545 
aphthous,  546 
catarrhal,  545 

prognosis  of,  546 
symptoms  of,  545 
definition  of,  545 
fetid,  546 
follicular,  546 
gangrenous,  548 

symptoms  of,  549 
treatment  of,  549 
in  measles,   112 
parasitic,  547 

monilia  Candida  in,  547 
oidium  albicans  in,  547 
prognosis  in,  548 
saccharomyces  albicans  in,  547 
symptoms  of,  547 
treatment  of,  548 
ulcerative,  546 

treatment  of,   546 
vesicular,  546 
Stone  in  kidney,  733 
Stools  in  cholera,  208 
in  dysentery,  233 
Strangulation,  internal,  of  bowel,  624,  626 
"  Strawberry  tongue"  in  scarlet  fever,  104 
Streptococcus  erisipelatus,  189 
Streptothrix  actinomyces,  273 
Stricture  of  bowel,  623 

of  oesophagus,  organic,  561 
Strongyloides  intestinalis,  898 
classification  of,  898 
definition  of,  898 
diarrhoea  in,  900 
distribution  of,  898 
emaciation  in,  900 
treatment  of,   900 
Struma,  749 

colloid,  749 
Strumitis,  echinococcic.  749 
parasitic,  749 


Strumitis,  syphiHtic,  749 

traumatic,  749 

tuberculous,  749 
StriimpeH's  family  type  of  lateral  sclerosis, 

Sudamina  in  miliary  fever,  357 

in  typhoid  fever,  31 
Suffocative  catarrh,  acute,  400,  402 
Sunstroke,   1080 

definition  of,  1080 

diagnosis  of,  1081 

etiology  of,  1080 

morbid  anatomy  of,  1081 

pathology  of,  1081 

prognosis  in,  1081 

symptoms  of,  1081 

treatment  of,   1082 

hydrotherapeutic,  1082 
venesection  in,  1082 
Suppression  of  urine,  737 
Suppuration  of  kidney  in  septicsemia,  195 
Suppurative  hsematitis,  780 

inflammation  of  bile-ducts,  673 

pancreatitis,  688 

pyelonephritis,  726 

pylephlebitis,  666 
Suprarenal  glands,  diseases  of,  760 
Surgical  emphysema,  413 

kidney,  727 

scarlet  fever,  102 
Sweating  sickness,  356 
Sydenham's   chorea,    1043.      See  Chorea 

iXLinor. 
Symmetrical  stricture  of  oesophagus,  561 
Syncope  in  pneumothorax,  450 
Syphilis,  276 

acquired,  276 

anajmia  in,  284 

arteritis  in,  281 

of  bones,  286 

of  brain  and  spinal  cord,  285,  286 

chancre  of,  280,  283,  284 

condylomata  in,  284 

definition  of,  276 

diagnosis  of,  286 

distribution  of,  276 

etiology  of,  277 

frequenc.y  of,  279 

gummata  in,  281 

headache  in,  285 

heart  changes  in,  281 

hereditary,  276,  286,  289 
epiphysitis  in,  286 
eruptions  in,  286 
Hutchinson  teeth  in,  286 
mucous  patches  in,  286 
rhinitis  in,  286 
symptoms  of,  286 

iritis  in,  284 

lesions  of,  primary,  280 
secondarv,  280 
tertiary,  "280 

of  liver,  281 

of  lungs,  281 

macular  syphilide  in,  284 


1126 

Syphilis,  morbid  anatomy  of,  280 

mucous  patches  in,  284,  286 

of  nervous  sj^stem,  283,  285 

neuroretinitis  in,  285 

paralyses  in,  285 

pathology  of,  280 

prevention  of,  279 

prognosis  of,  286 

roseola  in,  283 

skin  eruptions  in,  283 

stages  of,  276,  280 

symptoms  of,  283 

transmission  of,  277,  278 

treatment  of,  286 
Syphilitic  alopecia,  284 

arteritis,  281 

cirrhosis  of  liver,  664 

condylomata,  284 

dactylitis,  286 

epiphysitis,  286 

eruptions,  283 

gummata,  281,  284 

infantilism,  286 

iritis,  284 

keratitis,  286 

laryngitis,  376 

lymph  nodes,  283 

marasmus,  286 

nephritis,  281 

phthisis,  282 

rhinitis,  286 

spastic  spinal  paralysis,  980 

strumitis,  749 
Syringomyelia,  988 

claw-hand  in,  989 

definition  of,  988 

diagnosis  of,  989 

etiology  of,  988 

history  of,  988 

morbid  anatomy  of,  988 

pathology  of,  988 

prognosis  in,  990 

symptoms  of,  989 

treatment  of,  990 


TABES  of  brain,  952 
miesenterica,  300 
Tache  blenatre  in  typhoid  fever,  32 

cerebrale  in  typhoid  fever,  32 
Tachycardia,  521 

in  exophthalmic  goitre,  753 

in  hysteria,  1050 
Taenia  confusa,  901 

cucumerina,  903 

echinococcus,  901 

medio  canellata,  901 

nana,  901 

saginata,  901 

solium,  901 
Tapeworm,  900 

dog,  double-pored,  901 

dwarf,  901 

Russian,  901 

symptoms  of,  903 


INDEX 


Tapeworm,  treatment  of,  904 
Tapping  in  pleurisy  with  effusion,  441 
Teeth  in  syphihs,  286 
Telegraphers'  cramp,  1072 
Teratoma  of  mediastinum,  453 
Tertian  parasite  of  malarial  fever,  865 
Testicle,  tuberculosis  of,  338 
Test,  Widal,  in  typhoid  fever,  48 
Test-meal  in  gastric  cancer,  593 
Tests  for  albumin  in  urine,  742 

blood,  in  diabetes  mellitus,  798 

for  sugar  in  urine,  799 
Tetanilla,  1064 
Tetanus,  267 

bacillus  of,  267 

definition  of,  267 

diagnosis  of,  269 

from  hysteria,  269 

from  strychnine  poisoning,  269 

from  tetany,  269 

distribution  of,  267 

emprosthotonos  in,  269 

etiology  of,  267 

frequency  of,  267 

head,  271 

kopf-,  271 

"lock-jaw"  in,  269 

morbid  anatomy  of,  268 

muscular  rigidity  in,  268 

opisthotonos  in,  269 

pain  in,  269 

pathology  of,  268 

prevention  of,  268 

prognosis  of,  269 

risus  sardonicus  in,  269 

spasm  of  diaphragm  in,  269 
of  glottis  in,  269 

symptoms  of,  268 

treatment  of,  270 
antitoxin,  270 
Tetany,  1064 

Chvostek's  sign  of,   1065 

diagnosis  of,  1065 

from  Jacksonian  epilepsy,  1065 
from  hysteria,  1065 

Erb's  sign  of,  1065 

etiology  of,  1064 

gastric,  575 

Chvostek's  sign  in,  576 
Erb's  sign  in,  576 
Trousseau's  sign  in,  575 

Hoffmann's  sign  of,  1065 

morbid  anatomy  of,  1064 

pathology  of,   1064 

prognosis  in,  1065 

in  status  lymphaticus,  771 

symptoms  of,  1064 

treatment  of,  1065 

Trousseau's  sign  of,  1065 
svmptom  of,   1065 
Thermic  fever,  1080 
Thomson's  disease,  1038 
Thread-worm,  885 
Three-day  fever,   131 
Thrombosis,  cerebral,  913 


INDEX 


1127 


Thrombosis  in  croupous  pneumonia,  162 
of  portal  vein,  666 
in  typhoid  fever,  35 
venous,  in  croupous  pneumonia,  162 
sinuses,  946 

etiology  of,  946 
morbid  anatomy  of,  946 
pathology  of,  946 
prognosis  of,  946 
symptoms  of,  946 
treatment  of,  946 
Thrush,  547,     See  Stomatitis,  parasitic. 
Thymus  gland,  diseases  of,  772 
Thyreocele,  749 

Thyroid  gland,  adenoma  of,  751 
carcinoma  of,  751 
carcinosarcoma  of,  751 
diseases  of,  749 
endothelioma  of,  751 
sarcoma  of,  751 
swelling  of,  750 
tuberculosis  of,  343 
tumors  of,  751 
Tic  convulsif,  1027 
Tick  fever,  354 

albuminuria  in,  355 
definition  of,  354 
diagnosis  of,  355 
etiology  of,  354 
fever  in,  355 
prognosis  of,  356 
pyroplasma  hominis  in,  354 
rash  in,  355 
symptoms  of,  355 
treatment  of,  356 
Tinnitus,  1028 
Tongue,  eczema  of,  549 

treatment  of,  550 
geographical,  549 
smokers',  550 

strawberry,  in  scarlet  fever,  104 
Tonsillitis,  acute,  556 

definition  of,  556 
diffuse,  556 
endocarditis  in,  557 
etiology  of,  556 
follicular,  556 
forms  of,  556 
morbid  anatomy  of,  557 
pathology  of,  557 
symptoms  of,  557 
treatment  of,  558 
hypertrophic,  chronic,  558 

barrel-shaped  chest  in,  559 
definition  of,  558 
funnel  chest  in,  559 
mouth  breathing  in,  559 
pigeon-breast  in,  559 
symptoms  of,  559 
treatment  of,  559 
Tonsils,  diseases  of,  556 
tuberculosis  of,  334 
TorticoUis,  1033 
Toxic  gastrectasis,  578 
gastritis,  acute,  565 


Tracheotomy  in  acute  catarrhal  laryngitis^ 
371 
in  oedematous  laryngitis,  374 
Transverse  myelitis,  983 
Traumatic  abscess  of  liver,  653 
neuroses,  1070 
strumitis,  749 
Trematodes,  904 

definition  of,  904 
"Trembles"  in  cattle,  352 
Tremor  in  exophthalmic  goitre,  754 

in  paralysis  agitans,  1041 
Trichina  spiralis,  885 
Trichiniasis,  885 

diagnosis  of,  887 
etiology  of,  885 
morbid  anatomy  of,  886 
pathology  of,  886 
prognosis  in,  887 
symptoms  of,  887 
treatment  of,  887 
Trichocephalus  dispar,  900 
Trichomonas  hominis,  909 

vaginalis,  909 
Tricophyton,  909 
Tricuspid  regurgitation,  513 
definition  of,  513 
diagnosis  of,  514 
etiology  of,  513 
pathology  of,  513 
physical  signs  of,  514 
prognosis  in,  515 
symptoms  of,  514 
stenosis,  515 

diagnosis  of,  515 
Trifacial  nerve,  paralysis  of,  1020 

symptoms  of,  1020 
Trilocular  heart,  527 
Trip-hammer  pulse  in  aortic  regurgitation, 

511 
Trommer's  test  for  sugar  in  urine,  799 
Tropical  abscess  of  liver,  654 
adenitis,  226 
bubo,  226 
chlorosis,  888 
splenomegaly,  883 
Trousseau's  sign  in  gastric  tetany,  575 

of  tetany,   1065 
Trypanosoma  fever,  880 

treatment  of,  881 
Trypanosomata,  varieties  of,  879 
Trypanosomiasis,  879 
definition  of,  879 
human,   880 
Tubercle,  295 
of  brain,  932 
miliary,  295 
Tuberculin  treatment  of  tuberculosis,  332 
Tuberculosis,  290 

miliary,  acute,  297 

bacillus  in,  297 
diagnosis  of,  298 
prognosis  of,  299 
symptoms  of,  297 
treatment  of,  299 


1128 


INDEX 


Tuberciilosis  in  Addison's  disease,  760 
of  alimentary  canal,  334 
bacillus  of,  290 
of  bladder,  340 

diagnosis  of,  340 

symptoms  of,  340 

treatment  of,  341 
bovine,  291 
of  brain,  343 
of  csecum,  336 
of  cervical  glands,  300 
chronic  hyperplastic,  296 
definition  of,  290 
etiology  of,  290 
of  Fallopian  tubes,  342 
frequency  of,  293 
of  genitourinarv  svstem,  338 
glandular,  299- 

signs  of,  300 

treatment  of,  300 
of  heart,  343 
of  intestine,  335 

chronic  hyperplastic,  336 

prognosis  in,  337 

symptoms  of,  338 

treatment  of,  337 
of  kidneys,  341 

acute,  341 

chronic,  341 

hydronephrosis  in,  342 

pyonephrosis  in,  342 

sj'mptoms  of,  342 
of  hver,  338 

of  mediastinal  glands,  300 
meningeal,  acute,  301 

diagnosis  of,  302 

from    acute    meningitis, 

302 
from  cerebrospinal  men- 
ingitis, 302 
symptoms  of,  301 
of  mesenteric  glands,  300 
mode  of  infection  in,  290 
morbid  anatomy  of,  295 
mortality  of,  294 
of  myocardium,  343 
of  oesophagus,  334 
of  ovaries,  342 
pathology  of,  295 
of  pericardium,  304 

symptoms  of,  304 
of  peritoneum,  304 

acute  miliary,  305 

caseous  type  of,  306 

chronic  fibroid,  306 
s3^mptoms  of,  306 
of  pharynx,  334 
of  pleura,   303 

lesions  in,  303 
pneumonic,  acute,  diagnosis  of,  318 

physical  signs  of,  318 
predisposing  causes  of,  291,  292 
prevention  of,  293 
pulmonary,  309 

amphoric  breathing  in,  319 


Tuberculosis,     pulmonary,      bacillus      of, 
method  of  staining,  322 
caseation  in,  310 
cavities  in,  311 
complications  of,  316 
"cracked-pot  sound"  in,  319 
diagnosis  of,  318 

fluoroscope  in,  321 

microscopic,   322 

tuberculin  in,  321 
hsemoptysis  in,  316 

prognosis  of,  324 

treatnient  of,  333 
hemorrhage  in,  316 
infiltration  of  Laennec  in,  310 
lesions  in,  309 
metallic  tinkling  in,  319 
mode  of  infection  in,  309 
pectoriloquj'  in,  319 
phj^sical  signs  of,  318 
pneumothorax  in,  318 
prognosis  in,  323 
pulmonary  osteoarthropathy,  318 
reparation  in,  312 
symptoms  of,  314 

cough,   316 

dyspnoea,  316 

fever,  314,  315 

larjmgeal,  314 

loss  of  weight,  315 

sputum,  315,  316 

sweating,  315 
treatment  of,  324 

antistreptococcic     serum     in, 
332 

bronchitis  in,  330 

climatic,  326 

cough,  331 

diet  in,  324 

exercise  in,  326 

fever,  330 

medicinal,  329 

night-sweats,  330 

out-door  life  in,  326 

serum,  331 

special  symptoms,  330 

tuberculin  in,  332 
types  of,  309 

caseating,  309,  310 

chronic,  309 

fibroid,   309,  312 

miliary,  309 

ulceratiA-e,  309 
vascular  changes  in,  310 
vomiting  in,  treatment  of,  333 
of  rectum,  336 
of  retroperitoneal  glands,  300 
of  serous  membranes,  301 

acute,  301 

chronic,  301 

treatment  of,  308 
of  spinal  cord,  343 
of  stomach,  335 
of  testicle,  338 

diagnosis  of,  339 


INDEX 


1129 


Tuberculosis  of  testicle,  symptoms  of,  339 
treatment  of,  339 
of  thyroid  gland 
of  tonsils,  334 

of  uterus,  342 
Tuberculous  laryngitis,  375 
leprosy,  348 
pleurisy,  303 
strumitis,   749 

vegetative  endocarditis,  343 
Tubular  nephritis,  chronic,  704 
Tumors  of  bowel  as  cause  of  obstruction, 
624 
of  brain  and  its  membranes,  932 
of  kidney,  732 
of  liver,  668 
in  lungs,  428 
of  mediastinum,  452 
of  pancreas,  695 
of  thyroid  gland,  751 
Tungau,  911 
Tunnel  ansemia,  888 
disease,  887 

St,  Gothard's,  887 
Tiirck's  gyromele  in  gastric  dilatation,  575 
Tympanites,  639 

in  croupous  pneumonia,  154 
in  typhoid  fever,  28,  40 
treatment  of,  57 
Tympany  in  acute  peritonitis,  644 
Typhoid  fever,  17 

albuminuria  in,  41 
anaemia  in,  34 
antisepsis  in,  56 
appendicitis  in,  30,  39 
arthritis  in,  44 
atypical  forms  of,  30 
bacillus  of,  17 

in  blood,  25 
bathing  in,  53 
bed-sores  in,  33 

treatment  of,  58 
blood  in,  34 

bloodvessels,  lesions  of,  in,  35 
boils  in,  34 

bone  complications  in,  44 
Brand  bath  in,  53 

contraindications  to,  53 
cardiac  failure  in,  35 
in  children,  30 
chills  in,  30,  32 
cholecystitis  in,  40 
cholelithiasis  in,  41 
circulatory  complications  in,  34 
cold  in,   52 
coma  vigil  in,  43 
complicating  pregnancy,  45 
complications  of,  34,  35 
constipation  in,  27 

treatment  of,  56 
convulsions  in,  44 
cystitis  in,  42 
definition  of,  17 
delirium  in,  28,  30 
delusions  in,  43 


Typhoid  feA^er,  diagnosis  of,  45 
diarrhoea  in,  27,  30,  36 

treatment  of,  56 
diazo  reaction  of  urine  in,  50 
diet  in,  54 
differentiation    of,    from    other 

fevers,  46,  47 
disinfection  of  discharges  in,  18 
dislocation  of  hip  in,  spontaneous, 

44 
distribution  of,  17 
Ehrlich's  reaction  in,  50 
embolism  in,  35 
embryocardia  in,  34 
empyema  in,  43 
endarteritis  in,  26 
epididymitis  in,  42 
erysipelas  in,  34 
etiolog}^  of,   17 
facial  expression  in,  27 
frequency  of,  21 
gangrene  in,  33 

gastric  ulcer  in,  36 
genitourinary  complications  in,  41 
headache  in,  27,  30 
heart  clot  in,  35 

muscle  in,  changes  in,  26 

sounds  in,  34 
hemiplegia  in,  44 
hemorrhage  in,  30,  36 

diagnosis  of,  36 

symptoms  of,  36 

treatment  of,  57 
hepatic  complications  in,  40 
herpes  in,   32 
history  of,  17 
hydrotherapy  in,  52 
hypostatic  congestion  of  lung  in, 

42 
incubation  of,  27 
infarction  of  lung  in,  42 
insomnia  in,  27 

treatment  of,  58 
jaundice  in,  40 
joint  complications  in,  44 
kidneys  in,  26 
laryngeal  ulceration  in,  42 
leukocytosis  in,  34 
liver  in,  26,  40 
medicines  in,  55 
meningitis  in,  43,  44 
mesenteric  nodes  in,  25 
mixed  infection  in,  32 
mode  of  infection  in,  18 
morbid  anatomy  of,  23 
mortality  of,  22 
muscle,  complications  in,  44 
muscular  tremors  in,  28 
myocarditis  in,  35 
myositis  in,  45 
nephritis  in,  41 
nervous  complications  of,  43 
neuritis  in,  44 
nose-bleed  in,  26 
oesophagitis  in,  35 


1130 


INDEX 


Typhoid  fever,  oesophagus  in,  ulceration  of, 
35 
orchitis  in,  42 
osteomyeUtis  in,  44 
otitis  media,  acute,  in,  44 
^  parotitis  in,  35 

pathology  of,  23 
peliomata  in,  32 
pericarditis  in,  34 
perforation  in,  37 

diagnosis  of,  38 

signs  of,  38 

treatment  of,  58 
peritonitis  in,  38 

diagnosis  of,  38 
petechias  in,  34 
pharyngitis  in,  35 
phlebitis  in,  35 
pleurisy  in,  43 
pneumonia  in,  30,  42 
polyuria  in,  42 
prevention  of,  18 
preventive  inoculation  in,  20 
prognosis  of,  51 
pulmonary  abscess  in,  42 
pulse  in,  27 
pyuria  in,  42 
recrudescence  in,  31 
renal  disease,  acute,  in,  30 
respiratory  complications  in,  42 

lesions  in,  26 
rose  spots  in,  28 
sequelae  in,  34 
skin  changes  in,  32 
splenic  enlargement  in,  25,  27 
stimulants  in,  55 
stools  in,  36 
stupor  in,  28 
sudamina  in,  32 
symptoms  of,  27 
tache  blendtre  in,  32 

cerebrate  in,  32 
temperature  in,  27,  31 
tests  in,  48 
thirst  in,  27 
thrombosis  in,  35 
tongue  in,  27 
treatment  of,  52 

during  convalescence,  59 

medicinal,  55 

special  symptoms,  56 
tympanites  in,  28,  40 

treatment  of,  57 
typhoid  spine  in,  44 
ulcer  in,  23,  24 
vomiting  in,  36 

treatment  of,  56 
Widal's  test  in,  48 
Typhus  fever,  61 

chill  in,  63 
complications  of,  65 
definition  of,  61 
delirium  in,  64 
diagnosis  of,  65 
distribution  of,  61 


Typhus  fever,  eruption  in,  63,  64 

etiology  of,  62 

fever  in,  63 

hepatic  changes  in,  63 

history  of,  61 

hypostatic  congestion  of  lungs  in, 
63 

intestinal  lesions  in,  03 

kidneys  in,  63 

morbid  anatomy  of,  63 

myocarditis  in,  63 

pathology  of,  63 

petechias  in,  64 

prevention  of,  63 

prognosis  of,  66 

pulse  in,  64 

relapses  in,  65 

retention  of  urine  in,  67 

spleen  in,  64 

termination  of,  65 

treatment  of,  66 
siderans,  64 
Tyrotoxicon,  857 
Tyrotoxismus,  857 


ULCER,  duodenal,  628 
diagnosis  of,  630 

from  acute  fat-necrosis,  631 
from  gallstone  colic,  631 
from  gastric  ulcer,  630 
from    intestinal    obstruction, 
631 
etiology  of,  628 
hemorrhage  in,  630 
morbid  anatomy  of,  629 
pathology  of,  629 
perforation  in,  629 

symptoms  of,  630 
prognosis  in,  631 
symptoms  of,  629 
treatment  of,  632 
gastric,  579.     See  Gastric  ulcer. 

in  typhoid  fever,  36 
intestinal,  in  paratyphoid  fever,  59 
peptic,  579 
perforating,    of   foot,    in   locomotor 

ataxia,  964 
of  stomach,  579 
Ulceration,  laryngeal,  in  typhoid  fever,  42 

of  oesophagus  in  typhoid  fe^•er,  35 
Ulcerative  appendicitis,  617 
endocarditis,  485 
pharyngitis,  554 
stomatitis,  546 
Ulcus  ventriculi,  579 
Uncinaria  Americana,  888 

duodenale,  886 
Uncinariasis,  887 
ansemia  in,  890 
Charcot-Leyden  crystals  in,  890 
definition  of,  887 
diagnosis  of,  891 
etiology  of,  888 
frequency  of,  888 


INDEX 


1131 


Uncinariasis,  morbid  anatomy  of,  890 

pathology  of,  890 

prophylaxis  of,  889 

symptoms  of,  890 

treatment  of,  892 
Undulant  fever,  245 
Uraemia,  720 

amaurosis  in,  722 

convulsive  type  of,  721 

definition  of,  720 

diagnosis  of,  723 

from  heatstroke,   723 
from  opium  poisoning,  723 

etiology  of,  720 

hemiplegia  in,  722 

insomnia  in,  722 

latent,  722 

mania  in,  722 

monoplegia  in,  722 

odor  in,  722 

paralytic  form  of,  722 

pathology  of,  720 

prognosis  in,  723 

symptoms  of,  721 

treatment  of,  hot  pack  in,  724 
TJrsemic  apoplexy,  923 
Uric  acid  diathesis,  746 
Urinary  secretion,  disorders  of,  737 
Urine  acetone  in,  tests  for,  799,  800 

in  acute  diffuse  nephritis,  701 1 

albumin  in,  741 
tests  for,  742 

albumose  in,  746 

in  beriberi,  256 

blood  in,  738 

in  cholelithiasis,  679 

in  chronic  interstitial  nephritis,  712 
parenchymatous   nephritis,    706 

chyle  in,  744 

in  croupous  pneumonia,  153 

in  diabetes  insipidus,  807 
mellitus,  795 

haemoglobin  in,  739 

indican  in,  745 

melanin  in,  746 

oxalates  in,  745 

phosphates  in,  745 

pus  in,  744 

in  renal  calculus,  735 

in  rheumatic  fever,  acute,  199 

in  smallpox,  77 

sugar  in,  tests  for,  799 

suppression  of,  737 

in  scarlet  fever,  101 
uric  acid  in,  746 
in  yellow  fever,  216 
Urticaria  in  acute  rheumatic  fever,  201 
Uterus,  tuberculosis  of,  342 


VACCINATION,  88 
method  of,  88 
in  smallpox,  73,  88 
Vaccine  lymph,  glycerinated,  89 
Vaccinia,  88 


Vaccinia  in  man,  primary,  89 

secondary,  89 
^^agus  nerve,  disease  of,   1030 
Valvular  endocarditis,  482 
Varicella,  90 

definition  of,  90 

diagnosis  of,  92 

from  smallpox,  92 

eruption  in,  91 

erysipelas  in,  92 

etiology  of,  90 

incubation  in,  90 

nephritis  in,  92 

prognosis  in,  92 

symptoms  of,  90 

treatment  of,  92 
Varicose  aneurysm,  534 

groin  glands  in  filariasis,  896 
Variola,  70.     See  Smallpox. 

fulminans,  81 

pustulosa  hemorrhagica,  81 
Varioloid,  82 
Vascular  goitre,  749 

Venesection  in  pulmonary  emphysema,  419 
Venous  sinuses,  thrombosis  of,  946 

thrombosis   in    croupous    pneumonia, 
162 
Ver  macaque,  912 
Verrucous  endocarditis,  482 
Verruga,  360 

definition  of,  360 

distribution  of,  360 

etiology  of,  361 

incubation  of,  361 

joints  in,  361 

Peruviana,  360 

prognosis  in,  362 

symptoms  of,  361 

treatment  of,  362 
Vertebrae,  disease  of,  993 
diagnosis  of,  994 
prognosis  in,  994 
symptoms  of,  994 
treatment  of,  994 

malignant  growths  of,  994 
Vertigo,  1029 

in  brain  tumor,  933 
Vesical  crises  in  locomotor  ataxia,  962 

tuberculosis,  340 
Vesicular  stomatitis,  546 
Violinists'  cramp,  1072 
Visceroptosis,  632 
Visual  tract,  1016 
Volvulus,  627 

prognosis  of,  627 

symptoms  of,  627 

treatment  of,  627 
Vomiting,  cyclic,  607 

Von  Graefe's  sign  in  exophthalmic  goitre, 
753 


WATER-HAMMER  pulse  in  aortic  re- 
gurgitation, 511 
infection  by,  in  typhoid  fever,  18 


^ 


1132 


INDEX 


Weber's  syndrome  in  brain  tumor,  934 

Weil's  disease,  352 

Weisses  blut,  780 

Westphal's  symptom  in  locomotor  ataxia, 

961 
Wet  brain,  846 
Whipworm,  900 
White  flux,  242 
Whooping-cough,   119 

amblyopia  in,  122 

bacillus  pertussis  Eppendorf  in,  119 

bronchopneumonia  in,  122 

conjunctival  hemorrhages  in,  122 

complications  of,   122 

definition  of,  119 

diagnosis  of,   123 

distribution  of,  119 

duration  of,  121 

emphysema  in,  122 

etiology  of,  119 

frequency  of,   119 

glandular  enlargement  in,  122 

incubation  in,  120 

in  measles,   113 

morbid  anatomj^  of,  120 

mortality  in,  123 

paralysis  in,   122 

paroxysm  of,   120 

pathology  of,   120 

physical  signs  in,  121 

pneumothorax  in,   122 

prognosis  in,  123 

symptoms  of,  120 

treatment  of,  123 

bronchitis  tent  in,  123 

vomiting  in,   122 
Widal  test  in  typhoid  fever,  48 
Winckel's  disease,  786 
"Wooden  tongue,"  274 
Wool-sorters'  disease,  257 
Word  blindness,  931 

deafness,  931 
Worm,  beef-,  901 

guinea-,  896 

hook-,  888 

Medina,  896 

pin-,  885 

pork-,  901 

ring-,  909 

round-,  884 

screw-,  911 


Worm,  seat-,  885 

thread-,  885 

whip-,  900 
Wounds  of  heart,  481 
Wrist-drop  in  lead  poisoning,  853 
Writers'  cramp,  1072 
Wryneck,   1033 

congenital,   1033 

spasmodic,  1033 

spurious,   1034 


X 
Y 


EROSTOMIA,  551 


AWS,  358 

Yellow  atrophy  of  liver,  acute,  670 
fever,  212 

albuminuria  in,  216 

apoplectiform  type  of,  216 
.  blood  in,  214 

cardiac  changes  in,  214 

convulsions  in,  215 

definition  of,  212 

diagnosis  of,  217 

from  dengue,  217 

from   malarial   hsemoglo- 

binuric  fever,  217 
from   pernicious  malarial 
fever  217 

etiology  of,  212 

gastric  changes  in,  215 

hsematemesis  in,  605 

headache  in,  215 

intermittent  changes  in,  216' 

jaundice  in,  216 

morbid  anatomy  of,  214 

mortality  of,  217 

nephritic  changes  in,  215 

pain  in,  215 

pathology  of,  214 

prevention  of,  212 

prognosis  of,  217 

prophylaxis  of,  214 

remission  in,  215,  216 

respiration  in,  215 

sj^mptoms  of,  215 

tongue  in,  216 

treatment  of,  218 

urine  in,  216 

vomiting  in,  216 


% 


7 


Cv>'\ 


!    ! 


